荧光原位杂交技术在尿路上皮癌及前列腺癌的临床研究
|
摘要
荧光原位杂交技术(fluorescence in situ hybridization, FISH)是20世纪80年代末在已有放射性原位杂交技术基础上发展起来的一种非放射性分子细胞遗传学技术。采用荧光素直接标记DNA制备探针,根据探针与被检测样本中序列的碱基互补配对,通过荧光显微镜观察细胞内的荧光信号来判断有无染色体数目和结构的改变。由于其操作简单、安全有效、具有很好的特异性和灵敏性的特点,适于临床医学检测。目前,已广泛用于遗传疾病的诊断及血液肿瘤、实体肿瘤等方面的检测。近年来,随着分子遗传学的迅猛发展,研究发现了尿路上皮癌、前列腺癌中一些常发生、高特异性的染色体畸变,为FISH技术应用于这些泌尿生殖系肿瘤的检测奠定了理论基础。本研究分为三个部分,分别探讨FISH技术在上尿路尿路上皮癌、膀胱尿路上皮癌和前列腺癌的临床应用价值。
目的探索在中国人群中3号、7号、17号染色体及p16位点异常与膀胱尿路上皮癌发生、发展的关系。评估FISH诊断膀胱尿路上皮癌的可行性和有效性及对术后随访的临床应用价值。
方法分别对100例膀胱尿路上皮癌患者和30例非尿路上皮癌对照人群的新鲜尿液,进行尿脱落细胞学检查及FISH检测3号、7号及17号染色体、9号染色体p16位点异常,比较两种方法的敏感性和特异性。统计分析各染色体畸变与肿瘤数目、大小、既往复发率、临床分期及病理分级等临床参数的相关性。对66例非肌层浸润性膀胱癌术后三个月的膀胱冲洗液进行FISH检测,根据随访结果分析FISH在监测膀胱癌复发的作用。
结果FISH和细胞学两种检测方法诊断膀胱尿路上皮癌的敏感性分别为82%和36%,有显著性差异(p<0.001)；特异性分别为97%和100%,差异无统计学意义(p>0.05)。各染色体多倍性畸变率分别为63%(3)、72%(7)、31%(p16)、60%(17)；单体畸变率为53%(3)、49%(7)、47%(p16)、46%(17)；基因纯合性缺失仅见于p16位点为34%。各染色体畸变与患者的肿瘤数目、大小、既往复发率均未见显著相关性(p>0.05)；17号染色体多倍性畸变率与肿瘤分期、分级呈正相关性(p<0.05)；其余类型的染色体畸变与肿瘤分期、分级无明显相关性P>0.05)。根据术后平均随访22个月的结果,23例非肌层浸润性膀胱癌患者术后复发,FISH阳性患者术后复发率为54%,阴性患者复发率为13%,差异有显著统计学意义(p<0.001),术后FISH阴性患者无复发生存率明显优于FISH阳性患者。
结论FISH诊断膀胱尿路上皮癌具有较高的特异性和敏感性,可望成为早期诊断和术后监测膀胱癌复发有效、安全的检查方法。
目的探讨通过FISH检测3、7、17号染色体及P16位点畸变诊断上尿路上皮癌的可行性和有效性。
方法分别对29例上尿路上皮癌患者和20例非尿路上皮癌对照人群的新鲜尿液,进行尿脱落细胞学检查及FISH检测3号、7号及17号染色体、9号染色体p16位点异常,比较两种方法的敏感性和特异性。并对FISH诊断膀胱尿路上皮癌和上尿路上皮癌进行比较。
结果FISH和细胞学两种检测方法诊断膀胱尿路上皮癌的敏感性分别为90%和48%,有显著性差异(p<0.05)；特异性均为100%。FISH诊断膀胱尿路上皮癌和上尿路上皮癌的敏感性分别为82%和90%,差异无统计学意义(p>0.05)。
结论FISH用于检测上尿路移行细胞癌的敏感性高于细胞学检查,而特异性无差异。FISH技术有可能成为诊断和鉴别诊断上尿路尿路上皮癌可靠、无创的诊断方法。
目的探索在中国人群中TMPRSS2基因和ETS基因家族中ERG、ETV1、ETV4基因融合的遗传学改变与前列腺癌发生、发展的关系。评估FISH诊断和鉴别诊断前列腺癌的临床应用价值。
方法：分别对20例良性前列腺增生(BPH)、5例重度上皮内瘤样病变(HGPIN)和53例前列腺癌(Pca)石蜡切片进行FISH检测TMPRSS2基因和ERG、TV1、ETV4基因融合现象,比较不同前列腺疾病发生基因融合的情况。分析前列腺癌标本中ERG基因改变和Gleason评分、PSA、临床分期之间的关系。
结果在53例前列腺癌标本中32例(60%)检测到ERG基因改变,提示TMPRSS2/ERG融合基因,5例(9%)检测到TMPRSS2/ETV1融合基因,1例(2%)检测到ERG基因改变。5例高级别上皮内瘤样病变标本中检测到1例(20%)发生了ERG基因改变。20例良性前列腺增生标本未检测到基因融合现象。FISH诊断前列腺癌的敏感性为72%,特异性为96%。ERG基因改变与前列腺癌Gleason评分、临床分期呈正相关(p<0.05),与PSA水平无明显相关性(p>0.05)。
结论FISH诊断前列腺癌具有较高的特异性和敏感性,有助于前列腺癌的诊断和鉴别诊断。TMPRSS2基因和ETS家族基因的基因融合有助于前列腺癌的病因研究和探索,对后期治疗及预后有指导作用。
Fluorescence in situ hybridization(FISH) is a kind of technology of non-radioactive in situ Hybridization, which was deVeloped on the basis of radioactiVe hybridization in the later 1980s. The fluorescence molecules were labeled to genetic material to obtain the probes. Probes have the ability to selectively block target gene according to base-pair complementary, and then the quantity and structure change of the hybridized chromosome could be observed by the fluorescence signal under fluorescence microscope. Because of the advantages of simple operation, safety, effective, high security and specificity, fluorescence in situ hybridization has widely been used in the detection of genetic disease, hematological malignancy, solid tumor and so on. With the rapid development of molecular genetics, some specific chromosome aberrat-ions have been often found in urothelial cell carcinoma and prostate cancer, laying theoretical foundation for the application of fluorescence in situ hybridizatio in urogenital cancers. This study is divided into three parts and the clinical application of fluorescence in situ hybridizatio in bladder urothelial carcinomas, upper tract urothelial carcinomas or prostate cancer was evaluated in this study respectively.
Purpose To research the relations between aberrations of chromosome 3,7,17, p16 and bladder urothelial carcinoma, by the fluorescence in situ hybridization. To assess the clinical utility of fluorescence in situ hybridization as a non-invasive method in the diagnosis and postoperative follow-up of bladder urothelial carcinoma in Chinese group.
Methods Urine samples of both 100 patients with bladder urothelial carcinoma and 30 non-cancer controls were analyzed by means of cytology and fluorescence in situ hybridization. Fluorescence in situ hybridization were used to detect the abnormalities of chromosome 3, 7,17 and p16. We compared the sensitivity and specificity between fluorescence in situ hybridization and cytology and analyzed whether the rates of abnormalities in chromosome 3,7,17, p16 have significant associations with tumor size, tumor number recurrence, clinical and pathologic tumor stages statistically. Bladder washings collected from 66 patients with non-muscle invasive bladder urothelial carcinomas three months after operation were analyzed by the fluorescence in situ hybridization to assess the role of fluorescence in situ hybridization in surveillance of recurring bladder cancer.
Result The sensitivity of fluorescence in situ hybridization and cytology was 82% and 36%, and fluorescence in situ hybridization was significantly more sensitive than cytology (p< 0.001). The specificity of fluorescence in situ hybridization and cytology was 96%and 100%, and there was no significant difference between the two groups(p>0.05). The polysomic aberration rates were 63%(3),72%(7),31%(p16),60%(17); the monosomic aberration rates 53%(3),49%(7),47%(p16),46%(17); 34% presented a homozygous deletion of chromosome 9p21. There were no associations between abnormalities of chromosomes and tumor size, tumor number recurrence(p>0.05). The polysomic aberration rates of chromosome 17 were significantly associated with clinical and pathologic tumor stages(p< 0.05), while the other patterns of Chromosome aberrations were not(p>0.05). After a median follow-up of 22 months, 23 patients with non-muscle invasive bladder urothelial carcinomas developed tumor recurrence. The recurrence rate was significantly higher in patients with positive results of fluorescence in situ hybridization (54%) than in patients with negative results(13%) (p<0.001).
Conclusions Fluorescence in situ hybridization assay of chromosomes 3,7,17 and p16 is an effective method to detect bladder urothelial carcinomas with with high sensitivity and specificity. FISH might contribute to not only an effective and invasive diagnostic approach to bladder urothelial carcinomas, but also an available tool for predicting tumor recurrence.
Purpose To evaluate the possibility and validity of detecting the aberrations of chromosome 3,7,17and p16 by fluorescence in situ hybridization in order to diagnose upper tract urothelial carcinoma.
Methods Urine samples of both 23 patients with upper tract urothelial carcinomas and 20 patients without urothelial carcinomas served as control group were analyzed by means of cytology and fluorescence in situ hybridization. The mixtures of fluorescent labeled probes to the centromeres of chromosomes 3,7 and 17, and p16 were used to detect chromosomal abnormalities. Sensitivity and specificity of both methods were determined and cpmpared.The utility of FISH in upper tract urothelial carcinomas were compared to the utility in bladder urothelial carcinomas through statistical analysis.
Result The sensitivity of fluorescence in situ hybridization and cytology was 90% and 48%, fluorescence in situ hybridization was significantly more sensitive than cytology (p<0.001). The specificity of both methods wae 100%. The sensitivities of fluorescence in situ hybridization were no significant difference between upper tract urothelial carcinoma and bladder urothelial carcinoma.
Conclusions The sensitivity of fluorescence in situ hybridization for the detection of upper tract urothelial carcinomas is superior than that of cytology whilst maintaining a similar specificity, fluorescence in situ hybridization might become a very useful tool in the diagnosis and differential diagnosis of upper tract urothelial carcinoma.
Purpose To research the relations between fushion of TMPRSS2 and ETS transcription factor genes (ERG, ETV1, ETV4) and prostater caner, by the fluorescence in situ hybridization. To assess the clinical utility of fluorescence in situ hybridization in the diagnosis and differential diagnosis of prostater caner in Chinese group.
Methods The prostate specimens including 53 prostate cancers,20 benign prostatic hyperplasias (BPH),5 high grade prostatic intrae-pithelial neoplasias (HGPIN) were separetely analyzed by means of fluorescence in situ hybridization to assess the gene fushions indiative of malignancy. The relationship between aberration of ERG gene and Gleason's scores, PSA and clinical stage was analysed respectively.
Result Of 53 prostate cancer specimens,TMPRSS2/ERG fusion was detected in 32cases(60%); TMPRSS2/ETV1 fusion was detected in 5 cases(9%) and TMPRSS2/ETV1 fusion in 1 case(2%). 1case(20%) of HGPIN was detected with aberration of ERG gene. None of the three types of gene fushion was detected in all 20 cases of BPH. The sensitivity and specificity of FISH for the detection of prostate cancer was 72% and 96%. Aberration of ERG gene in prostate cancer was significantly associated with Gleason's scores and pathological stage(p<0.05), while not associated with PSA(p>0.05).
Conclusions Fluorescence in situ hybridization assay is an effective method to detect prostate cancer with high sensitivity and specificity, contributing to improving the current diagnosis and differential diagnosis of prostate cancer. The gene fushions of TMPRSS2 and ETS transcription factor genes could be a new approach for the study on etiology of prostate cancer, and an important direction in treatment and prediction of the prognosis.
目的探索在中国人群中3号、7号、17号染色体及p16位点异常与膀胱尿路上皮癌发生、发展的关系。评估FISH诊断膀胱尿路上皮癌的可行性和有效性及对术后随访的临床应用价值。
方法分别对100例膀胱尿路上皮癌患者和30例非尿路上皮癌对照人群的新鲜尿液,进行尿脱落细胞学检查及FISH检测3号、7号及17号染色体、9号染色体p16位点异常,比较两种方法的敏感性和特异性。统计分析各染色体畸变与肿瘤数目、大小、既往复发率、临床分期及病理分级等临床参数的相关性。对66例非肌层浸润性膀胱癌术后三个月的膀胱冲洗液进行FISH检测,根据随访结果分析FISH在监测膀胱癌复发的作用。
结果FISH和细胞学两种检测方法诊断膀胱尿路上皮癌的敏感性分别为82%和36%,有显著性差异(p<0.001)；特异性分别为97%和100%,差异无统计学意义(p>0.05)。各染色体多倍性畸变率分别为63%(3)、72%(7)、31%(p16)、60%(17)；单体畸变率为53%(3)、49%(7)、47%(p16)、46%(17)；基因纯合性缺失仅见于p16位点为34%。各染色体畸变与患者的肿瘤数目、大小、既往复发率均未见显著相关性(p>0.05)；17号染色体多倍性畸变率与肿瘤分期、分级呈正相关性(p<0.05)；其余类型的染色体畸变与肿瘤分期、分级无明显相关性P>0.05)。根据术后平均随访22个月的结果,23例非肌层浸润性膀胱癌患者术后复发,FISH阳性患者术后复发率为54%,阴性患者复发率为13%,差异有显著统计学意义(p<0.001),术后FISH阴性患者无复发生存率明显优于FISH阳性患者。
结论FISH诊断膀胱尿路上皮癌具有较高的特异性和敏感性,可望成为早期诊断和术后监测膀胱癌复发有效、安全的检查方法。
目的探讨通过FISH检测3、7、17号染色体及P16位点畸变诊断上尿路上皮癌的可行性和有效性。
方法分别对29例上尿路上皮癌患者和20例非尿路上皮癌对照人群的新鲜尿液,进行尿脱落细胞学检查及FISH检测3号、7号及17号染色体、9号染色体p16位点异常,比较两种方法的敏感性和特异性。并对FISH诊断膀胱尿路上皮癌和上尿路上皮癌进行比较。
结果FISH和细胞学两种检测方法诊断膀胱尿路上皮癌的敏感性分别为90%和48%,有显著性差异(p<0.05)；特异性均为100%。FISH诊断膀胱尿路上皮癌和上尿路上皮癌的敏感性分别为82%和90%,差异无统计学意义(p>0.05)。
结论FISH用于检测上尿路移行细胞癌的敏感性高于细胞学检查,而特异性无差异。FISH技术有可能成为诊断和鉴别诊断上尿路尿路上皮癌可靠、无创的诊断方法。
目的探索在中国人群中TMPRSS2基因和ETS基因家族中ERG、ETV1、ETV4基因融合的遗传学改变与前列腺癌发生、发展的关系。评估FISH诊断和鉴别诊断前列腺癌的临床应用价值。
方法：分别对20例良性前列腺增生(BPH)、5例重度上皮内瘤样病变(HGPIN)和53例前列腺癌(Pca)石蜡切片进行FISH检测TMPRSS2基因和ERG、TV1、ETV4基因融合现象,比较不同前列腺疾病发生基因融合的情况。分析前列腺癌标本中ERG基因改变和Gleason评分、PSA、临床分期之间的关系。
结果在53例前列腺癌标本中32例(60%)检测到ERG基因改变,提示TMPRSS2/ERG融合基因,5例(9%)检测到TMPRSS2/ETV1融合基因,1例(2%)检测到ERG基因改变。5例高级别上皮内瘤样病变标本中检测到1例(20%)发生了ERG基因改变。20例良性前列腺增生标本未检测到基因融合现象。FISH诊断前列腺癌的敏感性为72%,特异性为96%。ERG基因改变与前列腺癌Gleason评分、临床分期呈正相关(p<0.05),与PSA水平无明显相关性(p>0.05)。
结论FISH诊断前列腺癌具有较高的特异性和敏感性,有助于前列腺癌的诊断和鉴别诊断。TMPRSS2基因和ETS家族基因的基因融合有助于前列腺癌的病因研究和探索,对后期治疗及预后有指导作用。
Fluorescence in situ hybridization(FISH) is a kind of technology of non-radioactive in situ Hybridization, which was deVeloped on the basis of radioactiVe hybridization in the later 1980s. The fluorescence molecules were labeled to genetic material to obtain the probes. Probes have the ability to selectively block target gene according to base-pair complementary, and then the quantity and structure change of the hybridized chromosome could be observed by the fluorescence signal under fluorescence microscope. Because of the advantages of simple operation, safety, effective, high security and specificity, fluorescence in situ hybridization has widely been used in the detection of genetic disease, hematological malignancy, solid tumor and so on. With the rapid development of molecular genetics, some specific chromosome aberrat-ions have been often found in urothelial cell carcinoma and prostate cancer, laying theoretical foundation for the application of fluorescence in situ hybridizatio in urogenital cancers. This study is divided into three parts and the clinical application of fluorescence in situ hybridizatio in bladder urothelial carcinomas, upper tract urothelial carcinomas or prostate cancer was evaluated in this study respectively.
Purpose To research the relations between aberrations of chromosome 3,7,17, p16 and bladder urothelial carcinoma, by the fluorescence in situ hybridization. To assess the clinical utility of fluorescence in situ hybridization as a non-invasive method in the diagnosis and postoperative follow-up of bladder urothelial carcinoma in Chinese group.
Methods Urine samples of both 100 patients with bladder urothelial carcinoma and 30 non-cancer controls were analyzed by means of cytology and fluorescence in situ hybridization. Fluorescence in situ hybridization were used to detect the abnormalities of chromosome 3, 7,17 and p16. We compared the sensitivity and specificity between fluorescence in situ hybridization and cytology and analyzed whether the rates of abnormalities in chromosome 3,7,17, p16 have significant associations with tumor size, tumor number recurrence, clinical and pathologic tumor stages statistically. Bladder washings collected from 66 patients with non-muscle invasive bladder urothelial carcinomas three months after operation were analyzed by the fluorescence in situ hybridization to assess the role of fluorescence in situ hybridization in surveillance of recurring bladder cancer.
Result The sensitivity of fluorescence in situ hybridization and cytology was 82% and 36%, and fluorescence in situ hybridization was significantly more sensitive than cytology (p< 0.001). The specificity of fluorescence in situ hybridization and cytology was 96%and 100%, and there was no significant difference between the two groups(p>0.05). The polysomic aberration rates were 63%(3),72%(7),31%(p16),60%(17); the monosomic aberration rates 53%(3),49%(7),47%(p16),46%(17); 34% presented a homozygous deletion of chromosome 9p21. There were no associations between abnormalities of chromosomes and tumor size, tumor number recurrence(p>0.05). The polysomic aberration rates of chromosome 17 were significantly associated with clinical and pathologic tumor stages(p< 0.05), while the other patterns of Chromosome aberrations were not(p>0.05). After a median follow-up of 22 months, 23 patients with non-muscle invasive bladder urothelial carcinomas developed tumor recurrence. The recurrence rate was significantly higher in patients with positive results of fluorescence in situ hybridization (54%) than in patients with negative results(13%) (p<0.001).
Conclusions Fluorescence in situ hybridization assay of chromosomes 3,7,17 and p16 is an effective method to detect bladder urothelial carcinomas with with high sensitivity and specificity. FISH might contribute to not only an effective and invasive diagnostic approach to bladder urothelial carcinomas, but also an available tool for predicting tumor recurrence.
Purpose To evaluate the possibility and validity of detecting the aberrations of chromosome 3,7,17and p16 by fluorescence in situ hybridization in order to diagnose upper tract urothelial carcinoma.
Methods Urine samples of both 23 patients with upper tract urothelial carcinomas and 20 patients without urothelial carcinomas served as control group were analyzed by means of cytology and fluorescence in situ hybridization. The mixtures of fluorescent labeled probes to the centromeres of chromosomes 3,7 and 17, and p16 were used to detect chromosomal abnormalities. Sensitivity and specificity of both methods were determined and cpmpared.The utility of FISH in upper tract urothelial carcinomas were compared to the utility in bladder urothelial carcinomas through statistical analysis.
Result The sensitivity of fluorescence in situ hybridization and cytology was 90% and 48%, fluorescence in situ hybridization was significantly more sensitive than cytology (p<0.001). The specificity of both methods wae 100%. The sensitivities of fluorescence in situ hybridization were no significant difference between upper tract urothelial carcinoma and bladder urothelial carcinoma.
Conclusions The sensitivity of fluorescence in situ hybridization for the detection of upper tract urothelial carcinomas is superior than that of cytology whilst maintaining a similar specificity, fluorescence in situ hybridization might become a very useful tool in the diagnosis and differential diagnosis of upper tract urothelial carcinoma.
Purpose To research the relations between fushion of TMPRSS2 and ETS transcription factor genes (ERG, ETV1, ETV4) and prostater caner, by the fluorescence in situ hybridization. To assess the clinical utility of fluorescence in situ hybridization in the diagnosis and differential diagnosis of prostater caner in Chinese group.
Methods The prostate specimens including 53 prostate cancers,20 benign prostatic hyperplasias (BPH),5 high grade prostatic intrae-pithelial neoplasias (HGPIN) were separetely analyzed by means of fluorescence in situ hybridization to assess the gene fushions indiative of malignancy. The relationship between aberration of ERG gene and Gleason's scores, PSA and clinical stage was analysed respectively.
Result Of 53 prostate cancer specimens,TMPRSS2/ERG fusion was detected in 32cases(60%); TMPRSS2/ETV1 fusion was detected in 5 cases(9%) and TMPRSS2/ETV1 fusion in 1 case(2%). 1case(20%) of HGPIN was detected with aberration of ERG gene. None of the three types of gene fushion was detected in all 20 cases of BPH. The sensitivity and specificity of FISH for the detection of prostate cancer was 72% and 96%. Aberration of ERG gene in prostate cancer was significantly associated with Gleason's scores and pathological stage(p<0.05), while not associated with PSA(p>0.05).
Conclusions Fluorescence in situ hybridization assay is an effective method to detect prostate cancer with high sensitivity and specificity, contributing to improving the current diagnosis and differential diagnosis of prostate cancer. The gene fushions of TMPRSS2 and ETS transcription factor genes could be a new approach for the study on etiology of prostate cancer, and an important direction in treatment and prediction of the prognosis.
引文
[1]Nowell PC, Hungerford DA. Chromosome studies on normal and leukemic human leukocytes. J Natl Cancer Inst,1960,25:85-109.
[2]Lissens W, Sermon K, Preimplantation genetic diagnosis:current status and new developments. J J Human Reproduction,1997:2:1756-1761.
[3]Goldman JM, Druker BJ. Chronic myeloid leukemia:current treatment options. Blood,2002,99(8):3070-3071.
[4]Schrock E, du Manior S, Veldman T, et al. Multicolor spectral karyotyping othuman chromosome. Science,1996,273:494-497.
[5]Lan C, Liu JM, Liu TW, et al. ErbB2 amplification by fluorescence in situ hybridization in breast cancer specimens read as 2+in immunohistochemical analysis. Am J Clin Pathol,2005,124(1):97-102.
[6]Veeramachaneni R, Nordberg ML, Shi R, et al. Evaluation of fluorescence in situ hybridization as an ancillary tool to urine cytology in diagnosing urothelial carcinoma. Diagn Cytopathol,2003,28:301-307.
[7]Kumar A, Kumar R, Gupta NP. Comparison of NMP22 BladderChek Test and Urine Cytology for the Detection of Recurrent Bladder Cancer. Jpn J Ciin Oncol, 2006,36(3):172-175.
[8]Fadl-Elmula I, Oorunova L, Mandahl N, et al. Cytogenetic analysis of upper Urinary tract transitional cell carcinomas. Cancer Genet Cytogenet,1999,115: 123-127.
[9]Tomlins SA, Rhodes DR, Perner S, et al.. Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer. Science,2005,310:644-648.
[10]Sakai I, Miyake H, Harada K, et al. Analysis of factors predicting intravesical recurrence of superficial transitional cell carcinoma of the bladder without concomitant carcinoma in situ.Int J Urol,2006,13(11):1389-1392.
[11]Akagashi K, Tanda H, Kato S, et al. Int J Urol. Recurrence pattern for superficial bladder cancer,2006,13(6):686-691.
[12]Nguyen CT, Litt DB, Dolar SE, et al. Prognostic significance of nondiagnostic molecular changes in urine detected by UroVysion fluorescence in situ hybridization during surveillance for bladder cancer. Urology,2009,3(2): 347-350.
[13]Lokeshwar VB, Schroeder GL, Selzer MG, et al. Bladder tumor markers for monitoring recurrence and screening comparison of hyaluronic acid-hyaluronidase and BTA-Stat tests. Cancer,2002,95(1):61-72.
[14]Toma MI, Barak V, Hautmann SH, et al. Comparison of the Immunocyt test and urinary cytology with other urine tests in the detection and surveillance of bladder cancer. World J Urol,2004,22:145-149.
[15]Lokeshwar VB, Habuchi T, Grossman HB, et al. Bladder tumor markers beyond cytology:International Consensus Panel on bladder tumor markers. Urology, 2005,66(6 Suppl1):35-63.
[16]Friedrich MG, Toma MI, Hellstern A, et al. Comparison of multitarget fluorescence in situ hybridization in urine with other noninvasive tests for detecting bladder cancer. BJU Int,2003,92:911-914.
[17]Laudadio J, Keane TE, Reeves HM, et al. Fluorescence in situ hybridization for detecting transitional cell carcinoma:implications for clinical practice. BJU Int, 2005,96(9):1280-1285.
[18]Cordon CC. Molecular alterations in bladder cancer.Cancer. Surv,1998,32:115-131.
[19]Sandberg AA, Berger Cs. Review of chromo some studies in urological tumors. Cytogenetics and molecular genetics of bladder cancer. J Urol,1994,151(3): 545-560.
[20]Sokolova IA, Halling KC, Jenkins RB, et al. The development of a multitarget,multicolor fluo-rescence in situ hybridization assay for the detection of urothelial carcinoma in urine. J Mol Diagn,2000,2(3):116-123.
[21]Sauter G, Gasser T C, Moch H, et al. DNA aberrations in urinary bladder cancer detected by flow cytometry and FISH.Urol Res,1997,25(1):S37-S43.
[22]Michael F,Sarosdy MF,Schellhammer P,et al.Clinical evaluation of multi-target fluorescent in situ hybridization assay for detection of bladder cancer. J Urol, 2002,168(5):1950-1954.
[23]Lotan YRoehrbom CG Sensitivity and specificity of commonly available bladder tumor markers versus cytology; results of a comprehensive literature review and mcta-analyscs. Urology,2003,61:109-118.
[24]KonetyBK, Getzenberg RH.Urine based markers ofurological malignancy.J Urol, 2001,165:600-611.
[25]Kwak kw, Kim SH, Lee HM, et al.The Utility of Fluorescence In Situ Hybridization for Detection of Bladder Urothelial Carcinoma in Routine Clinical Practice. J Korean Med Sci,2009,24:1139-1144.
[26]Sarosdy MF, Kahn PR, Ziffer MD, et al.Use of a multitarget fluorescence in situ hybridization assay to diagnose bladder cancer in patients with hematuria. J Urol, 2006,176(1):44-47.
[27]Sanchez-Carbayo M, Urrutia M, Gonzalez de Buitrago JM, et al.Utility of serial urinary tumor markers to individualize intervals beteewn cystoscopies in the monitoring of patients with bladder carcinoma. Cancer,2001,92:2820-2828.
[28]Jones JS. DNA-based molecular cytology for bladder cancer surveillance. Urology,2006,67:35-45.
[29]Bubendorf L, Grilli B. UroVysion multiprobe FISH in urinary cytology. Methods Mol Med,2004,97:117-131.
[30]Michael F, Sarosdy, Paul R, et al. Use of a Multitarget Fluorescence In Situ Hybridization Assay to Diagnose Bladder Cancer in Patients With Hematuria. J Urol,2006,176:44-47.
[31]Placer J, Espinet B, Salido M, et al.Correlation between histologic findings and cytology abnormalities in bladder carcinoma;a FISH study. J Urol,2005,65: 913-918.
[32]Vecchione A, Sevignani C, Giarnieri E, et al. Inactivation of the FHIT gene favors bladder cancer development. Clin Cancer Res,2004,10(22):7607-7612.
[33]Mhawech-Fauceglia P, Fischer G, Beck A, et al. RAF.1,Aurora-A/STK15 and E-codherin biomarkers expression in patients with pTa/PT 1 urothelial bladder carcinoma; a retrospective TMA study of 246 patients with long-term follow-up. Eur Surg Ongol,2006,32:439-444.
[34]Krause FS, Rauch A, Schrott KM, et al. Clinical decisions for treatment of different staged bladder cancer based on multitarget fluorescence in situ hybridization assays? World J Urol,2006,24:418-422.
[35]Li M, Zhang ZF, Reuter VE, et al. Chromosome 3 allelic losses and microsatellite alterantions in transitional cell carcinoma of the urinary bladder. Am J Pathol 1996,149:229-235.
[36]Wada T, Louhelainen J, Hemminki K, et al. The prevalence of loss of heterozygosity in chromosome 3, including FHIT, in bladder cancer, using the
fluorescent multiplex polymerase chain reaction. BJU Int.2001,87(9):876-881.
[37]Jorissen RN, Walker F, Pouliot N, et al. Epidermal growth factor receptor: mechanisms of activation and Signaling. Exp Cell Res,2003,284(1):31-32.
[38]Colquhoun AJ, Mellon J K. Epidermal growth factor receptor and bladder cancer. Postgrad Med J,2002,78(924):584-589.
[39]Sokolova IA, Hailing KC, Jenkins RB, et al. The development of a multitarget, multicolor fluorescence in situ hybridization assay for detection of urothelial carcinoma in urine. Mol Diagn,2000,2:116-123.
[40]Bollmann M.Heller H.Bankfalvi A, et al. Quantitative molecular urinary cytology by fluorescence in situ hybridization.a tool for tailoring surveillance of patients with superficial bladder cancer BJU Int,2005,95 (9):1219-1225.
[41]Wolman SR, Goldman B, Slovak ML, et al. Aneusomy for detection of bladder cancer recurrence:a Southwest Oncology Group study. Cancer Genet Cytogenet, 2007,176(1):22-27.
[42]Rocco JW,Sidransky D. pl6(MTS-1/CDKN2/INK4a) in cancer progressionExp Cell Res,2001,264(1):42-55.
[43]Wheeless LL,Reeder JE,Han XY,et al.Bladder irrigation specimens assayed by fluorescence in situ hybridization to interphase nucleus. Cytometry,1994,1: 319-326.
[44]Balazs M,Carroll P,Kerschmann 1L et al.Frequent homozygous deletion of cyclin-dependent kinase inhibitor 2(MTS1,p 16)in superficial bladder cancer detected by fluorescence in situ hybridization. Genes Chromosomes Cancer. 1997,19:84-89.
[45]Yurakh A 0, Ramos D, Calabuig FS,et al.Molecular and immunohistochenmical analysis of the prognostic value of cell-cycle regulators in urothlial neoplasmas of the bladder.Eur Urol,2006,50(3):506-515.
[46]Kruger S, Mess F, Bohle A,et al. Numerical aberrations of chromosome 17 and the 9p21 locus are independent predictors of tumor recurrence in non-invasive transitional cell carcinoma of the urinary bladder. Int J Oncol.2003,23(1): 41-48.
[47]Gallucci M,Guadagni F,Marzano R,et al.Status of the p53,p16,RBI,and HER-2 genes and chromosomes 3,7,9,and 17 in advanced bladder cancer:correlation with adjacent mucosa and pathological parameters. J Clin Pathol,2005,58(4): 367-371.
[48]Kwak KW,Kim SH,Lee HM,et al.The utility of fluorescence in situ hybridization for detection of bladder urothelial carcinoma in routine clinical practice. J Korean Med Sci,2009,24(6):1139-1144.
[49]Bubendorf L, Grilli B, Sauter G, et al. Multiprobe FISH for enhanced detection of bladder cancer in voided urine specimens and bladder washings. Am J Clin Pathol,2001,116(1):79-86.
[50]Ribal MJ, Alcaraz A, Mengual L, et al. Chromosomal high-polysomies predict tumour progression in T1 transitional cell carcinoma of the bladder. Eur Urol, 2004,45(5):593-599.
[51]Gallucci M, Guadagni F, Marazano Ret al. Status of the p53, p16, RBI, and HER-2 genes and chromosome 3,7,9 and 17 in advanced bladder cancer: correlation with adjacent mucosa and pathological parameters. Clin Pathol,2005, 58:367-371.
[52]Winters ZE, Leck RD, Bradeburn MJ, et al. Cytoplasmic P2 express is correlted with HER-2/nuein breas tcancer and is a independent predicator of prognosis. Breast Cancer Res,2003,5(6):242-249.
[53]Gallucci M, Merola R, Leonardo C, et al. author reply 440-1.Analysis of HER2 expression in primary urinary bladder carcinoma and corresponding metastases. BJU Int,2005,95:982-986.
[54]Kastan MB, Bartek J. Cell2cycle checkpoints and cancer. Nature,2004,432 (7015):316-323.
[55]Massague J. G1 cel 12cycle control and cancer. Nature,2004,432(7015):298-306.
[56]Bernardini S, Billerey C, Martin M, et al. The predictive value of muscularis mucosae invasion and p53 over expression on progression of stage T1 bladder carcinoma. J Urol,2001,165(1):42-46.
[57]Edward M, Messing MD. Urothelial Tumors of the Urinary Tract. In: Campbell's Urology,8th ed. Walsh PC, Retik AB, Vaughan ED Jr, Wein AJ, eds. Philadelphia (PA):W. B. Saunders,2002.2732-2804.
[58]Choong NW, Quevedo JF, Kaur JS. Small cell carcinoma of urinary bladder:the Mayo Clinic experience. Cancer,2005,103:1172-1178.
[59]Schultz IJ, Kiemeney LA, Karthaus HF, et al. Survivin mRNA copy number in bladder washings predicts tumor recurrence in patients with superficial urothelial cell carcinomas. Clin Chem,2004,50(8):1425-1428.
[60]Esuvaranathan K, Chiong E, Thamboo TP, et al. Predictive value of p53 and pRb expression in superficial bladder cancer patients treated with BCG and interferon-alpha. Cancer,2007,109(6):1097-1105.
[61]Stavropoulos NE, Bouropoulos C, Ioachim IE, et al. Prognostic significance of angiogenesis in superficial bladder cancer. Int Urol Nephrol.2004,36(2): 163-167.
[62]Annamma Kurien,Joseph Thomas. Can Reflex UroVysion fluorescence in situ hybridization predict tumor recurrence during follow-up? Indian J Urol,2007, 23(3):333-334.
[63]Yoder BJ, Skacel M, Hedgepeth R, et al. Reflex UroVysion testing of bladder cancer surveillance patients with equivocal or negative urine cytology:A prospective study with focus on the natural history of anticipatory positive findings. Am J Clin Pathol,2007,127:295-301.
[64]Zellweger T, Benzl G, Cathomas G, et al. Multi-target fluorescence in situ hybridization in bladder washings for prediction of recurrent bladder cancer. Int J Cancer,2006,119:1660-1665.
[65]Bollmann M, Heller H, Bankfalvi A, et al. Quantitative molecular urinary cytology by fluorescence in situ hybridization:a tool for tailoring surveillance of patients with superficial bladder cancer? BJU Int,2005,95(9):1219-1225.
[66]Marano A, Pan Y, Li C, et al. Chromosomal numerical aberrations detected by fluorescence in situ hybridization on bladder washings from patients with bladder cancer. Eur Urol,2000,37(3):358-365.
[67]Chen GL, Bagley DH. Ureteroscopic surgery for upper tract transitional-cell carcinoma:complications and management. J Endourol,2001,15(4):399-404.
[68]Hall MC, Womack S, Sagalowsky AI, et al. Prognostic factors, recurrence, and survival in transitional cell carcinoma of the upper urinary tract:a 30-year experience in 252 patients. Urology,1998,52(4):594-601.
[69]Walsh IK, Keane PF,Ishak LM, et al. The BTA stat test:a tumor marker for the detection of upper tract transitional cell carcinoma. Urology,2001,58:532-535.
[70]Chen AA,Grasso M. Is there an role for FISH in the management and surveillance of patients with upper tract transitional-cell carcinoma? Journal of endourology,2008,2:1371-1374.
[71]Schatteman P, Chatzopoulos C, Assenmacher C, et al. Laparoscopic nephrouret-erectomy for upper urinary tract transitional cell carcinoma:Results of a belgian retrospective multicentre survey. Eur Urol,2007,51:1633-1638.
[72]Chen WJ, Kuo JY, Chen KK, et al. Primary urothelial carcinoma of the ureter: 11-year experience in Taipei Veterans General Hospital. J Chin Med Assoc.2005, 68(11):522-530.
[73]吴阶平.吴阶平泌尿外科学.济南：山东科学技术出版社,2004：417-418.
[74]Guarnizo E, Pavlovich CP, Seiba M, et al. Ureteroscopic biopsy of upper tract urothelial carcinoma:improved diagnostic accuracy and histopathological considerations using a multi-biopsy approach. J Urol,2000,163:52-55.
[75]Johnson DB, Pearle MS.Complications of ureteroscopy. Urol Clin North Am, 2004,31(1):157-171.
[76]Perez-Montiel D, Wakely PE, Hes O, et al. High-grade urothelial carcinoma of the renal pelvis:clinicopathologic study of 108 cases with emphasis on unusual morphologic variants. Mod Pathol,2006,19(4):494-503.
[77]Matsui Y, Utsunomiya N, Ichioka K, et al. Risk factors for subsequent development of bladder cancer after primary transitional cell carcinoma of the upper urinary tract.Urology,2005,65(2):279-283.
[78]Oehlschlager S, Baldauf A, Wiessner D, et al. Bladder tumor recurrence after primary surgery for transitional cell carcinoma of the upper urinary tract. Urol Int,2004,73(3):209-211.
[79]吴宏飞.现代泌尿外科诊疗指南.南京：东南大学出版社,2005：233-234.
[80]Mehra R, Tomlins SA, Shen R, et al. Comprehensive assessment of TMPRSS2 and ETS family gene aberrations in clinically localized prostate cancer. Mod Pathol,2007,20 (5):538-544.
[81]Che M, Grignon D. Pathology of prostate cancer. Cancer Metastasis Rev,2002, 21(3-4):381-395.
[82]Srigley J R. Benign mimickers of prostatic adenocarcinoma. Mod Pathol,2004, 17(3):328-348.
[83]Kusumi T, Koie T, Tanaka M, et al. Immunohistochemical detection of carcinoma in radical prostatectomy specimens following hormone therapy. Pathol Int,2008,58(11):687-694.
[84]Tomlins SA, Mehra R, Rhodes DR, et al.TMPRSS2:ETV4 gene fusions define a third molecular subtype of prostate cancer. Cancer Res,2006,66:3396-3400.
[85]Belaud-Rotureau MA, Parrens M, Dubus P, et al. A comparative analysis of FISH, RT-PCR, PCR and immunohistochemistry for the diagnosis of mantle cell lymphomas. Mod Pathol,2002,15(5):517-525.
[86]Bao F, Munker R, Lowery C, et al. Comparison of FISH and quantitative RT-PCR for the diagnosis and follow-up of BCR-ABL-positive leukemias. Mol Diagn Ther,2007,11(4):239-245.
[87]Han B, Mehra R, Dhanasekaran SM, et al. A fluorescence in situ hybridization screen for E26 transformation-specific aberrations:identification of DDX5-ETV4 fusion protein in prostate cancer. Cancer Res,2008,68(18):7629-7637.
[88]Tomlins SA, Bjartell A, Chinnaiyan AM,et al. ETS gene fusions in prostate cancer:from discovery to daily clinical practice. Eur Urol,2009,56(2):275-86.
[89]Mehra R, Han B, Tomlins SA, Heterogeneity of TMPRSS2 gene rearrangements in multifocal prostate adenocarcinoma:molecular evidence for an independent group of diseases. Cancer Res,2007,67(17):7991-7995.
[90]Hofer MD, Kuefer R, Maier C, et al.Genome-Wide Linkage Analysis of TMPRSS2-ERGFusion in Familial Prostate Cancer. Cancer Res,2009,69 (2): 640-646.
[91]Soller MJ, Isaksson M, Elfving P, etal. Confirmation of the high frequency of the TMPRSS2/ERG fusion gene in prostat cancer. Genes Chromosomes Cancer, 2006,45:717-719.
[92]Mehra R, Tomlins SA, Yu J, et al. Characterization of TMPRSS2-ETS gene aberrations in androgen-independent metastatic prostate cancer. Cancer Res, 2008,68(10):3584-3590.
[93]Perner S, Demichelis F, Beroukhim R, et al. TMPRSS2:ERG fusion-associated deletions provide insight into the heterogeneity of prostate cancer. Cancer Res, 2006,66:8337-8341.
[94]Iljin K, Wolf M, Edgren H, et al. TMPRSS2 fusions with oncogenic ETS factors in prostate cancer involve unbalanced genomic rearrangements and are associated with HDAC1 and epigenetic reprogramming. Cancer Res,2006, 66(21):10242-10246.
[95]Epstein JI, Herawi M. Prostate needle biopsies containing prostatic intraepithelial neoplasia or atypical foci suspicious for carcinoma:implications for patient care. J Urol,2006,175:820-834.
[96]Gallo F, Chiono L, Gastaldi E, et al. Prognostic significance of high-grade prostatic intraepithelial neoplasia (HGPIN):risk of prostatic cancer on repeat biopsies.Urology,2008,72(3):628-632.
[97]Mosquera JM, Perner S, Genega EM, et al. Characterization of TMPRSS2-ERG fusion high-grade prostatic intraepithelial neoplasia and potential clinical implications. Clin Cancer Res,2008,14:3380-3385.
[98]Furusato B, Gao CL, Ravindranath L, et al. Mapping of TMPRSS2-ERG fusions in the context of multi-focal prostate cancer. Mod Pathol,2008,21:67-75.
[99]Perner S, Mosquera JM, Demichelis F, et al. TMPRSS2-ERG fusion prostate cancer:an early molecular event associated with invasion. Am J Surg Pathol, 2007,31:882-888.
[100]Darnel AD, Lafargue CJ, Vollmer RT, Corcos J, Bismar TA. TMPRSS2-ERG fusion is frequently observed in Gleason pattern 3 prostate cancer in a Canadian cohort. Cancer Biol Ther,2009,8(2):125-130.
[101]Attard G, Clark J, Ambroisine L, et al. Duplication of the fusion of TMPRSS2 to ERG sequences identifies fatal human prostate cancer. Oncogene,2008,27: 253-263.
[102]Seth A, Watson DK. ETS transcription factors and their emerging roles in human cancer. Eur J Cancer,2005,41(16):2462-2478.
[103]Demichelis F, Fall K, Perner S, TMPRSS2:ERG gene fusion associated with lethal prostate cancer in a watchful waiting cohort. Oncogene,2007,26(31): 4596-4599.
[104]Petrovics G, Liu A, Shaheduzzaman S, et al. Frequent overexpression of ETS-related gene-1 (ERG1) in prostate cancer transcriptome. Oncogene,2005, 24(23):3847-3852.
[105]Attard G, Clark J, Ambroisine L, et al. Duplication of the fusion of TMPRSS2 to ERG sequences identifies fatal human prostate cancer.Oncogene,2008,27(3): 253-263.
[106]Nam RK.Sugar L.Wang Z Expression of TMPRSS2 ERG Gene Fusion in Prostate Cancer Cells is an Important Prognostic Factor for Cancer Progression.Cancer,2007,6(1):40-45.
[107]Cooperberg MR, Lubeck DP, Meng MV, et al. The changing face of low-risk prostate cancer:trends in clinical presentation and primary management. J Clin Oncol,2004,22(11):2141-2149.
[108]Perner S, Mosquera JM, Demichelis F,et al. TMPRSS-ERG fusion prostate cancer:an early molecular event associated with invasion. Am J Surg Pathol, 2007,31(6):882-888.
[109]Saramaki OR, Harjula AE, Martikainen PM, et al.TMPRSS2:ERG fusion identifies a subgroup of prostate cancers with a favorable prognosis. Clin Cancer Res,2008,14(11):3395-3400.
[1]Greenlee R,Hill-Harmon M,Murray T, et al. Cancer statistics. CA Cancer J Clin, 2001,51:15-36.
[2]Okamura T, Umemoto Y, Yasui T, et al. Noninvasive detection of alterations in chromosome numbers in urinary bladder cancer cells, using fluorescence in situ hybridization. Int J Clin Oncol,2004,9(5):373-377.
[3]Wolman SR, Goldman B, Slovak ML, et al. Aneusomy for detection of bladder cancer recurrence:a Southwest Oncology Group study. Cancer Genet Cytogenet. 2007,176(1):22-27.
[4]Mian C, Lodde M, Comploj E, et al. Multiprobe fluorescence in situ hybridisation:prognostic perspectives in superficial bladder cancer. J Clin Pathol,2006,9(9):984-987.
[5]Li M,Zhang ZF, Reuter VE, et al. Chromosome 3 allelic losses and microsatellite alterantions in transitional cell carcinoma of the urinary bladder. Am J Pathol 1996,149:229-235.
[6]Cairns P, Proctor AJ, Knowles MA. Loss of heterozygosity at the RB locus is frequent and correlates with muscle invasion in bladder carcinoma. Oncogene, 1991,6(12):2305-2309.
[7]Bart SH, GaylaO, Alan W, et al. Parsing ERK Activation Reveals quantitatively equivalent contributions from epidermal growthfactor receptor and HER2 in human mammary epithelial cells. J Biol Chem,2005,280(7):6157-6169.
[8].xu H,Yu Y,Marciniak D,et al. Epidermal growth factor receptor (EGFR)-related protein inhibits multiple members of the EGFR family in colon and breast cancer cells.Mol Cancer Ther,2005,4(3):435-442.
[9]Ding Y, Wang G, Ling MT, et al. Significance of Id-1 up-regulation and its association with EGFR in bladder cancer cell invasion. Int J Oncol.2006,28(4): 847-854.
[10]Mason RA, Morlock EV, Karagas MR, et al. EGFR pathway polymorphisms and bladder cancer susceptibility and prognosis. Carcinogenesis,2009,30(7): 1155-1160.
[11]Nguyen PL, Swanson PE, Jaszcz W, et al:Expression of epidermal growth factor receptor in invasive transitional cell carcinoma of the urinary bladder:a multivariate survival analysis. Am J Clin Pathol,1994,101:166-176.
[12]Mellon K, Wright C, Kelly P, et al. Long-term outcome related to epidermal growth factor receptor status in bladder cancer. J Urol,1995,153:919-925.
[13]Ravery V, Grignon D, Angulo J, et al:Evaluation of epidermal growth factor receptor, transforming growth factor and c-erbB2, epidermal growth factor and c-erbB2 in the progression of invasive bladder cancer. Urol Res,1997,25:9-17.
[14]Wester K, Sjostrom A, de la Torre M,et al. HER-2--a possible target for therapy of metastatic urinary bladder carcinoma. Acta Oncol.2002,41(3):282-288.
[15]Sato K, Moriyama M, Mori S, et al. An immunohistologic evaluation of C-erbB-2 gene product in patients with urinary bladder carcinoma. Cancer,1992, 70:2493-2498.
[16]Kruger S, Weitsch G, Buttner H, et al. Overexpression of c-erbB-2 oncoprotein in muscle-invasive bladder carcinoma:relationship with gene amplification, clinicopathological parameters and prognostic outcome. Int J Oncol,2002.21: 981-987.
[17]Chow NH, Chan SH, Tzai TS,Expression profiles of ErbB family receptors and prognosis in primary transitional cell carcinoma of the urinary bladder, Clin Cancer Res.2001,7(7):1957-1962.
[18]Jimenez RE, Hussain M, Bianco FJ Jr, et al:Her-2/neu overexpression in muscle-invasive urothelial carcinoma of the bladder:prognostic significance and comparative analysis in primary and metastatic tumors. Clin Cancer Res,2001, 7:2440-2447.
[19]Eissa S, Ali HS, Al Tonsi AH, et al. HER2/neu expression in bladder cancer: relationship to cell cycle kinetics. Clin Biochem,2005,38(2):142-148.
[20]Gandour-Edwards R, Lara PN Jr, Folkins AK, et al. Does HER2/neu expression provide prognostic information in patients with advanced urothelial carcinoma? Cancer,2002,95:1009-1015.
[21]Hemann M T, Bric A,Teruya-Feldstein J,et al. Evasion of the p53 tumour surveillance network by tumour-derived MYC mutants. Nature,2005, 436(7052):787-789.
[22]Shachaf C M,Felsher D W.Tumor dormancy and MYC inactivation:pushing cancer to the brink of normalcy.Cancer Res,2005,65(11):4471-4474.
[23]Lipponen PK. Expression of c-myc protein is related to cell proliferation and expression of growth factor receptors in transitional cell bladder cancer. J Pathol, 1995,175:203-210.
[24]Schmitz-Drager BJ, Schulz WA, Jurgens B, et al. c-myc in bladder cancer: clinical findings and analysis of mechanism. Urol Res,1997,25(1):45-49.
[25]Zaharieva B, Simon R, Ruiz C, et al. High-throughput tissue microarray analysis of CMYC amplificationin urinary bladder cancer. Int J Cancer, 2005,117(6):952-956.
[26]Karoui M, Hofmann R H, Zimmermann U, et al. No evidence of somatic FGFR3 mutation in various types of carcinoma. Oneogene,2001,20:5059-5061.
[27]Pollock PM, Gartside MG, Dejeza LC, et al. Frequent activating FGFR2 mutations in endometrial carcinomas parallel germline mutations associated with craniosynostosis and skeletal dysplasia syndromes.Oncogene,2007,26(50): 7158-7162.
[28]Cappellen D, De Oliveira C, Ricol D, et al. Frequent activating mutations of FGFR3 in human bladder and cervix carcinomas. Nat Genet,1999,23:18-20.
[29]Kimura T, Suzuki H, Ohashi T, et al. The incidence of thanatophoric dysplasia mutations in FGFR3 gene is higher in low-grade or superficial bladder carcinomas. Cancer,2001,92(10):2555-2561.
[30]Van Rhijn BW, Lurkin I, Radvanyi F, et al:The fibroblast growth factor receptor 3 (FGFR3) mutation is a strong indicator of superficial bladder cancer with low recurrence rate. Cancer Res,2001,61,1265-1268.
[31]Kompier LC, van der Aa MN, Lurkin I, et al. The development of multiple bladder tumour recurrences in relation to the FGFR3 mutation status of the primary tumour. J Pathol,2009,218(1):104-112.
[32]Ohashi H, Takagi H, Oh H, et al. Phosphatidylinositol 3-kinase/Akt regulates angiotensin II-induced inhibition of apoptosis in microvascular endothelial cells by governing survivin expression and suppression of caspase-3 activity. Circ Res,2004,94(6):785-793.
[33]Ambrosini G, Adida C, Altieri DC. A novel anti-apoptosis gene survivirl, expressed in cancer and lymphoma. J Nat Med,1997,3(8):917-921.
[34]Schultz IJ, Kiemeney LA, Willems JL, et al. Clin Chem. Survivin and MKI67 mRNA expression in bladder washings of patients with superficial urothelial cell carcinoma correlate with tumor stage and grade but do not predict tumor recurrence.2006,52(7):1440-1442.
[35]Shariat SF, Ashfaq R, Karakiewicz PI, et al. Survivin expression is associated with bladder cancer presence, stage, progression, and mortality. Cancer.2007, 109(6):1106-1113.
[36]Weiss C, von Romer F, Capalbo G, et al. Survivin expression as a predictive marker for local control in patients with high-risk T1 bladder cancer treated with transurethral resection and radiochemotherapy. Int J Radiat Oncol Biol Phys, 2009,74(5):1455-1460.
[37]Knowles MA, and Williamson M:Mutation of H-ras is infrequent in bladder cancer:confirmation by single-strand conformation polymorphism analysis, designed restriction fragment length polymorphisms, and direct sequencing. Cancer Res,1993,53:133-139.
[38]Fontana D, Bellina M, Scoffone C, et al:Evaluation of c-ras oncogene product (p21) in superficial bladder cancer. Eur Urol,1996,29:470-476.
[39]Ye DW, Zheng JF, Qian SX, et al. Correlation between the expression of oncogenes ras and c-erbB-2 and the biological behavior of bladder tumors. Urol Res,1993,21:39-43.
[40]Xu M, Jin Y L. The abnormal expression of retinoic acid receptor-beta,p53 and Ki67 protein in normal, premalignant esoph ageal tissue. Word J Gastroenterol, 2002,8:200-202.
[41]Kaur P, Kallakury B S, Sheehan C E, et al. Survivin and Bel-2 expressioon in prostatic adenocarcinomas. Arch Pathol Lab Med,2004,128:39-43.
[42]Esrig D, Elmajian D, Groshen S, Accumulation of nuclear p53 and tumor progression in bladder cancer. N Engl J Med.1994,331(19):1259-1264.
[43]Slaton JW, Benedict WF, Dinney CP. P53 in bladder cancer:mechanism of action, prognostic value, and target for therapy. Urology,2001,57(5):852-859.
[44]Schroeder JC, Conway K, Li Y, et al. p53 mutations in bladder cancer:evidence for exogenous versus endogenous risk factors. Cancer Res,2003,63(21): 7530-7538.
[45]Salinas-Sanchez AS, Lorenzo-Romero JG, Gimenez-Bachs JM, et al. Implications of p53 gene mutations on patient survival in transitional cell carcinoma of the bladder:a long-term study. Urol Oncol,2008,26(6):620-626.
[46]Malats N, Bustos A, Nascimento CM, et al. P53 as a prognostic marker for bladder cancer:a meta-analysis and review. Lancet Oncol,2005,6(9):678-686.
[47]Moonen PM, Balken-Ory B, Kiemeney LA, et al. Prognostic value of p53 for high risk superficial bladder cancer with long-term followup. J Urol,2007, 177(1):80-83.
[48]Elhefnawy ND, Shoeib M. evaluation of retinoblastoma gene product (RB) as a prognstic indicator in bladder carcinoma. J Egy Nat.2001,13:185-190.
[49]Logothetis CJ, Xu HJ, Ro JY, et al. Altered expression of retinoblastoma protein and known prognostic variables in locally advanced bladder cancer, J Natl Cancer, Inst,1992,84:1256-1261.
[50]Grossman HB, Liebert M, Antelo M, et al. p53 and RB expression predict progression in T1 bladder cancer. Clin Cancer Res,1998,4:829-834.
[51]Davies MA, Koul D, Dhesi H, et al. Regulation of AKT/PKB action, cellular growth, and apoptosis in rostate carcinoma cells by MMAC/PTEN. Cancer Res, 1999,59 (11):2551-2560.
[52]Aveyard J S, Skilleter A, Habuchi T, et al. Somatic mutation of PTEN in bladder carcinoma. Br J Cancer,1999,80:904-908.
[53]Tanaka M, Koul D, Davies MA, et al. MMACI/PTEN inhibits cell growth and induces chemosensitivity to doxorubicin in human bladder cancer cells. Oncogene,2000,19 (47):5406-5412.
[54]Kagi D, Vignaux F, Ledermann B, et al. Fas and perforin pathways as major mechanisms of T cell-mediated cytotoxicity. Science,1994,265(5171):528-530.
[55]Kim KS. Multifunctional role of Fas-associated death domain protein in apoptosis. J Biochem Mol Biol,2002,35(1):1-6.
[56]Chopin D,Barei-Moniri R,Maille P, et al. Human urinary bladder transitional cell carcinomas acquire the functional Fas ligand during tumor progression. Am J Pathol.2003,162(4):1139-1149.
[57]Sudarshan S, Holman DH, Hyer ML, et al. In vitro efficacy of Fas ligand gene therapy for the treatment of bladder cancer. Cancer Gene Ther.2005, 12(1):12-18.
[58]Inoue K, Kamada M, Slaton JW, Fukata S, et al. The prognostic value of angiogenesis and metastasis-related genes for progression of transitional cell carcinoma of the renal pelvis and ureter. Clin Cancer Res,2002,8(6):1863-1870.
[59]Stavropoulos NE, Bouropoulos C, Ioachim IE, et al. Int Urol Nephrol. Prognostic significance of angiogenesis in superficial bladder cancer.2004,36 (2):163-167.
[60]Streeter EH, Harris AL. Angiogenesis in bladder cancer--prognostic marker and target for future therapy. Surg Oncol,2002,11(1-2):85-100.
[61]Al-Abbasi DS, Al-Janabi AA, Al-Toriahi KM, et al. Expression of VEGF in urinary bladder transitional cell carcinoma in an Iraqi population subjected to depleted uranium:an immunohistochemical study. Appl Immunohistochem Mol Morphol.2009,17(4):307-311.
[62]Palmero Marti JL, Queipo Zaragoza JA, Ruiz Cerda JL, et al. Study of the angiogenesis as prognostic factor of pTl G3 bladder tumours. Actas Urol Esp, 2004,28:594-601.
[63]Stavropoulos N E, Bouropoulos C, Ioachim IE, et al. Prognostic significance of angiogenesis in superficial bladder cancer. Int Urol Nephrol,2004,36 (2):163-167.
[64]Tanaka K, Sonoo H, Kurebayashi J, et al. Inhibition of infiltration and angiogenesis by thrombospondin-1 in papillary thyroid carcinoma, Clin Cancer Res.2002,8(5):1125-1131.
[65]Kwak C, lin C, Lee C, et al, Thrombospondin-1, vascular endothelial growth factor expression and their relationship with p53 status in prostate cancer and benign prostatic hyperplasia, BJU Int,2002,89(3):1303-309.
[66]Goddard JC, Sutton CD, Jones JL, et al. Reduced thrombospondin-1 at presentation predicts disease progression in superficial bladder cancer. Eur Urol, 2002,42(5):464-468.
[67]Mohseni H, Zaslau S, McFadden D, et al. COX-2 inhibition demonstrates potent anti-proliferative effects on bladder cancer in vitro. J Surg Res,2004,119(2):138-42.
[68]Shirahama T, Arima J, Akiba S,et al. Relation between cyclooxygenase-2 expression and tumor invasiveness and patient survival in transitional cell carcinoma of the urinary bladder. Cancer.2001,92(1):188-193.
[69]Choi EM, Kwak SJ, Kim YM,et al. COX-2 inhibits anoikis by activation of the PI-3K/Akt pathway in human bladder cancer cells. Exp Mol Med,2005,37(3):199-203.
[70]Marinho A, Soares R, Ferro J, et al. Angiogenesis in breast cancer is related to age but not to other prognostic parameters. Pathol Res Pract,1997,193(4): 267-273.
[71]Stavropoulos NE, Bouropoulos C, Ioachim E, et al. Prognostic significance of thymidine phosphorylase in superficial bladder carcinoma. Int Urol Nephrol, 2005,37(1):55-60.
[72]Shimabukuro T, Matsuyama H, Baba Y, et al. Expression of thymidine phosphorylase in human superficial bladder cancer. Int J Urol,2005,12(1):29-34.
[73]Migaldi M, Sgambato A, Garagnani L, et al. Loss of p21Wafl expression is a strong predictor of reduced survival in primary superficial bladder cancers. Clin Cancer Res,2000,6:3131-3138.
[74]Shariat SF, Tokunaga H, Zhou J, p53, p21, pRB, and p16 expression predict clinical outcome in cystectomy with bladder cancer. J Clin Oncol.2004, 22(6):1014-1024.
[75]Stein JP, Ginsberg DA, Grossfeld GD, et al:Effect of p21WAF1/CIP1 expression on tumor progression in bladder cancer. J Natl Cancer Inst,1998,90: 1072-1079.
[76]Sui L, Dong Y, Watanabe Y, et al. Clinical significance of Skp2 expression, alone and combined with Jabl and p27 in epithelial ovarian tumom. Oncol Rep, 2006,15(4):765-771.
[77]Franke KH, Miklosi M, Goebell P, Cyclin-dependent kinase inhibitor P27(KIP1) is expressed preferentially in early stages of urothelial carcinoma. Urology,2000, 56(4):689-695.
[78]Burton PB, Anderson CJ, Corbishly CM. Caspase 3 and p27 as predictors of invasive bladder cancer. N Engl J Med,2000,343(19):1418-1420.
[79]Munoz E, Gomez F, Paz JI, et aL. Ki-67 immunolabeling in pre-malignant lesions and carcinoma of the prostate. Histologic correlation and prognostic evaluation. Eur J Histochem,2003,47(2):123-128.
[80]Santos L, Amaro T, Costa C, et al. Ki-67 index enhances the prognostic accuracy of the urothelial superficial bladder carcinoma risk group classification. Int J Cancer,2003,105:267-272.
[81]Wu TT, Chen JH, Lee YH, et al:The role of bcl-2, p53 and ki-67 index in predicting tumor recurrence for low grade superficial transitional cell bladder carcinoma. J Urol,2000,163:758-760,.
[82]Stavropoulos NE, Filiadis I, Ioachim E, et al:Prognostic significance of p53, bcl-2 and Ki-67 in high risk superficial bladder cancer. Anticancer Res,2002,22: 3759-3764.
[83]Gontero P, Casetta G, Zitella A, et al:Evaluation of P53 protein overexpression, Ki67 proliferative activity and mitotic index as markers of tumour recurrence in superficial transitional cell carcinoma of the bladder. Eur Urol,2000,38: 287-296,.
[84]Pfister C, Moore L, Allard P, et al:Predictive value of cell cycle markers p53, MDM2, p21, and Ki-67 in superficial bladder tumor recurrence. Clin Cancer Res,1999,5:4079-4084.
[85]Li Z, Hromehak R, Bloch A. Differendal expression of proteins regularting cell cycle progression in growth vs.differentiation. Bioehim Biophys Acts,1997, 1356(2):149-159.
[86]Sgambato A, Migaldi M,Faraglia B,et al:Cyclin Dl expression in papillary superficial bladder cancer:its association with other cell cycle-associated proteins, cell proliferation and clinical outcome. Int J Cancer,2002,97:671-678.
[87]Richter J, Wagner U, Kononen J, et al.High-throughput tissue microarray analysis of cyclin E gene amplification and overexpression in urinary bladder cancer. Am J Patho,2000,157:787-794.
[88]Shariat SF, Ashfaq R, Sagalowsky AI, et al. Correlation of cyclin D1 and El expression with bladder cancer presence, invasion, progression, and metastasis. Hum Pathol,2006,37(12):1568-1576.
[89]Stoimenov I, Helleday T. PCNA on the crossroad of cancer. Biochem Soc Trans. 2009,37(3):605-613.
[90]Inagaki T, Ebisuno S, Uekado Y, PCNA and p53 in urinary bladder cancer: correlation with histological findings and prognosis. Int J Urol,1997,4(2): 172-177.
[91]Zhu Z, Xing S, Lin C, et al. Bladder cancer therapy using combined proliferating cell nuclear antigen antisense oligonucleotides and recombinant adenovirus p53.Chin Med J,2003,116(12):1860-1863.
[92]El-Kott AF, Khalil AM, El-Kenawy Ael-M. Immunohistochemical expressions of uPA and its receptor uPAR and their prognostic significant in urinary bladder carcinoma. Int Urol Nephrol.2004,36(3):417-423.
[93]Li YJ, Zheng BZ, Zhou ZL,et al. Association of uPA and uPAR expression with invasive behaviors of urinary transitional cell carcinoma. Ai Zheng,2004, 23(6):704-706.
[94]Shin SJ, Kim KO, Kim MK,et al. Expression of E-cadherin and uPA and their association with the prognosis of pancreatic cancer. Jpn J Clin Oncol.2005, 35(6):342-348.
[95]Marhaba R, Zoller M. CD44 in cancer progression:adhesion, migration and growth regulation. J Mol Histol,2004,35(3):311-321.
[96]Stavropoulos NE, Filliadis I, Ioachim E, CD44 standard form expression as a predictor of progression in high risk superficial bladder tumors. Int Urol Nephrol, 2001,33(3):479-483.
[97]Miyake H, Hara I, Kamidono S,et al:Multifocal transitional cell carcinoma of the bladder and upper urinary tract:molecular screening of clonal origin by characterizing CD44 alternative splicing patterns. J Urol,2004,172(3):1127-1129.
[98]Wijnhoven BP, Dinjens WN, et al. E-cadherin-catenin cell-cell adhesion complex and human cancer. Br J Surg,2000,87(8):992-1005.
[99]Popov Z, Medina SG, Belda ML, et al. Low E-cadherin expression in bladder cancer at the transcriptional and protein level provides prognostic information. British Journal of Cancer,2000,83:209-214.
[100]Shariat SF, Pahlavan S, Baseman AG, E-cadherin expression predicts clinical outcome in carcinoma in situ of the urinary bladder. Urology,2001,57(1):60-65.
[101]Shin SJ, Kim KO, Kim MK,et al. Expression of E-cadherin and uPA and their association with the prognosis of pancreatic cancer. Jpn J Clin Oncol,2005, 35(6):342-348.
[102]Nutt JE, Durkan GC, Mellon JK, et al.Matrix metalloproteinases (MMPs) in bladder cancer:the induction of MMP9 by epidermal growth factor and its detection in urine. BJU Int,2003,91(1):99-104.
[103]Schmalfeldt B, Prechtel D, Harting K, et al. Increased expression of matrix metalloproteinases (MMP)-2, MMP-9 and the urokinase-type plasminogen activator is associated with progression from benign to advanced ovarian cancer. Clin Cancer Res,2001,7(8):2396-2404.
[1]Schnitt SJ. Breast cancer in 21st century:neu opportunities and neu challenges. Mod Pathol,2001,14(3):213-218.
[2]Winters ZE, Leck RD, Bradeburn MJ, etal. Cytoplasmic P2 express is correlted with HER-2/nuein breas tcancer and is a independent predicator of prognosis. Breas tCancer Res,2003,5(6):242-249.
[3]Junker K, Stachetzki U, Rademacher D, etal. HER2/neu expression and amplification in non-small cell lung cancer prior to and after neoadjuvant therapy. Lung Cancer,2005,49(2):279-80.
[4]Yazici H, Altun M, Alatli C, etal. c-erbB-2 Gene Amplification in Naso-pharyngeal Carcinoma. Cancer Invest,2000,18(1):6-10
[5]Tsutsui S, Ohno S, Murakam IS, et al. Progno stic value of CerbB2 expression in breast cancer. Surg Onco1 2002,79(4),216-223.
[6]Peter B, Howard A, Mannuela C, etal.Therapy for pancreatic cancer With a recombinant humanizied antibody anti-HER2(Hercepitin).J Gastrointestinal Surgery,2001,31(5):139-141.
[7]Karan D, Lin MF, Johansson SL, et al. Current status of themolecular genetics of human prostatic adenocarcinomas. Int J Cancer,2003,103(3):285-293.
[8]Corps AN, SowterHM, Smith S. Hepatocyte growth factor stimulates motility, chemotax is and mitogenesis inovarian carcinomace expressing high levels of c-met.Int J Cancer,1997,73:151-155.
[9]Knudsen BS, Gmyrek GA, Inra J, et al. High Expression of the Met receptor in prostate cancer metastasis to bone. Urology,2002,60 (60):1113-1117.
[10]Kim SJ, Johnson M, Koterba K, et al. Reduced c-Met Expression by an Adenovirus Expressing a c-Met Ribozyme Inhibits Tumorigenic Growth and Lymph Node Metastases of PC3-LN4 Prostate Tumor Cells in an Orthotopic Nude Mouse Model. Clin Cancer Res,2003,14:5161-5170.
[11]Zhang S, Zhau HE, Osunkoya AO, et al. Vascular endothelial growth factor regulates myeloid cell leukemia-1 expression through neuropilin-1-dependent activation of c-MET signaling in human prostate cancer cells. Mol Cancer,2010 19:9-19.
[12]Edwards J, Krishna NS, Witton C3, et al. Gene ampHficafions associated with the development of hormone-resistant prostate eantmr. Clin Cancer Res,2003, 9(14):5271-5281.
[13]McPherson RA, Conaway MC, Gregory CW, et al. The novel Ras antagonist, farnesylthiosalicylate, suppresses growth of prostate cancer in vitro. Prostate, 2004,58(4):325-334.
[14]Paik S, Bryant J, Tan-chiu E, et al. Real-world performance of HER2 testing-National Surgical Adjuvant Breast and Bowel Project Experience. J Natl Cancer Inst,2002,94:852-854.
[15]Agnantis NJ, C9nstantinidou AE, Papaevagelou M, et al. Comparative immunohistechemical study of rag-p21 oncopmtein in adenomatous hyperplaaia and adenoearcinoma of the prostate gland. Antieancor Res,1994,14(5a): 2135-2140.
[16]Han WD, Mu YM, Lu XC, et al. Upregulation of LRP16 mRNA by 17βestradiol through activation of estrogen receptor a (ERa), but not estrogen receptor β(ERβ), and promotes human breast cancer MCF7 cell proliferation:A preliminary report. Endoc Relat Cancer,2003,10(3):215-222.
[17]Walker VR, Korach KS. Estrogen recepto rknockout mice as a model fo rendocriner esearch. ILAR J,2004,45(4):455-461.
[18]Nupponen NN, Kakkola L, Koivisto P, et al. Genetic alterations in hormone-refractory recurrent prostate carcinomas. Am. J. Pathol,1998.153: 141-148.
[19]Kaltz-Wittmer, C, et al. FISH analysis of gene aberrations (MYC, CCND1, ERBB2, RB, and AR) in advanced prostatic carcinomas before and after androgen deprivation therapy. Lab Invest,2000,80:1455-1464.
[20]Iversen PL, Arora V, Acker AJ, et al. Efficacy of antisense morpholino oligomer targeted to c-myc in prostate cancer xenograft murine model and a Phase Ⅰ safety study in humans. Clinical Cancer Research,2003,9:2510-2519.
[21]Kuzmichev A, Jenuwein T, Tempst P, et al. Different EZH2-containing complexes target methylation of histone H1 or nucleosomal histone H3. Mol Cell,2004,14(2):183-193.
[22]Hanson RD, Hess JL, Yu BD, et al. Mammalian Trithorax and polycomb-group homologues are antagonistic regulators of homeotic development. Proc Nat Acad Sci USA,1999,96:14372-1437.
[23]Kleer CG., Cao Q, Varambally S, et al. EZH2 is a marker of aggressive breast cancer and promotes neoplastic transformation of breast epithelial cells. Proc Natl Acad Sci,2003,100:1606-11611.
[24]Varambally S, Dhanasekaran SM, Zhou M, et al. The polycomb group protein EZH2 iS involved in progression of prostate caDcer. Nature,2002,419:624-629.
[25]Tomlins SA, Rhodes DR, Perner S, et al.. Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer. Science.2005,310:644-648.
[26]Kumar-Sinha C, Tomlins SA, Chinnaiyan AM, et al. Recurrent gene fusions in prostate cancer. Nat Rev. Cancer,2008,8:497-511.
[27]Han B, Mehra R, Dhanasekaran SM, et al. A fluorescence in situ hybridization screen for E26 transformation-specific aberrations:identification of DDX5-ETV4 fusion protein in prostate cancer. Cancer Res,2008,68:7629-7637.
[28]Gopalan A, Leversha MA, Satagopan JM, et al. TMPRSS2-ERG gene fusion is not associated with outcome in patients treated by prostatectomy. Cancer Res, 2009,69:1400-1406.
[29]Yoshimoto M, Joshua AM, Cunha IW, et al. Absence of TMPRSS2:ERG fusions and PTEN losses in prostate cancer is associated with a favorable outcome. Mod Pathol,2008,21(12):1451-1460.
[30]Rostad K, Hellwinkel OJ, Haukaas SA, et al. TMPRSS2:ERG fusion transcripts in urine from prostate cancer patients correlate with a less favorable prognosis. APMIS,2009,117(8):575-582
[31]Merz VW, Arnold AM, Studer UE, et al. Differential expression of transforming growth factor-bota 1 and beta 3 as well as c-fos mRNA in normal human prostate, benign prostatic hyperplasia and prostatic Cancer. world J Urol,1994, 12(2):96-98.
[32]Zhou W, Janulis L, Park Ⅱ, et al. A novel anti-proliferative property of elusterinin prostate cancer coils. Life Sci,2002,72(1):11-21.
[33]Zhang X, Li W, Olumi AF. et al. Low-dose 2-O-tetradecanoylphorbol-13-acetate enhances tumor necrosis factor related apoptosis-inducing ligand induced apoptosis in prostate cancer cells.Clin Cancer Res,2007,13(23):7181-7190.
[34]Kim HS, Shiraki K, Rark SH, et al. Expression of survivin CIN and invasive squamous cell carcinoma of uterine cervix. Anticanee Res,2002,22(2A): 805-808.
[35]Sonnemann J, Gekeler V, SagrauskeA, et al. Apoptotic responsiveness of PC-3 prostate cancer cells to tumor necrosis factor-related apoptosisinducing ligand:e vidence for differential effects of Bcl-xL and Bcl-2 down-regulation. Int J Oncol, 2004,25(4):1171-1181.
[36]Lin Y, Fukuchi J, Hiipakka RA, et al. Up-regulation of Bcl-2 is required for the progression of prostate cancer cells from an androgen-dependent to an androgen-independent growth stage. Cell Res.2007,17(6):531-536.
[37]Yoshino T, Shiina H, Urakami S, et al. Bcl-2 expression as a predictive marker of hormone-refractory prostate cancer treated with taxane-based chemotherapy.Clin Cancer Res,2006,12(20):6116-6124.
[38]Ambrosin iG, Adida C, Alteri DC. Anovel ant-iapotosisgene, Surviving, Expressin cancer and lymphoma. NatureMed,1997, (8):917-921.
[39]Gazzaniga P, Gradilone A, Giuliani L, et al. Expressionandprognostic Significance of livin, survivin and other apoptosis-related genes in the progression of superficial bladde rcancer. Annals of Oncology,2003,14(2): 85-90.
[40]Shariat SF, Lotan Y, Saboorion H, et al. Survivin expression is associated with eatures of biologically aggressive prostate carcinoma. Cancer,2004,15(4): 751-757.
[41]Kishi H, Igawa M, Kikuno N, et al. Expression of survivin gene in prostate cancer:correlation with clinicopathological characteristics, proliferative activity and apoptosis. J Urol,2004,171 (5):1855-1860.
[42]Paduano F, Villa R, Pennati M, et al. Silencing of survivin gene by small interfering RNAs produces supra-additive growth suppression in combination with 17-allylamino-17-demethoxygeldanamycin in human prostate cancer cells. Mol Cancer Ther,2006,5(1):179-186.
[43]Pins MR, Fiadjoe JE, Korley F, et al. Clusterin as a possible predictor for biochemical recurrence of prostate cancer following radical prostatectomy with intermediate Gleason scores:a preliminary report. Prostate Cancer Prostatic Dis, 2004,7(3):243-8.
[44]Bettuzzi S, Davalli P, Astancolle S, et al. Tumor progression is accompanied by significant changes in the levels of expression of polyamine metabolism regulatory genes and clusterin(sulfated glycoprotein 2)in human prostate cancer specimens. Cancer Res,2000,60(1):28-24.
[45]Henderson J. Liver transplantation and rejection:an overview. Hepato-Gastro-enterol,1999,46(2):1480-1484.
[46]Liu H, Gong NQ, LiGS, et al. Changes of express/on of Bcl-2 protein in rat liver during ischemia-reperfusion injury. Zhongguo Xiandai Yixue Zazhi,2002, 12(12):16-18.
[47]Dominguez A, Ramos, Morales F, Romero F,et al.Hpttg, a human homologue of rat pttg, is overexpressed in hematopoietic neoplasms. Evidence for a trans-criptional activation function of hPTTG.Oncogene,1998,17(17):2187-2193.
[48]Zhu X, Mao Z, Na Y, Guo Y, et al.Significance of pituitary tumor transforming gene 1 (PTTG1) in prostate cancer. Anticancer Res,2006,26(2):1253-1259.
[49]Wang Z, Bhattacharya N, W emver M, et al. Pim-1:a Serine/hreonine kinase with 8 role in cell survival, proliferation, differentiation and tumorigenesis. J Vet Sef,2001,2(3):167-179.
[50]Cibull TL, Jones TD, Li L, et al. Overexpression of Pim-1 during progression of prostatic adenoearclnoma. J Clin Pathol,2006,59(3):285-288.
[51]Thompson J, Pehola IcJ, Koskinen PJ, et al. Attenuation of andgogen recepto-r dependent transcription by sefine/threonine kinase Pim-1. Lab Invest,2003,83: 1301-1309.
[52]Xie Y, Xu K, Lima DE, et al. ne44-kDa Pim-kinase phesphorylates BCRP/ABCG2 and thereby promotes its mulfimerization and drug-resistant activity in human prostate cancer cells. J Biol Chem,2008,283(6):3359-3356.
[53]Hu XF, Li J, Vandervalk S, et al. PIM-1-specific mAbsuppreses human and mourse tumuseor growth by decreasing PIM-1 levels, reducing Akt phosphorylation, and activating apoptosis. I Clin Invest,2009,119(2):362-375.
[54]Bai Hz, Pollman MJ, Inishi Y, et al. Regulation of vascular smooth muxcle cell apoptosis.Modulation of bad by a phosphatidylinositol 3-kinase de pendent pathway. Circ Res,1999,85(3):229-237.
[55]Matsui T, Li L, Del Monte F, et al. Adenoviral gene transfer of activated phosphatidylinositol 3'-kinase and Akt inhibits apoptosis of hypoxic cardio-myocytes in vitro. Circulation,1999,100:2373-2379.
[56]Kaplan P J, Mohan S, Cohen P, et al. The insulin-like growth factor axis and prostate cancer:lessons from the transgenic adenocarcinoma of mouse prostate (TRAMP) model. Cancer res,1999,59(9):2203-2209.
[57]Mucci LA, Stark JR, Pollak MN, et al. Plasma levels of acid-labile subunit, free insulin-like growth factor-Ⅰ, and prostate cancer risk:a prospective study. Cancer Epidemiol Biomarkers Prev.2010,19(2):484-491.
[58]Shukla S, Gupta S. Apigenin suppresses insulin-like growth factor I receptor signaling in human prostate cancer:an in vitro and in vivo study. Mol Carcinog, 2009,48(3):243-252.
[59]Rufinova MB, Schoer RA. Effect of angiogenes isinhibition by Id loss and the contribution of bone-marrow-derived endothelial cell sinsponta-FIeOUS mufine tumors. J Allergy Carcinoma Cell,2003,4(10):277-289.
[60]Lasorella A.Uo T.Iavarone A Id proteins at the cross-road of development and cancer Oncogene,2001,20:8326-8333.
[61]Lyden D, Hauofi K, Dias S, et al. Impaired imcmitment of bone-Marrow-derived endothelial and hematepoietic precursor cells blockstunIor ansingenesis and gowth. Nature,2001,7(11):1194-1201.
[62]Ouyang XS, Wang X, Lee DT, Over expression of 1D-1 in prostate cance. Urol 2002,167:2598-2602.
[63]Lin JC, Chang SY, Hsieh DS, et al. Modulation ofmitogen-activated protein kinase cascades by differentiation-1 protein:acquired drug resistance of hormone independent prostate cancer ceils. Urol,2005,174:2022-2026.
[64]Ling MT, Wang X, Lee DT, et al. Id-1 expression induces androgen-independent prostate cancor ceU growth through activation of epidermal growth factor receptor (EGF-R). Carcinogenesis,2004,5:517-525.
[65]Zhang X, Ling MT, Wang X, et al. Inactivation of Id-1 in prostate cancer cells:A potential therapeutic target in inducing chemosensitization to taxol through activation of JNK pathway. Int J Cancer,2006,118(8):2072-2081.
[66]Kaur P, Kallakury B S, Sheehan C E, et al. Survivin and Bel-2 expressioon in prostatic adenocarcinomas. Arch Pathol Lab Med,2004,128:39-43.
[67]Kastan MB, Bartek J. Cell2cycle checkpoints and cancer. Nature,2004,432 (7015):316-323.
[68]Massague J. G1 cell2cycle control and cancer. Nature,2004,432(7015):298-306.
[69]Bert Vogelstein, David Lane, Arnold J L. Surfing the p53 net-work. Nature, 2000,408:307-310.
[70]Schlomm T, Iwers L, Kirstein P, et al. Clinical significance of p53 alterations in surgically treated prostate cancers. Modern pathology,2008,21 (11):1371-1378.
[71]Pisters LL, Pettaway CA, Troncoso P, et al. Evidence that transfer of functional p53 protein results in increased apoptosis in prostate cancer. Clin Cancer Res, 2004,10(8):2587-2593.
[72]Maddison LA, Sutherland BW, Barrios RJ, el al. Conditional delefinn of Rb causes early stage prostate cancer. Cancer Res,2004,64(17):6018-6025.
[73]Nakamura T, Ide H, Eguchi R, el al.Concomitant analysis of p16/INK4, cyclin Dl,and retinoblastoma protein expression in esophageal squamous cell. Carcinoma,2003,50(53):1321-1326.
[74]Hayward SW, Wang Y, Day ML. Rescue and isolation of Rb-deficient prostate epithelium by tissue recombination. Methods Mol Biol,2003,218:17-33.
[75]Ito G, Uchiyama M, Kondo M, et al. Mori S Usami N Maeda O Kawabe T Hasegawa Y Shimokata K Sekido Y Kruppel-like factor 6 is frequently down-regulated and induces apoptosis in non-small cell lung cancer cells. Cancer Res,2004,64(11):3838-3843.
[76]Narla G, Heath KE, Reeves HL, et al. KLF6,a candidate tumor suppressor gene mutated in prostate. Science,2001,294(5551):2563-2566.
[77]Narla G, Difeo A, Reeves HL, et al. A germline DNA polymorphism enhances alternative splicing of the KLF6 tumor suppressor gene and is associated with increased prostate cancer risk. Cancer Res,2005,65:1213-1222.
[78]Narla G, DiFeo A, Yao S. Targeted inhibition of the KLF6 splice variant, KLF6 SV1, suppresses prostate cancer cell growth and spread. Cancer Res,2005, 65(13):5761-5768
[79]Li J, Yen C, Liaw D, et al. PTEN, a putative protein tyrosine phosphatase gene mutated in human brain, breast, and prostate cancer. Science,1997,275(5308): 1943-1947.
[80]Hu TH, Huang CC, Lin PR, el al. Expression and prognostic role of tumor suppressor gene PTEN/MMACI/TEPI in hepatocellular carcinoma. Cancer, 2003,97:1929.
[81]Cairns P, Okami K, Halachmi S, et al. Frequent inactivation of mN/MMAC1 in primary prostate cancer. Cancer Res,1997,57(22):4997-5000.
[82]Mulholland DJ, Jiao J, Wu H, et al. Hormone refractory prostate cancer: Lessons learned from the PTEN prostate cancer model. Adv Exp Med Biol. 2008,617:87-95.
[83]Yoshimoto M, Joshua AM, Cunha IW, et al. bsence of TMPRSS2:ERG fusions and PTEN losses in prostate cancer is associated with a favorable outcome. Mod Pathol,2008,21(12):1451-1460.
[84]85 Wu Z, McRoberts KS, Theodorescu D. The role of PTEN in prostate cancer cell tropism to the bone micro-environment. Carcinogenesis,2007,28(7): 1393-1400.
[85]Weinberg W C, Denning M F. P21 Wafl Control of Epithetlial Cell Cycle and Cell Fate. Crit Rev Oral Biol Med,2002,13(6):453-464.
[86]Romics I, Banfi G, Szekely E, et al. Expression of p21(wafl/cipl), p27 (kip1), p63 and androgen receptor in low and high Gleason score prostate cancer. Pathol Oncol Res.2008,14(3):307-311.
[87]Karim F, izazi, Luis A, et al. The Association of p21(wAF+1, clPl) with Progression to Androgen-independent Prostate Cancer. Clinical Cancer Research,2002,8:775-781.
[88]Rocco JW, Sidransky D. pl6(MTS-1/CDKN2/INK4a) in cancer progression. Exp Cell Res,2001,264(1):42-55.
[89]Chakravarti A, Heydon K, Wu CL, et al. Loss of p16 expression is of prognostic significance in locally advanced prostate cancer:an analysis from the Radiation Therapy Oncology Group protocol 86-10. J Clin Oncol,2003, 21(17):3328-3334.
[90]Allay JA, Steiner MS, Zhang Y, et al. Adenovirus p16 gene therapy for prostate cancer. World J Urol,2000,18(2):111-120.
[91]Sheng S. The promise and challenge toward the clinical application of maspin in cancer. Front Biosci,2004,1(9):2733-2745.
[92]Li Z, Shi HY, Zhang M. et al. Targeted expression of maspin in tumor vasculartures induces endothelial cell apoptosis. Ocogene,2005,24:2008-2019.
[93]Liu J,Yin S,Reddy N, et al. Bax mediates the apoptosis-sensitizing effect of maspin Cancer Res,2004,64:1703-1711.
[94]Odero-Mamh VA, Khalkhali-Ellis Z, Chunthapong J, et al. Maspin regulates difkrent signaling patllways for motility and adhesion in aggressive breast cancer cells. Cancer Biol Ner,2003,2(4):398-403.
[95]Pierson CR, McGowen R, Grignon D, et al. Maspinis upregulated in prema-lignant prostate epithelia. Prostate,2002,53:255-262.
[96]Machtens S, Serth J, Bokemeyer C, et al. Expression of the p53 and Maspin protein in primary prostate cancer:correlation with clinical features. Int J Cancer,2001,95(5):337-342.
[97]Li X, Chen D, Yin S, Maspin augments proteasome inhibitor-induced apoptosis in prostate cancer cells. J Cell Physiol,2007,212(2):298-306.
[2]Lissens W, Sermon K, Preimplantation genetic diagnosis:current status and new developments. J J Human Reproduction,1997:2:1756-1761.
[3]Goldman JM, Druker BJ. Chronic myeloid leukemia:current treatment options. Blood,2002,99(8):3070-3071.
[4]Schrock E, du Manior S, Veldman T, et al. Multicolor spectral karyotyping othuman chromosome. Science,1996,273:494-497.
[5]Lan C, Liu JM, Liu TW, et al. ErbB2 amplification by fluorescence in situ hybridization in breast cancer specimens read as 2+in immunohistochemical analysis. Am J Clin Pathol,2005,124(1):97-102.
[6]Veeramachaneni R, Nordberg ML, Shi R, et al. Evaluation of fluorescence in situ hybridization as an ancillary tool to urine cytology in diagnosing urothelial carcinoma. Diagn Cytopathol,2003,28:301-307.
[7]Kumar A, Kumar R, Gupta NP. Comparison of NMP22 BladderChek Test and Urine Cytology for the Detection of Recurrent Bladder Cancer. Jpn J Ciin Oncol, 2006,36(3):172-175.
[8]Fadl-Elmula I, Oorunova L, Mandahl N, et al. Cytogenetic analysis of upper Urinary tract transitional cell carcinomas. Cancer Genet Cytogenet,1999,115: 123-127.
[9]Tomlins SA, Rhodes DR, Perner S, et al.. Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer. Science,2005,310:644-648.
[10]Sakai I, Miyake H, Harada K, et al. Analysis of factors predicting intravesical recurrence of superficial transitional cell carcinoma of the bladder without concomitant carcinoma in situ.Int J Urol,2006,13(11):1389-1392.
[11]Akagashi K, Tanda H, Kato S, et al. Int J Urol. Recurrence pattern for superficial bladder cancer,2006,13(6):686-691.
[12]Nguyen CT, Litt DB, Dolar SE, et al. Prognostic significance of nondiagnostic molecular changes in urine detected by UroVysion fluorescence in situ hybridization during surveillance for bladder cancer. Urology,2009,3(2): 347-350.
[13]Lokeshwar VB, Schroeder GL, Selzer MG, et al. Bladder tumor markers for monitoring recurrence and screening comparison of hyaluronic acid-hyaluronidase and BTA-Stat tests. Cancer,2002,95(1):61-72.
[14]Toma MI, Barak V, Hautmann SH, et al. Comparison of the Immunocyt test and urinary cytology with other urine tests in the detection and surveillance of bladder cancer. World J Urol,2004,22:145-149.
[15]Lokeshwar VB, Habuchi T, Grossman HB, et al. Bladder tumor markers beyond cytology:International Consensus Panel on bladder tumor markers. Urology, 2005,66(6 Suppl1):35-63.
[16]Friedrich MG, Toma MI, Hellstern A, et al. Comparison of multitarget fluorescence in situ hybridization in urine with other noninvasive tests for detecting bladder cancer. BJU Int,2003,92:911-914.
[17]Laudadio J, Keane TE, Reeves HM, et al. Fluorescence in situ hybridization for detecting transitional cell carcinoma:implications for clinical practice. BJU Int, 2005,96(9):1280-1285.
[18]Cordon CC. Molecular alterations in bladder cancer.Cancer. Surv,1998,32:115-131.
[19]Sandberg AA, Berger Cs. Review of chromo some studies in urological tumors. Cytogenetics and molecular genetics of bladder cancer. J Urol,1994,151(3): 545-560.
[20]Sokolova IA, Halling KC, Jenkins RB, et al. The development of a multitarget,multicolor fluo-rescence in situ hybridization assay for the detection of urothelial carcinoma in urine. J Mol Diagn,2000,2(3):116-123.
[21]Sauter G, Gasser T C, Moch H, et al. DNA aberrations in urinary bladder cancer detected by flow cytometry and FISH.Urol Res,1997,25(1):S37-S43.
[22]Michael F,Sarosdy MF,Schellhammer P,et al.Clinical evaluation of multi-target fluorescent in situ hybridization assay for detection of bladder cancer. J Urol, 2002,168(5):1950-1954.
[23]Lotan YRoehrbom CG Sensitivity and specificity of commonly available bladder tumor markers versus cytology; results of a comprehensive literature review and mcta-analyscs. Urology,2003,61:109-118.
[24]KonetyBK, Getzenberg RH.Urine based markers ofurological malignancy.J Urol, 2001,165:600-611.
[25]Kwak kw, Kim SH, Lee HM, et al.The Utility of Fluorescence In Situ Hybridization for Detection of Bladder Urothelial Carcinoma in Routine Clinical Practice. J Korean Med Sci,2009,24:1139-1144.
[26]Sarosdy MF, Kahn PR, Ziffer MD, et al.Use of a multitarget fluorescence in situ hybridization assay to diagnose bladder cancer in patients with hematuria. J Urol, 2006,176(1):44-47.
[27]Sanchez-Carbayo M, Urrutia M, Gonzalez de Buitrago JM, et al.Utility of serial urinary tumor markers to individualize intervals beteewn cystoscopies in the monitoring of patients with bladder carcinoma. Cancer,2001,92:2820-2828.
[28]Jones JS. DNA-based molecular cytology for bladder cancer surveillance. Urology,2006,67:35-45.
[29]Bubendorf L, Grilli B. UroVysion multiprobe FISH in urinary cytology. Methods Mol Med,2004,97:117-131.
[30]Michael F, Sarosdy, Paul R, et al. Use of a Multitarget Fluorescence In Situ Hybridization Assay to Diagnose Bladder Cancer in Patients With Hematuria. J Urol,2006,176:44-47.
[31]Placer J, Espinet B, Salido M, et al.Correlation between histologic findings and cytology abnormalities in bladder carcinoma;a FISH study. J Urol,2005,65: 913-918.
[32]Vecchione A, Sevignani C, Giarnieri E, et al. Inactivation of the FHIT gene favors bladder cancer development. Clin Cancer Res,2004,10(22):7607-7612.
[33]Mhawech-Fauceglia P, Fischer G, Beck A, et al. RAF.1,Aurora-A/STK15 and E-codherin biomarkers expression in patients with pTa/PT 1 urothelial bladder carcinoma; a retrospective TMA study of 246 patients with long-term follow-up. Eur Surg Ongol,2006,32:439-444.
[34]Krause FS, Rauch A, Schrott KM, et al. Clinical decisions for treatment of different staged bladder cancer based on multitarget fluorescence in situ hybridization assays? World J Urol,2006,24:418-422.
[35]Li M, Zhang ZF, Reuter VE, et al. Chromosome 3 allelic losses and microsatellite alterantions in transitional cell carcinoma of the urinary bladder. Am J Pathol 1996,149:229-235.
[36]Wada T, Louhelainen J, Hemminki K, et al. The prevalence of loss of heterozygosity in chromosome 3, including FHIT, in bladder cancer, using the
fluorescent multiplex polymerase chain reaction. BJU Int.2001,87(9):876-881.
[37]Jorissen RN, Walker F, Pouliot N, et al. Epidermal growth factor receptor: mechanisms of activation and Signaling. Exp Cell Res,2003,284(1):31-32.
[38]Colquhoun AJ, Mellon J K. Epidermal growth factor receptor and bladder cancer. Postgrad Med J,2002,78(924):584-589.
[39]Sokolova IA, Hailing KC, Jenkins RB, et al. The development of a multitarget, multicolor fluorescence in situ hybridization assay for detection of urothelial carcinoma in urine. Mol Diagn,2000,2:116-123.
[40]Bollmann M.Heller H.Bankfalvi A, et al. Quantitative molecular urinary cytology by fluorescence in situ hybridization.a tool for tailoring surveillance of patients with superficial bladder cancer BJU Int,2005,95 (9):1219-1225.
[41]Wolman SR, Goldman B, Slovak ML, et al. Aneusomy for detection of bladder cancer recurrence:a Southwest Oncology Group study. Cancer Genet Cytogenet, 2007,176(1):22-27.
[42]Rocco JW,Sidransky D. pl6(MTS-1/CDKN2/INK4a) in cancer progressionExp Cell Res,2001,264(1):42-55.
[43]Wheeless LL,Reeder JE,Han XY,et al.Bladder irrigation specimens assayed by fluorescence in situ hybridization to interphase nucleus. Cytometry,1994,1: 319-326.
[44]Balazs M,Carroll P,Kerschmann 1L et al.Frequent homozygous deletion of cyclin-dependent kinase inhibitor 2(MTS1,p 16)in superficial bladder cancer detected by fluorescence in situ hybridization. Genes Chromosomes Cancer. 1997,19:84-89.
[45]Yurakh A 0, Ramos D, Calabuig FS,et al.Molecular and immunohistochenmical analysis of the prognostic value of cell-cycle regulators in urothlial neoplasmas of the bladder.Eur Urol,2006,50(3):506-515.
[46]Kruger S, Mess F, Bohle A,et al. Numerical aberrations of chromosome 17 and the 9p21 locus are independent predictors of tumor recurrence in non-invasive transitional cell carcinoma of the urinary bladder. Int J Oncol.2003,23(1): 41-48.
[47]Gallucci M,Guadagni F,Marzano R,et al.Status of the p53,p16,RBI,and HER-2 genes and chromosomes 3,7,9,and 17 in advanced bladder cancer:correlation with adjacent mucosa and pathological parameters. J Clin Pathol,2005,58(4): 367-371.
[48]Kwak KW,Kim SH,Lee HM,et al.The utility of fluorescence in situ hybridization for detection of bladder urothelial carcinoma in routine clinical practice. J Korean Med Sci,2009,24(6):1139-1144.
[49]Bubendorf L, Grilli B, Sauter G, et al. Multiprobe FISH for enhanced detection of bladder cancer in voided urine specimens and bladder washings. Am J Clin Pathol,2001,116(1):79-86.
[50]Ribal MJ, Alcaraz A, Mengual L, et al. Chromosomal high-polysomies predict tumour progression in T1 transitional cell carcinoma of the bladder. Eur Urol, 2004,45(5):593-599.
[51]Gallucci M, Guadagni F, Marazano Ret al. Status of the p53, p16, RBI, and HER-2 genes and chromosome 3,7,9 and 17 in advanced bladder cancer: correlation with adjacent mucosa and pathological parameters. Clin Pathol,2005, 58:367-371.
[52]Winters ZE, Leck RD, Bradeburn MJ, et al. Cytoplasmic P2 express is correlted with HER-2/nuein breas tcancer and is a independent predicator of prognosis. Breast Cancer Res,2003,5(6):242-249.
[53]Gallucci M, Merola R, Leonardo C, et al. author reply 440-1.Analysis of HER2 expression in primary urinary bladder carcinoma and corresponding metastases. BJU Int,2005,95:982-986.
[54]Kastan MB, Bartek J. Cell2cycle checkpoints and cancer. Nature,2004,432 (7015):316-323.
[55]Massague J. G1 cel 12cycle control and cancer. Nature,2004,432(7015):298-306.
[56]Bernardini S, Billerey C, Martin M, et al. The predictive value of muscularis mucosae invasion and p53 over expression on progression of stage T1 bladder carcinoma. J Urol,2001,165(1):42-46.
[57]Edward M, Messing MD. Urothelial Tumors of the Urinary Tract. In: Campbell's Urology,8th ed. Walsh PC, Retik AB, Vaughan ED Jr, Wein AJ, eds. Philadelphia (PA):W. B. Saunders,2002.2732-2804.
[58]Choong NW, Quevedo JF, Kaur JS. Small cell carcinoma of urinary bladder:the Mayo Clinic experience. Cancer,2005,103:1172-1178.
[59]Schultz IJ, Kiemeney LA, Karthaus HF, et al. Survivin mRNA copy number in bladder washings predicts tumor recurrence in patients with superficial urothelial cell carcinomas. Clin Chem,2004,50(8):1425-1428.
[60]Esuvaranathan K, Chiong E, Thamboo TP, et al. Predictive value of p53 and pRb expression in superficial bladder cancer patients treated with BCG and interferon-alpha. Cancer,2007,109(6):1097-1105.
[61]Stavropoulos NE, Bouropoulos C, Ioachim IE, et al. Prognostic significance of angiogenesis in superficial bladder cancer. Int Urol Nephrol.2004,36(2): 163-167.
[62]Annamma Kurien,Joseph Thomas. Can Reflex UroVysion fluorescence in situ hybridization predict tumor recurrence during follow-up? Indian J Urol,2007, 23(3):333-334.
[63]Yoder BJ, Skacel M, Hedgepeth R, et al. Reflex UroVysion testing of bladder cancer surveillance patients with equivocal or negative urine cytology:A prospective study with focus on the natural history of anticipatory positive findings. Am J Clin Pathol,2007,127:295-301.
[64]Zellweger T, Benzl G, Cathomas G, et al. Multi-target fluorescence in situ hybridization in bladder washings for prediction of recurrent bladder cancer. Int J Cancer,2006,119:1660-1665.
[65]Bollmann M, Heller H, Bankfalvi A, et al. Quantitative molecular urinary cytology by fluorescence in situ hybridization:a tool for tailoring surveillance of patients with superficial bladder cancer? BJU Int,2005,95(9):1219-1225.
[66]Marano A, Pan Y, Li C, et al. Chromosomal numerical aberrations detected by fluorescence in situ hybridization on bladder washings from patients with bladder cancer. Eur Urol,2000,37(3):358-365.
[67]Chen GL, Bagley DH. Ureteroscopic surgery for upper tract transitional-cell carcinoma:complications and management. J Endourol,2001,15(4):399-404.
[68]Hall MC, Womack S, Sagalowsky AI, et al. Prognostic factors, recurrence, and survival in transitional cell carcinoma of the upper urinary tract:a 30-year experience in 252 patients. Urology,1998,52(4):594-601.
[69]Walsh IK, Keane PF,Ishak LM, et al. The BTA stat test:a tumor marker for the detection of upper tract transitional cell carcinoma. Urology,2001,58:532-535.
[70]Chen AA,Grasso M. Is there an role for FISH in the management and surveillance of patients with upper tract transitional-cell carcinoma? Journal of endourology,2008,2:1371-1374.
[71]Schatteman P, Chatzopoulos C, Assenmacher C, et al. Laparoscopic nephrouret-erectomy for upper urinary tract transitional cell carcinoma:Results of a belgian retrospective multicentre survey. Eur Urol,2007,51:1633-1638.
[72]Chen WJ, Kuo JY, Chen KK, et al. Primary urothelial carcinoma of the ureter: 11-year experience in Taipei Veterans General Hospital. J Chin Med Assoc.2005, 68(11):522-530.
[73]吴阶平.吴阶平泌尿外科学.济南：山东科学技术出版社,2004：417-418.
[74]Guarnizo E, Pavlovich CP, Seiba M, et al. Ureteroscopic biopsy of upper tract urothelial carcinoma:improved diagnostic accuracy and histopathological considerations using a multi-biopsy approach. J Urol,2000,163:52-55.
[75]Johnson DB, Pearle MS.Complications of ureteroscopy. Urol Clin North Am, 2004,31(1):157-171.
[76]Perez-Montiel D, Wakely PE, Hes O, et al. High-grade urothelial carcinoma of the renal pelvis:clinicopathologic study of 108 cases with emphasis on unusual morphologic variants. Mod Pathol,2006,19(4):494-503.
[77]Matsui Y, Utsunomiya N, Ichioka K, et al. Risk factors for subsequent development of bladder cancer after primary transitional cell carcinoma of the upper urinary tract.Urology,2005,65(2):279-283.
[78]Oehlschlager S, Baldauf A, Wiessner D, et al. Bladder tumor recurrence after primary surgery for transitional cell carcinoma of the upper urinary tract. Urol Int,2004,73(3):209-211.
[79]吴宏飞.现代泌尿外科诊疗指南.南京：东南大学出版社,2005：233-234.
[80]Mehra R, Tomlins SA, Shen R, et al. Comprehensive assessment of TMPRSS2 and ETS family gene aberrations in clinically localized prostate cancer. Mod Pathol,2007,20 (5):538-544.
[81]Che M, Grignon D. Pathology of prostate cancer. Cancer Metastasis Rev,2002, 21(3-4):381-395.
[82]Srigley J R. Benign mimickers of prostatic adenocarcinoma. Mod Pathol,2004, 17(3):328-348.
[83]Kusumi T, Koie T, Tanaka M, et al. Immunohistochemical detection of carcinoma in radical prostatectomy specimens following hormone therapy. Pathol Int,2008,58(11):687-694.
[84]Tomlins SA, Mehra R, Rhodes DR, et al.TMPRSS2:ETV4 gene fusions define a third molecular subtype of prostate cancer. Cancer Res,2006,66:3396-3400.
[85]Belaud-Rotureau MA, Parrens M, Dubus P, et al. A comparative analysis of FISH, RT-PCR, PCR and immunohistochemistry for the diagnosis of mantle cell lymphomas. Mod Pathol,2002,15(5):517-525.
[86]Bao F, Munker R, Lowery C, et al. Comparison of FISH and quantitative RT-PCR for the diagnosis and follow-up of BCR-ABL-positive leukemias. Mol Diagn Ther,2007,11(4):239-245.
[87]Han B, Mehra R, Dhanasekaran SM, et al. A fluorescence in situ hybridization screen for E26 transformation-specific aberrations:identification of DDX5-ETV4 fusion protein in prostate cancer. Cancer Res,2008,68(18):7629-7637.
[88]Tomlins SA, Bjartell A, Chinnaiyan AM,et al. ETS gene fusions in prostate cancer:from discovery to daily clinical practice. Eur Urol,2009,56(2):275-86.
[89]Mehra R, Han B, Tomlins SA, Heterogeneity of TMPRSS2 gene rearrangements in multifocal prostate adenocarcinoma:molecular evidence for an independent group of diseases. Cancer Res,2007,67(17):7991-7995.
[90]Hofer MD, Kuefer R, Maier C, et al.Genome-Wide Linkage Analysis of TMPRSS2-ERGFusion in Familial Prostate Cancer. Cancer Res,2009,69 (2): 640-646.
[91]Soller MJ, Isaksson M, Elfving P, etal. Confirmation of the high frequency of the TMPRSS2/ERG fusion gene in prostat cancer. Genes Chromosomes Cancer, 2006,45:717-719.
[92]Mehra R, Tomlins SA, Yu J, et al. Characterization of TMPRSS2-ETS gene aberrations in androgen-independent metastatic prostate cancer. Cancer Res, 2008,68(10):3584-3590.
[93]Perner S, Demichelis F, Beroukhim R, et al. TMPRSS2:ERG fusion-associated deletions provide insight into the heterogeneity of prostate cancer. Cancer Res, 2006,66:8337-8341.
[94]Iljin K, Wolf M, Edgren H, et al. TMPRSS2 fusions with oncogenic ETS factors in prostate cancer involve unbalanced genomic rearrangements and are associated with HDAC1 and epigenetic reprogramming. Cancer Res,2006, 66(21):10242-10246.
[95]Epstein JI, Herawi M. Prostate needle biopsies containing prostatic intraepithelial neoplasia or atypical foci suspicious for carcinoma:implications for patient care. J Urol,2006,175:820-834.
[96]Gallo F, Chiono L, Gastaldi E, et al. Prognostic significance of high-grade prostatic intraepithelial neoplasia (HGPIN):risk of prostatic cancer on repeat biopsies.Urology,2008,72(3):628-632.
[97]Mosquera JM, Perner S, Genega EM, et al. Characterization of TMPRSS2-ERG fusion high-grade prostatic intraepithelial neoplasia and potential clinical implications. Clin Cancer Res,2008,14:3380-3385.
[98]Furusato B, Gao CL, Ravindranath L, et al. Mapping of TMPRSS2-ERG fusions in the context of multi-focal prostate cancer. Mod Pathol,2008,21:67-75.
[99]Perner S, Mosquera JM, Demichelis F, et al. TMPRSS2-ERG fusion prostate cancer:an early molecular event associated with invasion. Am J Surg Pathol, 2007,31:882-888.
[100]Darnel AD, Lafargue CJ, Vollmer RT, Corcos J, Bismar TA. TMPRSS2-ERG fusion is frequently observed in Gleason pattern 3 prostate cancer in a Canadian cohort. Cancer Biol Ther,2009,8(2):125-130.
[101]Attard G, Clark J, Ambroisine L, et al. Duplication of the fusion of TMPRSS2 to ERG sequences identifies fatal human prostate cancer. Oncogene,2008,27: 253-263.
[102]Seth A, Watson DK. ETS transcription factors and their emerging roles in human cancer. Eur J Cancer,2005,41(16):2462-2478.
[103]Demichelis F, Fall K, Perner S, TMPRSS2:ERG gene fusion associated with lethal prostate cancer in a watchful waiting cohort. Oncogene,2007,26(31): 4596-4599.
[104]Petrovics G, Liu A, Shaheduzzaman S, et al. Frequent overexpression of ETS-related gene-1 (ERG1) in prostate cancer transcriptome. Oncogene,2005, 24(23):3847-3852.
[105]Attard G, Clark J, Ambroisine L, et al. Duplication of the fusion of TMPRSS2 to ERG sequences identifies fatal human prostate cancer.Oncogene,2008,27(3): 253-263.
[106]Nam RK.Sugar L.Wang Z Expression of TMPRSS2 ERG Gene Fusion in Prostate Cancer Cells is an Important Prognostic Factor for Cancer Progression.Cancer,2007,6(1):40-45.
[107]Cooperberg MR, Lubeck DP, Meng MV, et al. The changing face of low-risk prostate cancer:trends in clinical presentation and primary management. J Clin Oncol,2004,22(11):2141-2149.
[108]Perner S, Mosquera JM, Demichelis F,et al. TMPRSS-ERG fusion prostate cancer:an early molecular event associated with invasion. Am J Surg Pathol, 2007,31(6):882-888.
[109]Saramaki OR, Harjula AE, Martikainen PM, et al.TMPRSS2:ERG fusion identifies a subgroup of prostate cancers with a favorable prognosis. Clin Cancer Res,2008,14(11):3395-3400.
[1]Greenlee R,Hill-Harmon M,Murray T, et al. Cancer statistics. CA Cancer J Clin, 2001,51:15-36.
[2]Okamura T, Umemoto Y, Yasui T, et al. Noninvasive detection of alterations in chromosome numbers in urinary bladder cancer cells, using fluorescence in situ hybridization. Int J Clin Oncol,2004,9(5):373-377.
[3]Wolman SR, Goldman B, Slovak ML, et al. Aneusomy for detection of bladder cancer recurrence:a Southwest Oncology Group study. Cancer Genet Cytogenet. 2007,176(1):22-27.
[4]Mian C, Lodde M, Comploj E, et al. Multiprobe fluorescence in situ hybridisation:prognostic perspectives in superficial bladder cancer. J Clin Pathol,2006,9(9):984-987.
[5]Li M,Zhang ZF, Reuter VE, et al. Chromosome 3 allelic losses and microsatellite alterantions in transitional cell carcinoma of the urinary bladder. Am J Pathol 1996,149:229-235.
[6]Cairns P, Proctor AJ, Knowles MA. Loss of heterozygosity at the RB locus is frequent and correlates with muscle invasion in bladder carcinoma. Oncogene, 1991,6(12):2305-2309.
[7]Bart SH, GaylaO, Alan W, et al. Parsing ERK Activation Reveals quantitatively equivalent contributions from epidermal growthfactor receptor and HER2 in human mammary epithelial cells. J Biol Chem,2005,280(7):6157-6169.
[8].xu H,Yu Y,Marciniak D,et al. Epidermal growth factor receptor (EGFR)-related protein inhibits multiple members of the EGFR family in colon and breast cancer cells.Mol Cancer Ther,2005,4(3):435-442.
[9]Ding Y, Wang G, Ling MT, et al. Significance of Id-1 up-regulation and its association with EGFR in bladder cancer cell invasion. Int J Oncol.2006,28(4): 847-854.
[10]Mason RA, Morlock EV, Karagas MR, et al. EGFR pathway polymorphisms and bladder cancer susceptibility and prognosis. Carcinogenesis,2009,30(7): 1155-1160.
[11]Nguyen PL, Swanson PE, Jaszcz W, et al:Expression of epidermal growth factor receptor in invasive transitional cell carcinoma of the urinary bladder:a multivariate survival analysis. Am J Clin Pathol,1994,101:166-176.
[12]Mellon K, Wright C, Kelly P, et al. Long-term outcome related to epidermal growth factor receptor status in bladder cancer. J Urol,1995,153:919-925.
[13]Ravery V, Grignon D, Angulo J, et al:Evaluation of epidermal growth factor receptor, transforming growth factor and c-erbB2, epidermal growth factor and c-erbB2 in the progression of invasive bladder cancer. Urol Res,1997,25:9-17.
[14]Wester K, Sjostrom A, de la Torre M,et al. HER-2--a possible target for therapy of metastatic urinary bladder carcinoma. Acta Oncol.2002,41(3):282-288.
[15]Sato K, Moriyama M, Mori S, et al. An immunohistologic evaluation of C-erbB-2 gene product in patients with urinary bladder carcinoma. Cancer,1992, 70:2493-2498.
[16]Kruger S, Weitsch G, Buttner H, et al. Overexpression of c-erbB-2 oncoprotein in muscle-invasive bladder carcinoma:relationship with gene amplification, clinicopathological parameters and prognostic outcome. Int J Oncol,2002.21: 981-987.
[17]Chow NH, Chan SH, Tzai TS,Expression profiles of ErbB family receptors and prognosis in primary transitional cell carcinoma of the urinary bladder, Clin Cancer Res.2001,7(7):1957-1962.
[18]Jimenez RE, Hussain M, Bianco FJ Jr, et al:Her-2/neu overexpression in muscle-invasive urothelial carcinoma of the bladder:prognostic significance and comparative analysis in primary and metastatic tumors. Clin Cancer Res,2001, 7:2440-2447.
[19]Eissa S, Ali HS, Al Tonsi AH, et al. HER2/neu expression in bladder cancer: relationship to cell cycle kinetics. Clin Biochem,2005,38(2):142-148.
[20]Gandour-Edwards R, Lara PN Jr, Folkins AK, et al. Does HER2/neu expression provide prognostic information in patients with advanced urothelial carcinoma? Cancer,2002,95:1009-1015.
[21]Hemann M T, Bric A,Teruya-Feldstein J,et al. Evasion of the p53 tumour surveillance network by tumour-derived MYC mutants. Nature,2005, 436(7052):787-789.
[22]Shachaf C M,Felsher D W.Tumor dormancy and MYC inactivation:pushing cancer to the brink of normalcy.Cancer Res,2005,65(11):4471-4474.
[23]Lipponen PK. Expression of c-myc protein is related to cell proliferation and expression of growth factor receptors in transitional cell bladder cancer. J Pathol, 1995,175:203-210.
[24]Schmitz-Drager BJ, Schulz WA, Jurgens B, et al. c-myc in bladder cancer: clinical findings and analysis of mechanism. Urol Res,1997,25(1):45-49.
[25]Zaharieva B, Simon R, Ruiz C, et al. High-throughput tissue microarray analysis of CMYC amplificationin urinary bladder cancer. Int J Cancer, 2005,117(6):952-956.
[26]Karoui M, Hofmann R H, Zimmermann U, et al. No evidence of somatic FGFR3 mutation in various types of carcinoma. Oneogene,2001,20:5059-5061.
[27]Pollock PM, Gartside MG, Dejeza LC, et al. Frequent activating FGFR2 mutations in endometrial carcinomas parallel germline mutations associated with craniosynostosis and skeletal dysplasia syndromes.Oncogene,2007,26(50): 7158-7162.
[28]Cappellen D, De Oliveira C, Ricol D, et al. Frequent activating mutations of FGFR3 in human bladder and cervix carcinomas. Nat Genet,1999,23:18-20.
[29]Kimura T, Suzuki H, Ohashi T, et al. The incidence of thanatophoric dysplasia mutations in FGFR3 gene is higher in low-grade or superficial bladder carcinomas. Cancer,2001,92(10):2555-2561.
[30]Van Rhijn BW, Lurkin I, Radvanyi F, et al:The fibroblast growth factor receptor 3 (FGFR3) mutation is a strong indicator of superficial bladder cancer with low recurrence rate. Cancer Res,2001,61,1265-1268.
[31]Kompier LC, van der Aa MN, Lurkin I, et al. The development of multiple bladder tumour recurrences in relation to the FGFR3 mutation status of the primary tumour. J Pathol,2009,218(1):104-112.
[32]Ohashi H, Takagi H, Oh H, et al. Phosphatidylinositol 3-kinase/Akt regulates angiotensin II-induced inhibition of apoptosis in microvascular endothelial cells by governing survivin expression and suppression of caspase-3 activity. Circ Res,2004,94(6):785-793.
[33]Ambrosini G, Adida C, Altieri DC. A novel anti-apoptosis gene survivirl, expressed in cancer and lymphoma. J Nat Med,1997,3(8):917-921.
[34]Schultz IJ, Kiemeney LA, Willems JL, et al. Clin Chem. Survivin and MKI67 mRNA expression in bladder washings of patients with superficial urothelial cell carcinoma correlate with tumor stage and grade but do not predict tumor recurrence.2006,52(7):1440-1442.
[35]Shariat SF, Ashfaq R, Karakiewicz PI, et al. Survivin expression is associated with bladder cancer presence, stage, progression, and mortality. Cancer.2007, 109(6):1106-1113.
[36]Weiss C, von Romer F, Capalbo G, et al. Survivin expression as a predictive marker for local control in patients with high-risk T1 bladder cancer treated with transurethral resection and radiochemotherapy. Int J Radiat Oncol Biol Phys, 2009,74(5):1455-1460.
[37]Knowles MA, and Williamson M:Mutation of H-ras is infrequent in bladder cancer:confirmation by single-strand conformation polymorphism analysis, designed restriction fragment length polymorphisms, and direct sequencing. Cancer Res,1993,53:133-139.
[38]Fontana D, Bellina M, Scoffone C, et al:Evaluation of c-ras oncogene product (p21) in superficial bladder cancer. Eur Urol,1996,29:470-476.
[39]Ye DW, Zheng JF, Qian SX, et al. Correlation between the expression of oncogenes ras and c-erbB-2 and the biological behavior of bladder tumors. Urol Res,1993,21:39-43.
[40]Xu M, Jin Y L. The abnormal expression of retinoic acid receptor-beta,p53 and Ki67 protein in normal, premalignant esoph ageal tissue. Word J Gastroenterol, 2002,8:200-202.
[41]Kaur P, Kallakury B S, Sheehan C E, et al. Survivin and Bel-2 expressioon in prostatic adenocarcinomas. Arch Pathol Lab Med,2004,128:39-43.
[42]Esrig D, Elmajian D, Groshen S, Accumulation of nuclear p53 and tumor progression in bladder cancer. N Engl J Med.1994,331(19):1259-1264.
[43]Slaton JW, Benedict WF, Dinney CP. P53 in bladder cancer:mechanism of action, prognostic value, and target for therapy. Urology,2001,57(5):852-859.
[44]Schroeder JC, Conway K, Li Y, et al. p53 mutations in bladder cancer:evidence for exogenous versus endogenous risk factors. Cancer Res,2003,63(21): 7530-7538.
[45]Salinas-Sanchez AS, Lorenzo-Romero JG, Gimenez-Bachs JM, et al. Implications of p53 gene mutations on patient survival in transitional cell carcinoma of the bladder:a long-term study. Urol Oncol,2008,26(6):620-626.
[46]Malats N, Bustos A, Nascimento CM, et al. P53 as a prognostic marker for bladder cancer:a meta-analysis and review. Lancet Oncol,2005,6(9):678-686.
[47]Moonen PM, Balken-Ory B, Kiemeney LA, et al. Prognostic value of p53 for high risk superficial bladder cancer with long-term followup. J Urol,2007, 177(1):80-83.
[48]Elhefnawy ND, Shoeib M. evaluation of retinoblastoma gene product (RB) as a prognstic indicator in bladder carcinoma. J Egy Nat.2001,13:185-190.
[49]Logothetis CJ, Xu HJ, Ro JY, et al. Altered expression of retinoblastoma protein and known prognostic variables in locally advanced bladder cancer, J Natl Cancer, Inst,1992,84:1256-1261.
[50]Grossman HB, Liebert M, Antelo M, et al. p53 and RB expression predict progression in T1 bladder cancer. Clin Cancer Res,1998,4:829-834.
[51]Davies MA, Koul D, Dhesi H, et al. Regulation of AKT/PKB action, cellular growth, and apoptosis in rostate carcinoma cells by MMAC/PTEN. Cancer Res, 1999,59 (11):2551-2560.
[52]Aveyard J S, Skilleter A, Habuchi T, et al. Somatic mutation of PTEN in bladder carcinoma. Br J Cancer,1999,80:904-908.
[53]Tanaka M, Koul D, Davies MA, et al. MMACI/PTEN inhibits cell growth and induces chemosensitivity to doxorubicin in human bladder cancer cells. Oncogene,2000,19 (47):5406-5412.
[54]Kagi D, Vignaux F, Ledermann B, et al. Fas and perforin pathways as major mechanisms of T cell-mediated cytotoxicity. Science,1994,265(5171):528-530.
[55]Kim KS. Multifunctional role of Fas-associated death domain protein in apoptosis. J Biochem Mol Biol,2002,35(1):1-6.
[56]Chopin D,Barei-Moniri R,Maille P, et al. Human urinary bladder transitional cell carcinomas acquire the functional Fas ligand during tumor progression. Am J Pathol.2003,162(4):1139-1149.
[57]Sudarshan S, Holman DH, Hyer ML, et al. In vitro efficacy of Fas ligand gene therapy for the treatment of bladder cancer. Cancer Gene Ther.2005, 12(1):12-18.
[58]Inoue K, Kamada M, Slaton JW, Fukata S, et al. The prognostic value of angiogenesis and metastasis-related genes for progression of transitional cell carcinoma of the renal pelvis and ureter. Clin Cancer Res,2002,8(6):1863-1870.
[59]Stavropoulos NE, Bouropoulos C, Ioachim IE, et al. Int Urol Nephrol. Prognostic significance of angiogenesis in superficial bladder cancer.2004,36 (2):163-167.
[60]Streeter EH, Harris AL. Angiogenesis in bladder cancer--prognostic marker and target for future therapy. Surg Oncol,2002,11(1-2):85-100.
[61]Al-Abbasi DS, Al-Janabi AA, Al-Toriahi KM, et al. Expression of VEGF in urinary bladder transitional cell carcinoma in an Iraqi population subjected to depleted uranium:an immunohistochemical study. Appl Immunohistochem Mol Morphol.2009,17(4):307-311.
[62]Palmero Marti JL, Queipo Zaragoza JA, Ruiz Cerda JL, et al. Study of the angiogenesis as prognostic factor of pTl G3 bladder tumours. Actas Urol Esp, 2004,28:594-601.
[63]Stavropoulos N E, Bouropoulos C, Ioachim IE, et al. Prognostic significance of angiogenesis in superficial bladder cancer. Int Urol Nephrol,2004,36 (2):163-167.
[64]Tanaka K, Sonoo H, Kurebayashi J, et al. Inhibition of infiltration and angiogenesis by thrombospondin-1 in papillary thyroid carcinoma, Clin Cancer Res.2002,8(5):1125-1131.
[65]Kwak C, lin C, Lee C, et al, Thrombospondin-1, vascular endothelial growth factor expression and their relationship with p53 status in prostate cancer and benign prostatic hyperplasia, BJU Int,2002,89(3):1303-309.
[66]Goddard JC, Sutton CD, Jones JL, et al. Reduced thrombospondin-1 at presentation predicts disease progression in superficial bladder cancer. Eur Urol, 2002,42(5):464-468.
[67]Mohseni H, Zaslau S, McFadden D, et al. COX-2 inhibition demonstrates potent anti-proliferative effects on bladder cancer in vitro. J Surg Res,2004,119(2):138-42.
[68]Shirahama T, Arima J, Akiba S,et al. Relation between cyclooxygenase-2 expression and tumor invasiveness and patient survival in transitional cell carcinoma of the urinary bladder. Cancer.2001,92(1):188-193.
[69]Choi EM, Kwak SJ, Kim YM,et al. COX-2 inhibits anoikis by activation of the PI-3K/Akt pathway in human bladder cancer cells. Exp Mol Med,2005,37(3):199-203.
[70]Marinho A, Soares R, Ferro J, et al. Angiogenesis in breast cancer is related to age but not to other prognostic parameters. Pathol Res Pract,1997,193(4): 267-273.
[71]Stavropoulos NE, Bouropoulos C, Ioachim E, et al. Prognostic significance of thymidine phosphorylase in superficial bladder carcinoma. Int Urol Nephrol, 2005,37(1):55-60.
[72]Shimabukuro T, Matsuyama H, Baba Y, et al. Expression of thymidine phosphorylase in human superficial bladder cancer. Int J Urol,2005,12(1):29-34.
[73]Migaldi M, Sgambato A, Garagnani L, et al. Loss of p21Wafl expression is a strong predictor of reduced survival in primary superficial bladder cancers. Clin Cancer Res,2000,6:3131-3138.
[74]Shariat SF, Tokunaga H, Zhou J, p53, p21, pRB, and p16 expression predict clinical outcome in cystectomy with bladder cancer. J Clin Oncol.2004, 22(6):1014-1024.
[75]Stein JP, Ginsberg DA, Grossfeld GD, et al:Effect of p21WAF1/CIP1 expression on tumor progression in bladder cancer. J Natl Cancer Inst,1998,90: 1072-1079.
[76]Sui L, Dong Y, Watanabe Y, et al. Clinical significance of Skp2 expression, alone and combined with Jabl and p27 in epithelial ovarian tumom. Oncol Rep, 2006,15(4):765-771.
[77]Franke KH, Miklosi M, Goebell P, Cyclin-dependent kinase inhibitor P27(KIP1) is expressed preferentially in early stages of urothelial carcinoma. Urology,2000, 56(4):689-695.
[78]Burton PB, Anderson CJ, Corbishly CM. Caspase 3 and p27 as predictors of invasive bladder cancer. N Engl J Med,2000,343(19):1418-1420.
[79]Munoz E, Gomez F, Paz JI, et aL. Ki-67 immunolabeling in pre-malignant lesions and carcinoma of the prostate. Histologic correlation and prognostic evaluation. Eur J Histochem,2003,47(2):123-128.
[80]Santos L, Amaro T, Costa C, et al. Ki-67 index enhances the prognostic accuracy of the urothelial superficial bladder carcinoma risk group classification. Int J Cancer,2003,105:267-272.
[81]Wu TT, Chen JH, Lee YH, et al:The role of bcl-2, p53 and ki-67 index in predicting tumor recurrence for low grade superficial transitional cell bladder carcinoma. J Urol,2000,163:758-760,.
[82]Stavropoulos NE, Filiadis I, Ioachim E, et al:Prognostic significance of p53, bcl-2 and Ki-67 in high risk superficial bladder cancer. Anticancer Res,2002,22: 3759-3764.
[83]Gontero P, Casetta G, Zitella A, et al:Evaluation of P53 protein overexpression, Ki67 proliferative activity and mitotic index as markers of tumour recurrence in superficial transitional cell carcinoma of the bladder. Eur Urol,2000,38: 287-296,.
[84]Pfister C, Moore L, Allard P, et al:Predictive value of cell cycle markers p53, MDM2, p21, and Ki-67 in superficial bladder tumor recurrence. Clin Cancer Res,1999,5:4079-4084.
[85]Li Z, Hromehak R, Bloch A. Differendal expression of proteins regularting cell cycle progression in growth vs.differentiation. Bioehim Biophys Acts,1997, 1356(2):149-159.
[86]Sgambato A, Migaldi M,Faraglia B,et al:Cyclin Dl expression in papillary superficial bladder cancer:its association with other cell cycle-associated proteins, cell proliferation and clinical outcome. Int J Cancer,2002,97:671-678.
[87]Richter J, Wagner U, Kononen J, et al.High-throughput tissue microarray analysis of cyclin E gene amplification and overexpression in urinary bladder cancer. Am J Patho,2000,157:787-794.
[88]Shariat SF, Ashfaq R, Sagalowsky AI, et al. Correlation of cyclin D1 and El expression with bladder cancer presence, invasion, progression, and metastasis. Hum Pathol,2006,37(12):1568-1576.
[89]Stoimenov I, Helleday T. PCNA on the crossroad of cancer. Biochem Soc Trans. 2009,37(3):605-613.
[90]Inagaki T, Ebisuno S, Uekado Y, PCNA and p53 in urinary bladder cancer: correlation with histological findings and prognosis. Int J Urol,1997,4(2): 172-177.
[91]Zhu Z, Xing S, Lin C, et al. Bladder cancer therapy using combined proliferating cell nuclear antigen antisense oligonucleotides and recombinant adenovirus p53.Chin Med J,2003,116(12):1860-1863.
[92]El-Kott AF, Khalil AM, El-Kenawy Ael-M. Immunohistochemical expressions of uPA and its receptor uPAR and their prognostic significant in urinary bladder carcinoma. Int Urol Nephrol.2004,36(3):417-423.
[93]Li YJ, Zheng BZ, Zhou ZL,et al. Association of uPA and uPAR expression with invasive behaviors of urinary transitional cell carcinoma. Ai Zheng,2004, 23(6):704-706.
[94]Shin SJ, Kim KO, Kim MK,et al. Expression of E-cadherin and uPA and their association with the prognosis of pancreatic cancer. Jpn J Clin Oncol.2005, 35(6):342-348.
[95]Marhaba R, Zoller M. CD44 in cancer progression:adhesion, migration and growth regulation. J Mol Histol,2004,35(3):311-321.
[96]Stavropoulos NE, Filliadis I, Ioachim E, CD44 standard form expression as a predictor of progression in high risk superficial bladder tumors. Int Urol Nephrol, 2001,33(3):479-483.
[97]Miyake H, Hara I, Kamidono S,et al:Multifocal transitional cell carcinoma of the bladder and upper urinary tract:molecular screening of clonal origin by characterizing CD44 alternative splicing patterns. J Urol,2004,172(3):1127-1129.
[98]Wijnhoven BP, Dinjens WN, et al. E-cadherin-catenin cell-cell adhesion complex and human cancer. Br J Surg,2000,87(8):992-1005.
[99]Popov Z, Medina SG, Belda ML, et al. Low E-cadherin expression in bladder cancer at the transcriptional and protein level provides prognostic information. British Journal of Cancer,2000,83:209-214.
[100]Shariat SF, Pahlavan S, Baseman AG, E-cadherin expression predicts clinical outcome in carcinoma in situ of the urinary bladder. Urology,2001,57(1):60-65.
[101]Shin SJ, Kim KO, Kim MK,et al. Expression of E-cadherin and uPA and their association with the prognosis of pancreatic cancer. Jpn J Clin Oncol,2005, 35(6):342-348.
[102]Nutt JE, Durkan GC, Mellon JK, et al.Matrix metalloproteinases (MMPs) in bladder cancer:the induction of MMP9 by epidermal growth factor and its detection in urine. BJU Int,2003,91(1):99-104.
[103]Schmalfeldt B, Prechtel D, Harting K, et al. Increased expression of matrix metalloproteinases (MMP)-2, MMP-9 and the urokinase-type plasminogen activator is associated with progression from benign to advanced ovarian cancer. Clin Cancer Res,2001,7(8):2396-2404.
[1]Schnitt SJ. Breast cancer in 21st century:neu opportunities and neu challenges. Mod Pathol,2001,14(3):213-218.
[2]Winters ZE, Leck RD, Bradeburn MJ, etal. Cytoplasmic P2 express is correlted with HER-2/nuein breas tcancer and is a independent predicator of prognosis. Breas tCancer Res,2003,5(6):242-249.
[3]Junker K, Stachetzki U, Rademacher D, etal. HER2/neu expression and amplification in non-small cell lung cancer prior to and after neoadjuvant therapy. Lung Cancer,2005,49(2):279-80.
[4]Yazici H, Altun M, Alatli C, etal. c-erbB-2 Gene Amplification in Naso-pharyngeal Carcinoma. Cancer Invest,2000,18(1):6-10
[5]Tsutsui S, Ohno S, Murakam IS, et al. Progno stic value of CerbB2 expression in breast cancer. Surg Onco1 2002,79(4),216-223.
[6]Peter B, Howard A, Mannuela C, etal.Therapy for pancreatic cancer With a recombinant humanizied antibody anti-HER2(Hercepitin).J Gastrointestinal Surgery,2001,31(5):139-141.
[7]Karan D, Lin MF, Johansson SL, et al. Current status of themolecular genetics of human prostatic adenocarcinomas. Int J Cancer,2003,103(3):285-293.
[8]Corps AN, SowterHM, Smith S. Hepatocyte growth factor stimulates motility, chemotax is and mitogenesis inovarian carcinomace expressing high levels of c-met.Int J Cancer,1997,73:151-155.
[9]Knudsen BS, Gmyrek GA, Inra J, et al. High Expression of the Met receptor in prostate cancer metastasis to bone. Urology,2002,60 (60):1113-1117.
[10]Kim SJ, Johnson M, Koterba K, et al. Reduced c-Met Expression by an Adenovirus Expressing a c-Met Ribozyme Inhibits Tumorigenic Growth and Lymph Node Metastases of PC3-LN4 Prostate Tumor Cells in an Orthotopic Nude Mouse Model. Clin Cancer Res,2003,14:5161-5170.
[11]Zhang S, Zhau HE, Osunkoya AO, et al. Vascular endothelial growth factor regulates myeloid cell leukemia-1 expression through neuropilin-1-dependent activation of c-MET signaling in human prostate cancer cells. Mol Cancer,2010 19:9-19.
[12]Edwards J, Krishna NS, Witton C3, et al. Gene ampHficafions associated with the development of hormone-resistant prostate eantmr. Clin Cancer Res,2003, 9(14):5271-5281.
[13]McPherson RA, Conaway MC, Gregory CW, et al. The novel Ras antagonist, farnesylthiosalicylate, suppresses growth of prostate cancer in vitro. Prostate, 2004,58(4):325-334.
[14]Paik S, Bryant J, Tan-chiu E, et al. Real-world performance of HER2 testing-National Surgical Adjuvant Breast and Bowel Project Experience. J Natl Cancer Inst,2002,94:852-854.
[15]Agnantis NJ, C9nstantinidou AE, Papaevagelou M, et al. Comparative immunohistechemical study of rag-p21 oncopmtein in adenomatous hyperplaaia and adenoearcinoma of the prostate gland. Antieancor Res,1994,14(5a): 2135-2140.
[16]Han WD, Mu YM, Lu XC, et al. Upregulation of LRP16 mRNA by 17βestradiol through activation of estrogen receptor a (ERa), but not estrogen receptor β(ERβ), and promotes human breast cancer MCF7 cell proliferation:A preliminary report. Endoc Relat Cancer,2003,10(3):215-222.
[17]Walker VR, Korach KS. Estrogen recepto rknockout mice as a model fo rendocriner esearch. ILAR J,2004,45(4):455-461.
[18]Nupponen NN, Kakkola L, Koivisto P, et al. Genetic alterations in hormone-refractory recurrent prostate carcinomas. Am. J. Pathol,1998.153: 141-148.
[19]Kaltz-Wittmer, C, et al. FISH analysis of gene aberrations (MYC, CCND1, ERBB2, RB, and AR) in advanced prostatic carcinomas before and after androgen deprivation therapy. Lab Invest,2000,80:1455-1464.
[20]Iversen PL, Arora V, Acker AJ, et al. Efficacy of antisense morpholino oligomer targeted to c-myc in prostate cancer xenograft murine model and a Phase Ⅰ safety study in humans. Clinical Cancer Research,2003,9:2510-2519.
[21]Kuzmichev A, Jenuwein T, Tempst P, et al. Different EZH2-containing complexes target methylation of histone H1 or nucleosomal histone H3. Mol Cell,2004,14(2):183-193.
[22]Hanson RD, Hess JL, Yu BD, et al. Mammalian Trithorax and polycomb-group homologues are antagonistic regulators of homeotic development. Proc Nat Acad Sci USA,1999,96:14372-1437.
[23]Kleer CG., Cao Q, Varambally S, et al. EZH2 is a marker of aggressive breast cancer and promotes neoplastic transformation of breast epithelial cells. Proc Natl Acad Sci,2003,100:1606-11611.
[24]Varambally S, Dhanasekaran SM, Zhou M, et al. The polycomb group protein EZH2 iS involved in progression of prostate caDcer. Nature,2002,419:624-629.
[25]Tomlins SA, Rhodes DR, Perner S, et al.. Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer. Science.2005,310:644-648.
[26]Kumar-Sinha C, Tomlins SA, Chinnaiyan AM, et al. Recurrent gene fusions in prostate cancer. Nat Rev. Cancer,2008,8:497-511.
[27]Han B, Mehra R, Dhanasekaran SM, et al. A fluorescence in situ hybridization screen for E26 transformation-specific aberrations:identification of DDX5-ETV4 fusion protein in prostate cancer. Cancer Res,2008,68:7629-7637.
[28]Gopalan A, Leversha MA, Satagopan JM, et al. TMPRSS2-ERG gene fusion is not associated with outcome in patients treated by prostatectomy. Cancer Res, 2009,69:1400-1406.
[29]Yoshimoto M, Joshua AM, Cunha IW, et al. Absence of TMPRSS2:ERG fusions and PTEN losses in prostate cancer is associated with a favorable outcome. Mod Pathol,2008,21(12):1451-1460.
[30]Rostad K, Hellwinkel OJ, Haukaas SA, et al. TMPRSS2:ERG fusion transcripts in urine from prostate cancer patients correlate with a less favorable prognosis. APMIS,2009,117(8):575-582
[31]Merz VW, Arnold AM, Studer UE, et al. Differential expression of transforming growth factor-bota 1 and beta 3 as well as c-fos mRNA in normal human prostate, benign prostatic hyperplasia and prostatic Cancer. world J Urol,1994, 12(2):96-98.
[32]Zhou W, Janulis L, Park Ⅱ, et al. A novel anti-proliferative property of elusterinin prostate cancer coils. Life Sci,2002,72(1):11-21.
[33]Zhang X, Li W, Olumi AF. et al. Low-dose 2-O-tetradecanoylphorbol-13-acetate enhances tumor necrosis factor related apoptosis-inducing ligand induced apoptosis in prostate cancer cells.Clin Cancer Res,2007,13(23):7181-7190.
[34]Kim HS, Shiraki K, Rark SH, et al. Expression of survivin CIN and invasive squamous cell carcinoma of uterine cervix. Anticanee Res,2002,22(2A): 805-808.
[35]Sonnemann J, Gekeler V, SagrauskeA, et al. Apoptotic responsiveness of PC-3 prostate cancer cells to tumor necrosis factor-related apoptosisinducing ligand:e vidence for differential effects of Bcl-xL and Bcl-2 down-regulation. Int J Oncol, 2004,25(4):1171-1181.
[36]Lin Y, Fukuchi J, Hiipakka RA, et al. Up-regulation of Bcl-2 is required for the progression of prostate cancer cells from an androgen-dependent to an androgen-independent growth stage. Cell Res.2007,17(6):531-536.
[37]Yoshino T, Shiina H, Urakami S, et al. Bcl-2 expression as a predictive marker of hormone-refractory prostate cancer treated with taxane-based chemotherapy.Clin Cancer Res,2006,12(20):6116-6124.
[38]Ambrosin iG, Adida C, Alteri DC. Anovel ant-iapotosisgene, Surviving, Expressin cancer and lymphoma. NatureMed,1997, (8):917-921.
[39]Gazzaniga P, Gradilone A, Giuliani L, et al. Expressionandprognostic Significance of livin, survivin and other apoptosis-related genes in the progression of superficial bladde rcancer. Annals of Oncology,2003,14(2): 85-90.
[40]Shariat SF, Lotan Y, Saboorion H, et al. Survivin expression is associated with eatures of biologically aggressive prostate carcinoma. Cancer,2004,15(4): 751-757.
[41]Kishi H, Igawa M, Kikuno N, et al. Expression of survivin gene in prostate cancer:correlation with clinicopathological characteristics, proliferative activity and apoptosis. J Urol,2004,171 (5):1855-1860.
[42]Paduano F, Villa R, Pennati M, et al. Silencing of survivin gene by small interfering RNAs produces supra-additive growth suppression in combination with 17-allylamino-17-demethoxygeldanamycin in human prostate cancer cells. Mol Cancer Ther,2006,5(1):179-186.
[43]Pins MR, Fiadjoe JE, Korley F, et al. Clusterin as a possible predictor for biochemical recurrence of prostate cancer following radical prostatectomy with intermediate Gleason scores:a preliminary report. Prostate Cancer Prostatic Dis, 2004,7(3):243-8.
[44]Bettuzzi S, Davalli P, Astancolle S, et al. Tumor progression is accompanied by significant changes in the levels of expression of polyamine metabolism regulatory genes and clusterin(sulfated glycoprotein 2)in human prostate cancer specimens. Cancer Res,2000,60(1):28-24.
[45]Henderson J. Liver transplantation and rejection:an overview. Hepato-Gastro-enterol,1999,46(2):1480-1484.
[46]Liu H, Gong NQ, LiGS, et al. Changes of express/on of Bcl-2 protein in rat liver during ischemia-reperfusion injury. Zhongguo Xiandai Yixue Zazhi,2002, 12(12):16-18.
[47]Dominguez A, Ramos, Morales F, Romero F,et al.Hpttg, a human homologue of rat pttg, is overexpressed in hematopoietic neoplasms. Evidence for a trans-criptional activation function of hPTTG.Oncogene,1998,17(17):2187-2193.
[48]Zhu X, Mao Z, Na Y, Guo Y, et al.Significance of pituitary tumor transforming gene 1 (PTTG1) in prostate cancer. Anticancer Res,2006,26(2):1253-1259.
[49]Wang Z, Bhattacharya N, W emver M, et al. Pim-1:a Serine/hreonine kinase with 8 role in cell survival, proliferation, differentiation and tumorigenesis. J Vet Sef,2001,2(3):167-179.
[50]Cibull TL, Jones TD, Li L, et al. Overexpression of Pim-1 during progression of prostatic adenoearclnoma. J Clin Pathol,2006,59(3):285-288.
[51]Thompson J, Pehola IcJ, Koskinen PJ, et al. Attenuation of andgogen recepto-r dependent transcription by sefine/threonine kinase Pim-1. Lab Invest,2003,83: 1301-1309.
[52]Xie Y, Xu K, Lima DE, et al. ne44-kDa Pim-kinase phesphorylates BCRP/ABCG2 and thereby promotes its mulfimerization and drug-resistant activity in human prostate cancer cells. J Biol Chem,2008,283(6):3359-3356.
[53]Hu XF, Li J, Vandervalk S, et al. PIM-1-specific mAbsuppreses human and mourse tumuseor growth by decreasing PIM-1 levels, reducing Akt phosphorylation, and activating apoptosis. I Clin Invest,2009,119(2):362-375.
[54]Bai Hz, Pollman MJ, Inishi Y, et al. Regulation of vascular smooth muxcle cell apoptosis.Modulation of bad by a phosphatidylinositol 3-kinase de pendent pathway. Circ Res,1999,85(3):229-237.
[55]Matsui T, Li L, Del Monte F, et al. Adenoviral gene transfer of activated phosphatidylinositol 3'-kinase and Akt inhibits apoptosis of hypoxic cardio-myocytes in vitro. Circulation,1999,100:2373-2379.
[56]Kaplan P J, Mohan S, Cohen P, et al. The insulin-like growth factor axis and prostate cancer:lessons from the transgenic adenocarcinoma of mouse prostate (TRAMP) model. Cancer res,1999,59(9):2203-2209.
[57]Mucci LA, Stark JR, Pollak MN, et al. Plasma levels of acid-labile subunit, free insulin-like growth factor-Ⅰ, and prostate cancer risk:a prospective study. Cancer Epidemiol Biomarkers Prev.2010,19(2):484-491.
[58]Shukla S, Gupta S. Apigenin suppresses insulin-like growth factor I receptor signaling in human prostate cancer:an in vitro and in vivo study. Mol Carcinog, 2009,48(3):243-252.
[59]Rufinova MB, Schoer RA. Effect of angiogenes isinhibition by Id loss and the contribution of bone-marrow-derived endothelial cell sinsponta-FIeOUS mufine tumors. J Allergy Carcinoma Cell,2003,4(10):277-289.
[60]Lasorella A.Uo T.Iavarone A Id proteins at the cross-road of development and cancer Oncogene,2001,20:8326-8333.
[61]Lyden D, Hauofi K, Dias S, et al. Impaired imcmitment of bone-Marrow-derived endothelial and hematepoietic precursor cells blockstunIor ansingenesis and gowth. Nature,2001,7(11):1194-1201.
[62]Ouyang XS, Wang X, Lee DT, Over expression of 1D-1 in prostate cance. Urol 2002,167:2598-2602.
[63]Lin JC, Chang SY, Hsieh DS, et al. Modulation ofmitogen-activated protein kinase cascades by differentiation-1 protein:acquired drug resistance of hormone independent prostate cancer ceils. Urol,2005,174:2022-2026.
[64]Ling MT, Wang X, Lee DT, et al. Id-1 expression induces androgen-independent prostate cancor ceU growth through activation of epidermal growth factor receptor (EGF-R). Carcinogenesis,2004,5:517-525.
[65]Zhang X, Ling MT, Wang X, et al. Inactivation of Id-1 in prostate cancer cells:A potential therapeutic target in inducing chemosensitization to taxol through activation of JNK pathway. Int J Cancer,2006,118(8):2072-2081.
[66]Kaur P, Kallakury B S, Sheehan C E, et al. Survivin and Bel-2 expressioon in prostatic adenocarcinomas. Arch Pathol Lab Med,2004,128:39-43.
[67]Kastan MB, Bartek J. Cell2cycle checkpoints and cancer. Nature,2004,432 (7015):316-323.
[68]Massague J. G1 cell2cycle control and cancer. Nature,2004,432(7015):298-306.
[69]Bert Vogelstein, David Lane, Arnold J L. Surfing the p53 net-work. Nature, 2000,408:307-310.
[70]Schlomm T, Iwers L, Kirstein P, et al. Clinical significance of p53 alterations in surgically treated prostate cancers. Modern pathology,2008,21 (11):1371-1378.
[71]Pisters LL, Pettaway CA, Troncoso P, et al. Evidence that transfer of functional p53 protein results in increased apoptosis in prostate cancer. Clin Cancer Res, 2004,10(8):2587-2593.
[72]Maddison LA, Sutherland BW, Barrios RJ, el al. Conditional delefinn of Rb causes early stage prostate cancer. Cancer Res,2004,64(17):6018-6025.
[73]Nakamura T, Ide H, Eguchi R, el al.Concomitant analysis of p16/INK4, cyclin Dl,and retinoblastoma protein expression in esophageal squamous cell. Carcinoma,2003,50(53):1321-1326.
[74]Hayward SW, Wang Y, Day ML. Rescue and isolation of Rb-deficient prostate epithelium by tissue recombination. Methods Mol Biol,2003,218:17-33.
[75]Ito G, Uchiyama M, Kondo M, et al. Mori S Usami N Maeda O Kawabe T Hasegawa Y Shimokata K Sekido Y Kruppel-like factor 6 is frequently down-regulated and induces apoptosis in non-small cell lung cancer cells. Cancer Res,2004,64(11):3838-3843.
[76]Narla G, Heath KE, Reeves HL, et al. KLF6,a candidate tumor suppressor gene mutated in prostate. Science,2001,294(5551):2563-2566.
[77]Narla G, Difeo A, Reeves HL, et al. A germline DNA polymorphism enhances alternative splicing of the KLF6 tumor suppressor gene and is associated with increased prostate cancer risk. Cancer Res,2005,65:1213-1222.
[78]Narla G, DiFeo A, Yao S. Targeted inhibition of the KLF6 splice variant, KLF6 SV1, suppresses prostate cancer cell growth and spread. Cancer Res,2005, 65(13):5761-5768
[79]Li J, Yen C, Liaw D, et al. PTEN, a putative protein tyrosine phosphatase gene mutated in human brain, breast, and prostate cancer. Science,1997,275(5308): 1943-1947.
[80]Hu TH, Huang CC, Lin PR, el al. Expression and prognostic role of tumor suppressor gene PTEN/MMACI/TEPI in hepatocellular carcinoma. Cancer, 2003,97:1929.
[81]Cairns P, Okami K, Halachmi S, et al. Frequent inactivation of mN/MMAC1 in primary prostate cancer. Cancer Res,1997,57(22):4997-5000.
[82]Mulholland DJ, Jiao J, Wu H, et al. Hormone refractory prostate cancer: Lessons learned from the PTEN prostate cancer model. Adv Exp Med Biol. 2008,617:87-95.
[83]Yoshimoto M, Joshua AM, Cunha IW, et al. bsence of TMPRSS2:ERG fusions and PTEN losses in prostate cancer is associated with a favorable outcome. Mod Pathol,2008,21(12):1451-1460.
[84]85 Wu Z, McRoberts KS, Theodorescu D. The role of PTEN in prostate cancer cell tropism to the bone micro-environment. Carcinogenesis,2007,28(7): 1393-1400.
[85]Weinberg W C, Denning M F. P21 Wafl Control of Epithetlial Cell Cycle and Cell Fate. Crit Rev Oral Biol Med,2002,13(6):453-464.
[86]Romics I, Banfi G, Szekely E, et al. Expression of p21(wafl/cipl), p27 (kip1), p63 and androgen receptor in low and high Gleason score prostate cancer. Pathol Oncol Res.2008,14(3):307-311.
[87]Karim F, izazi, Luis A, et al. The Association of p21(wAF+1, clPl) with Progression to Androgen-independent Prostate Cancer. Clinical Cancer Research,2002,8:775-781.
[88]Rocco JW, Sidransky D. pl6(MTS-1/CDKN2/INK4a) in cancer progression. Exp Cell Res,2001,264(1):42-55.
[89]Chakravarti A, Heydon K, Wu CL, et al. Loss of p16 expression is of prognostic significance in locally advanced prostate cancer:an analysis from the Radiation Therapy Oncology Group protocol 86-10. J Clin Oncol,2003, 21(17):3328-3334.
[90]Allay JA, Steiner MS, Zhang Y, et al. Adenovirus p16 gene therapy for prostate cancer. World J Urol,2000,18(2):111-120.
[91]Sheng S. The promise and challenge toward the clinical application of maspin in cancer. Front Biosci,2004,1(9):2733-2745.
[92]Li Z, Shi HY, Zhang M. et al. Targeted expression of maspin in tumor vasculartures induces endothelial cell apoptosis. Ocogene,2005,24:2008-2019.
[93]Liu J,Yin S,Reddy N, et al. Bax mediates the apoptosis-sensitizing effect of maspin Cancer Res,2004,64:1703-1711.
[94]Odero-Mamh VA, Khalkhali-Ellis Z, Chunthapong J, et al. Maspin regulates difkrent signaling patllways for motility and adhesion in aggressive breast cancer cells. Cancer Biol Ner,2003,2(4):398-403.
[95]Pierson CR, McGowen R, Grignon D, et al. Maspinis upregulated in prema-lignant prostate epithelia. Prostate,2002,53:255-262.
[96]Machtens S, Serth J, Bokemeyer C, et al. Expression of the p53 and Maspin protein in primary prostate cancer:correlation with clinical features. Int J Cancer,2001,95(5):337-342.
[97]Li X, Chen D, Yin S, Maspin augments proteasome inhibitor-induced apoptosis in prostate cancer cells. J Cell Physiol,2007,212(2):298-306.