不同亚型的大肠侧向发育型肿瘤的KRAS、APC、p53表达
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摘要
目的比较不同亚型的大肠侧向发育型肿瘤(LST)、≥10 mm隆起型腺瘤、进展期大肠癌的KRAS、APC、p53的基因表达情况,探讨不同亚型LST的分子发生途径。方法应用高分辨率溶解曲线法(HRM)分别检测2016年1月～2018年7月我院收治的38例颗粒型LST(LST-G)和13例非颗粒型LST(LST-NG)以及60例隆起型腺瘤、48例进展期大肠癌的KRAS、APC、p53的基因表达情况,应用统计学方法比较四组病变的基因表达差异。结果 LST-G,LST-NG,隆起型腺瘤、进展期大肠癌的KRAS、APC、p53突变率分别为52.6%、7.7%、46.7%和60.4%,15.8%、53.8%、20.0%和58.3%,7.9%、46.2%、11.7%和66.7%。LST-NG组KRAS突变率均低于LST-G组、隆起型腺瘤组和进展期大肠癌组,差异有统计学意义(P<0.05),而LST-G组和隆起型腺瘤组KRAS突变率比较,差异无统计学意义(P>0.05);LST-NG组APC和p53突变率高于LST-G组和隆起型腺瘤组,差异有统计学意义(P<0.05),而LST-G组和隆起型腺瘤组APC和p53突变率比较,差异无统计学意义(P>0.05),LST-NG组的APC和p53突变率低于进展期大肠癌组,但差异无统计学意义(P>0.05)。结论 LST-G和LST-NG的基因表达不同,2种不同亚型的LST可能存在不同的分子发生途径。
Objective To compare the gene expression of KRAS, APC and p53 in different subtypes of colorectal lateral developmental tumors(LST), polypoid colorectal adenomas(≥10 mm) and advanced colorectal cancer, and to investigate the molecular pathogenesis of the different subtypes of colorectal lateral developmental tumors. Methods The gene expression of KRAS, APC and p53 in our hospital from January 2016 to July 2018, 38 cases of granular categories(LST-G), 13 cases of nongranular categories(LST-NG), 60 cases of polypoid colorectal adenomas and 48 cases of advanced colorectal cancer were detected by High Resolution Melting(HRM). Results The mutation rate of KRAS, APC and p53 in LST-G group, LST-NG group, polypoid adenoma group and colorectal cancer group were 52.6%, 7.7%,46.7%and 60.4%, 15.8%; 53.8%, 20.0% and 58.3%, 7.9%, 46.2%, 11.7%, and 6.7% respectively. The KRAS mutation rate of LST-NG group were significantly lower than LST-G group, polypoid adenomas group and advanced colorectal cancer group respectively(P<0.05). But there was no significant difference between LST-G group and polypoid adenomas group(P>0.05). The APC and p53 mutation rate of LST-NG group were significantly higher than LST-G and polypoid adenomas group(P<0.05), whereas the APC and p53 mutation rate were no significant difference between LST-G group and polypoid adenomas group(P>0.05), the APC and p53 mutation rate in LST-NG group were lower than the advanced colorectal cancer group, but there were no statistically significant difference(P>0.05). Conclusion The differences of gene expression between LST-G and LST-NG may remind the different molecular pathways.
Objective To compare the gene expression of KRAS, APC and p53 in different subtypes of colorectal lateral developmental tumors(LST), polypoid colorectal adenomas(≥10 mm) and advanced colorectal cancer, and to investigate the molecular pathogenesis of the different subtypes of colorectal lateral developmental tumors. Methods The gene expression of KRAS, APC and p53 in our hospital from January 2016 to July 2018, 38 cases of granular categories(LST-G), 13 cases of nongranular categories(LST-NG), 60 cases of polypoid colorectal adenomas and 48 cases of advanced colorectal cancer were detected by High Resolution Melting(HRM). Results The mutation rate of KRAS, APC and p53 in LST-G group, LST-NG group, polypoid adenoma group and colorectal cancer group were 52.6%, 7.7%,46.7%and 60.4%, 15.8%; 53.8%, 20.0% and 58.3%, 7.9%, 46.2%, 11.7%, and 6.7% respectively. The KRAS mutation rate of LST-NG group were significantly lower than LST-G group, polypoid adenomas group and advanced colorectal cancer group respectively(P<0.05). But there was no significant difference between LST-G group and polypoid adenomas group(P>0.05). The APC and p53 mutation rate of LST-NG group were significantly higher than LST-G and polypoid adenomas group(P<0.05), whereas the APC and p53 mutation rate were no significant difference between LST-G group and polypoid adenomas group(P>0.05), the APC and p53 mutation rate in LST-NG group were lower than the advanced colorectal cancer group, but there were no statistically significant difference(P>0.05). Conclusion The differences of gene expression between LST-G and LST-NG may remind the different molecular pathways.
引文
[1]张艳飞,丁士刚.大肠侧向发育型肿瘤的诊断及内镜治疗进展[J].中国微创外科杂志,2017,17(12).1117-11125.
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[10]钟选芳,张晓慧,甘爱华,等.大肠侧向发育型肿瘤的临床和病理特征回顾性研究[J].中华消化内镜杂志,2015,32(9):624-625.
[11]Sakai E,Fukuyo M,Matsusaka K,et al.TP53 mutation at early stage of colorectal cancer progression from two types of laterallyspreading tumors[J].Cancer Sci,2016,107(6):820-827.
[12]Sugimoto T,Ohta M,Ikenoue T,et al.Macroscopic morphologic subtypes of laterallyspreadingcolorectal tumors showing distinct molecular alterations[J].Int J Cancer,2010,127(7):1562-1569.
[13]Shi L,Wu YX,Yu JH,et al.Research of the relationship betweenβ-catenin and c-myc-mediated Wnt pathway and laterallyspreading tumors occurrence[J].Eur Rev Med Pharmacol Sci,2017,21(2):252-257.
[14]Nagai K,Hayashi Y,Honma K,et al.Adenoma of colorectal laterally spreading tumor nongranular type with biological phenotypic features similar to cancer[J].J Gastroenterol Hepatol,2018,33(11):1853-1863.
[15]Sakai E,Ohata K,Chiba H,et al.Methylation epigenotypes and genetic features in colorectal laterally spreading tumors[J].Int J Cancer,2014,135(7):1586-1595.
[2]Ni HB,Wang FY,Xu J,et al.Screening and identification of a tumor specific methylation phenotype in the colorectal laterallyspreading tumor[J].Eur Rev Med Pharmacol Sci,2017,21(11):2611-2616.
[3]Wu J,Huo JR,Wang D,et al.Expression of Wnt and integrin pathways in colorectal laterally spreading tumors and their correlation with endoscopic subtypes[J].Nan Fang Yi Ke Da Xue Xue Bao,2017,37(9):1234-1241.
[4]兰世迁,廖仙红,谢如飞.结直肠侧向发育型肿瘤行内镜黏膜下剥离术治疗的临床效果观察[J].实用医技杂志,2018,25(1):71-72.
[5]Wang J,Wang X,Gong W,et al.Increased expression of beta-catenin, phosphorylated glycogen synthase kinase 3beta,cyclin D1,and c-myc in laterallyspreadingcolorectal tumors[J].J Histochem Cytochem,2009,57(4):363-371.
[6]朱良亮,于恩达.大肠侧向发育型肿瘤分子生物学特征的研究进展[J].海南医学院学报,2018,24(4):573-576.
[7]Takahashi T,Nosho K,Yamamoto H,et al.Flat-type colorectal advanced adenomas(laterally spreading tumors)have different genetic and epigenetic alterations from protrudedtype advanced adenomas[J].Mod Pathol,2007,20(1):139-147.
[8]Myung DS,Kweon SS,Lee J,et al.Clinicopathological features of laterally spreading colorectal tumors and their association with advanced histology and invasiveness:an experience from Honam province of South Korea:a Honam Association for the Study of Intestinal Diseases(HASID)[J].PLoS One,2017,12(10):e184205.
[9]Sugai T,Habano W,Takagi R,et al.Analysis of molecular alterations in laterally spreading tumors of the colorectum[J].J Gastroenterol,2017,52(6):715-723.
[10]钟选芳,张晓慧,甘爱华,等.大肠侧向发育型肿瘤的临床和病理特征回顾性研究[J].中华消化内镜杂志,2015,32(9):624-625.
[11]Sakai E,Fukuyo M,Matsusaka K,et al.TP53 mutation at early stage of colorectal cancer progression from two types of laterallyspreading tumors[J].Cancer Sci,2016,107(6):820-827.
[12]Sugimoto T,Ohta M,Ikenoue T,et al.Macroscopic morphologic subtypes of laterallyspreadingcolorectal tumors showing distinct molecular alterations[J].Int J Cancer,2010,127(7):1562-1569.
[13]Shi L,Wu YX,Yu JH,et al.Research of the relationship betweenβ-catenin and c-myc-mediated Wnt pathway and laterallyspreading tumors occurrence[J].Eur Rev Med Pharmacol Sci,2017,21(2):252-257.
[14]Nagai K,Hayashi Y,Honma K,et al.Adenoma of colorectal laterally spreading tumor nongranular type with biological phenotypic features similar to cancer[J].J Gastroenterol Hepatol,2018,33(11):1853-1863.
[15]Sakai E,Ohata K,Chiba H,et al.Methylation epigenotypes and genetic features in colorectal laterally spreading tumors[J].Int J Cancer,2014,135(7):1586-1595.
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