透明质酸测定鉴别诊断肾细胞癌和移行细胞癌
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摘要
目的
肾肿瘤在泌尿外科比较常见,且多数为恶性。肾癌患者主诉和临床表现多变,尤其在浸润生长至肾盂后,与肾盂癌很难鉴别。鉴于肾癌和肾盂癌诊断后治疗方法的不同,对肾癌和肾盂癌进行鉴别诊断是尤为重要的。
目前有很多体液中肿瘤标志物的研究,其中与泌尿系肿瘤相关的标志物检测主要集中在对尿液中肿瘤标志物的研究。肾盂癌作为一种上尿路移行细胞癌,其尿液中表达肿瘤标志物水平很高。目前用于进行移行细胞癌的诊断和预后的尿液肿瘤标志物主要有细胞角质蛋白(Cytokeratins,CK)、核基质蛋白22(Nuclear matrix protein 22,NMP22)、膀胱癌相关核基质蛋白(BLCA4)、膀胱肿瘤抗原(Bladder tumor antigen,BTA)、纤维蛋白降解产物(Fibrin degradation products,FDP)、端粒酶(Telomerase)、基质金属蛋白酶(Matrix metalloproteinase,MMP)以及透明质酸和透明质酸酶(Hyahronic acid/Hyaluronidase,HA/HAase)。其中透明质酸是组织基质中的一种粘多糖,可以促进肿瘤细胞的粘符合转移,低分子量的透明质酸,还可以促进血管生成。研究表明,使用酶联免疫法测定膀胱癌病人尿液中的透明质酸明显升高,其敏感性和特异性可以达到92%和93%。而且只有高级别的膀胱癌病人样本中才有刺激血管生成的透明质酸。此外,透明质酸在很多肿瘤组织和肿瘤患者体液内有明显升高。如胃癌,结肠癌,肾母细胞癌和恶性间皮瘤患者血液中透明质酸水平都明显升高。有关肾癌、肾盂癌患者血液和尿液中透明质酸的表达水平,尚没有相关的报道。
实验材料和方法
1。实验材料:收集中国医科大学附属一院和附属二院2003年12月至2005年1月共41例患者血液和尿液样本。其中,肾癌17例,肾盂癌14例,
ObjectRenal tumor is a common diease in surgical urology, whereas most of them are malignant. Renal carcinoma can be mainly divided into two kinds: primary and secondary. In primary renal carcinoma, renal cell cancer(RCC) occupies 85% , renal transitional cell carcinoma(TCC) 7 -8% , Wilm's tumor 5 -6% , renal sarcoma 3% (the renal transitional cell carcinoma rate is higher than this value in our nation). Renal cancer patients'symptoms and signs are very diversity , especially after the invasion into pelvis, it is very difficult to perform differential diagnosis. For the different operation way to RCC and TCC, this differential diagnosis is very important.Nowadays there are many articles about tumor markers in body fluid, the research about urology cancer is mainly in urine markers. As Renal pelvic carcinoma is a transitional cancer, the level of tumor marker in the urine is quietly high. The tumor markers using to check in urine for the diagnosis and prognosis are Cytokeratins (CK) , Nuclear matrix protein 22 (NMP22) , BLCA4, Bladder tumor antigen (BTA) , Fibrin degradation products (FDP) , Telomerase, Matrix metalloproteinase (MMP) , Hyaluronic acid/Hyaluronidase (HA/HAase). HA is a glycosaminoglycan in tissue matrix, it can improve the adhersion and trans-mition of tumor cell, whereas the low molecular HA can promote the angiogeno-sis. As say in many researches, HA is obviously high in bladder cancer patients 'urine, the sensitivity and specificity is 92% and 93% separately. And, only in high grade bladder cancer, there are HA which can stimulate the angiogenosis. Still, HA is obviously high in the tissue and body fluid in other cancer. For example, the blood levels of HA in gastric cancer, colon cancer, Wilm's tumor
and malignant mesothelioma are all higher than normal. However, the HA level of TCC and RCC in urine and blood samples are still not researched.Materials and Methods1. Sample collections: this study include 41 patients, all take both urine and blood samples, in which there are 17 cases of renal cell carcinoma, 14 cases of renal transitional carcinoma and 10 cases of normal persons.2. Methods: After dealing samples with standard way, the samples are kept within deep freezer. And do the experiment all together. We use ELISA to test HA in urine and blood samples and use chemoluminescence immunoassay to test the protein in urine samples. Use the urine protein to adjust the HA in urine samples. SPSS 11.0 for windows is used to analyse the data.Results1. HA in blood samples; In 41 cases of blood samples, the data in different groups are not different in statistics.2. HA in urine samples: HA concentration in urine samples are adjusted by urine protein. The HA value after adjustment is compared by statistics. Urine HA in the renal TCC group is obviously high than the other two groups (p <0. 01) , but the RCC group has no different with the control group (P >0.05). A-malgamate the TCC and RCC groups to be cancer group, the HA in urine after adjustment is different with control group. ( p <0.01)3. Blood HA/urine HA after adjustment; This value is different between the renal TCC group and the other two groups ( p < 0. 01) , but no difference is -shown between RCC and control group. Amalgamate the TCC and RCC groups tobe cancer group, the rate is different in statistics.Conclusions1. There are no different between renal TCC and RCC and normal persons
肾肿瘤在泌尿外科比较常见,且多数为恶性。肾癌患者主诉和临床表现多变,尤其在浸润生长至肾盂后,与肾盂癌很难鉴别。鉴于肾癌和肾盂癌诊断后治疗方法的不同,对肾癌和肾盂癌进行鉴别诊断是尤为重要的。
目前有很多体液中肿瘤标志物的研究,其中与泌尿系肿瘤相关的标志物检测主要集中在对尿液中肿瘤标志物的研究。肾盂癌作为一种上尿路移行细胞癌,其尿液中表达肿瘤标志物水平很高。目前用于进行移行细胞癌的诊断和预后的尿液肿瘤标志物主要有细胞角质蛋白(Cytokeratins,CK)、核基质蛋白22(Nuclear matrix protein 22,NMP22)、膀胱癌相关核基质蛋白(BLCA4)、膀胱肿瘤抗原(Bladder tumor antigen,BTA)、纤维蛋白降解产物(Fibrin degradation products,FDP)、端粒酶(Telomerase)、基质金属蛋白酶(Matrix metalloproteinase,MMP)以及透明质酸和透明质酸酶(Hyahronic acid/Hyaluronidase,HA/HAase)。其中透明质酸是组织基质中的一种粘多糖,可以促进肿瘤细胞的粘符合转移,低分子量的透明质酸,还可以促进血管生成。研究表明,使用酶联免疫法测定膀胱癌病人尿液中的透明质酸明显升高,其敏感性和特异性可以达到92%和93%。而且只有高级别的膀胱癌病人样本中才有刺激血管生成的透明质酸。此外,透明质酸在很多肿瘤组织和肿瘤患者体液内有明显升高。如胃癌,结肠癌,肾母细胞癌和恶性间皮瘤患者血液中透明质酸水平都明显升高。有关肾癌、肾盂癌患者血液和尿液中透明质酸的表达水平,尚没有相关的报道。
实验材料和方法
1。实验材料:收集中国医科大学附属一院和附属二院2003年12月至2005年1月共41例患者血液和尿液样本。其中,肾癌17例,肾盂癌14例,
ObjectRenal tumor is a common diease in surgical urology, whereas most of them are malignant. Renal carcinoma can be mainly divided into two kinds: primary and secondary. In primary renal carcinoma, renal cell cancer(RCC) occupies 85% , renal transitional cell carcinoma(TCC) 7 -8% , Wilm's tumor 5 -6% , renal sarcoma 3% (the renal transitional cell carcinoma rate is higher than this value in our nation). Renal cancer patients'symptoms and signs are very diversity , especially after the invasion into pelvis, it is very difficult to perform differential diagnosis. For the different operation way to RCC and TCC, this differential diagnosis is very important.Nowadays there are many articles about tumor markers in body fluid, the research about urology cancer is mainly in urine markers. As Renal pelvic carcinoma is a transitional cancer, the level of tumor marker in the urine is quietly high. The tumor markers using to check in urine for the diagnosis and prognosis are Cytokeratins (CK) , Nuclear matrix protein 22 (NMP22) , BLCA4, Bladder tumor antigen (BTA) , Fibrin degradation products (FDP) , Telomerase, Matrix metalloproteinase (MMP) , Hyaluronic acid/Hyaluronidase (HA/HAase). HA is a glycosaminoglycan in tissue matrix, it can improve the adhersion and trans-mition of tumor cell, whereas the low molecular HA can promote the angiogeno-sis. As say in many researches, HA is obviously high in bladder cancer patients 'urine, the sensitivity and specificity is 92% and 93% separately. And, only in high grade bladder cancer, there are HA which can stimulate the angiogenosis. Still, HA is obviously high in the tissue and body fluid in other cancer. For example, the blood levels of HA in gastric cancer, colon cancer, Wilm's tumor
and malignant mesothelioma are all higher than normal. However, the HA level of TCC and RCC in urine and blood samples are still not researched.Materials and Methods1. Sample collections: this study include 41 patients, all take both urine and blood samples, in which there are 17 cases of renal cell carcinoma, 14 cases of renal transitional carcinoma and 10 cases of normal persons.2. Methods: After dealing samples with standard way, the samples are kept within deep freezer. And do the experiment all together. We use ELISA to test HA in urine and blood samples and use chemoluminescence immunoassay to test the protein in urine samples. Use the urine protein to adjust the HA in urine samples. SPSS 11.0 for windows is used to analyse the data.Results1. HA in blood samples; In 41 cases of blood samples, the data in different groups are not different in statistics.2. HA in urine samples: HA concentration in urine samples are adjusted by urine protein. The HA value after adjustment is compared by statistics. Urine HA in the renal TCC group is obviously high than the other two groups (p <0. 01) , but the RCC group has no different with the control group (P >0.05). A-malgamate the TCC and RCC groups to be cancer group, the HA in urine after adjustment is different with control group. ( p <0.01)3. Blood HA/urine HA after adjustment; This value is different between the renal TCC group and the other two groups ( p < 0. 01) , but no difference is -shown between RCC and control group. Amalgamate the TCC and RCC groups tobe cancer group, the rate is different in statistics.Conclusions1. There are no different between renal TCC and RCC and normal persons
引文
1. Tammi MI, Day AJ, Turley EA. Signaling properties of hyaluronan receptors. J Biol Chem 2002; 277: 4598 -92
2. Stern R. Hyaluronan catabolism: a new metabolic pathway. Eur J Cell Biol. 2004 Aug;83(7):317-25.
3. Suzuki M, Asplund T, Yamashita H, Heldin CH, Heldin P. Stimulation of hyaluronan biosynthesis by platelet - derived growth factor - BB and transforming growth factor - beta 1 involves activation of protein kinase C. Biochem J. 1995 May 1 ;307 ( Pt 3) :817 -21.
4. Langner C, Ratschek M, Tsybrovskyy 0, Schips L, Zigeuner R. P63 immunoreactivity distinguishes upper urinary tract transitional - cell carcinoma and renal - cell carcinoma even in poorly differentiated tumors. J Histochem Cytochem. 2003 Aug;51(8) :1097 -9.
5. Heldin P. Importance of hyaluronan biosynthesis and degradation in cell differentiation and tumor formation. Braz J Med Biol Res. 2003 Aug;36(8) : 967 -73. Epub 2003 Jul 23. Review.
6. Rahmanian M, Heldin P. Testicular hyaluronidase induces tubular structures of endothelial cells grown in three - dimensional collagen gel through a CD44 - mediated mechanism. Int J Cancer. 2002 Feb 10;97(5) :601 -7.
7. Li Y, Heldin P. Hyaluronan production increases the malignant properties of mesothelioma cells. Br J Cancer. 2001 Aug 17;85(4) :600 -7.
8. Toole BP. Hyaluronan in morphogenesis. Semin Cell Dev Biol. 2001 Apr; 12(2):79-87.
9. Wang C, Tammi M, Guo H, Tammi R. Hyaluronan distribution in the normal epithelium of esophagus, stomach, and colon and their cancers. Am J Pathol. 1996 Jun;148(6):1861-9.
10. Auvinen P, Tammi R, Parkkinen J, Tammi M, Agren U, Johansson R, Hirvikoski P, Eskelinen M, Kosma VM. Hyaluronan in peritumoral stroma and malignant cells associates with breast cancer spreading and predicts survival. Am J Pathol. 2000 Feb;156(2):529-36.
2. Stern R. Hyaluronan catabolism: a new metabolic pathway. Eur J Cell Biol. 2004 Aug;83(7):317-25.
3. Suzuki M, Asplund T, Yamashita H, Heldin CH, Heldin P. Stimulation of hyaluronan biosynthesis by platelet - derived growth factor - BB and transforming growth factor - beta 1 involves activation of protein kinase C. Biochem J. 1995 May 1 ;307 ( Pt 3) :817 -21.
4. Langner C, Ratschek M, Tsybrovskyy 0, Schips L, Zigeuner R. P63 immunoreactivity distinguishes upper urinary tract transitional - cell carcinoma and renal - cell carcinoma even in poorly differentiated tumors. J Histochem Cytochem. 2003 Aug;51(8) :1097 -9.
5. Heldin P. Importance of hyaluronan biosynthesis and degradation in cell differentiation and tumor formation. Braz J Med Biol Res. 2003 Aug;36(8) : 967 -73. Epub 2003 Jul 23. Review.
6. Rahmanian M, Heldin P. Testicular hyaluronidase induces tubular structures of endothelial cells grown in three - dimensional collagen gel through a CD44 - mediated mechanism. Int J Cancer. 2002 Feb 10;97(5) :601 -7.
7. Li Y, Heldin P. Hyaluronan production increases the malignant properties of mesothelioma cells. Br J Cancer. 2001 Aug 17;85(4) :600 -7.
8. Toole BP. Hyaluronan in morphogenesis. Semin Cell Dev Biol. 2001 Apr; 12(2):79-87.
9. Wang C, Tammi M, Guo H, Tammi R. Hyaluronan distribution in the normal epithelium of esophagus, stomach, and colon and their cancers. Am J Pathol. 1996 Jun;148(6):1861-9.
10. Auvinen P, Tammi R, Parkkinen J, Tammi M, Agren U, Johansson R, Hirvikoski P, Eskelinen M, Kosma VM. Hyaluronan in peritumoral stroma and malignant cells associates with breast cancer spreading and predicts survival. Am J Pathol. 2000 Feb;156(2):529-36.