人表皮生长因子-2、突变型p53、Ki-67在早期子宫内膜腺癌组织中的表达及意义
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摘要
目的检测人表皮生长因子-2(C-erb B-2)、突变型p53、Ki-67在早期子宫内膜癌组织中的表达及其与临床病理参数的关系。方法采用免疫组织化学法检测C-erb B-2、突变型p53、Ki-67蛋白在增生期子宫内膜15例(增生期子宫内膜组),非典型增生子宫内膜15例(非典型增生子宫内膜组),子宫内膜癌60例(子宫内膜癌组)中的表达情况。结果C-erb B-2、突变型p53、Ki-67在子宫内膜癌组中的阳性表达率分别为33.33%、35.00%、75.00%。子宫内膜癌组中Cerb B-2阳性表达率明显高于增生期子宫内膜组及非典型增生子宫内膜组;突变型p53、Ki-67的阳性表达率明显高于增生期子宫内膜组及非典型增生子宫内膜组,差异有统计学意义(χ~2值分别为7.292,23.627,P<0.05),增生期子宫内膜组与非典型增生子宫内膜组间的差异无统计学意义(χ~2=4.647,P>0.05)。C-erb B-2在子宫内膜癌组中阳性表达随手术病理分期、组织学分级、肌层浸润深度的增加阳性表达逐渐升高,但差异均无统计学意义(χ~2=0.313,P>0.05)。突变型p53在子宫内膜癌组Ⅰ期与Ⅱ期之间差异无统计学意义(χ~2=0.659,P>0.05);而在G1与G3两者比较差异有统计学意义(χ~2=12.290,P=0.001);突变型P53随肌层浸润深度增加阳性表达逐渐升高,但差异无统计学意义(χ~2=3.956,P>0.05)。Ki-67随肌层浸润深度增加阳性表达逐渐升高,差异有统计学意义(χ~2=19.622,P<0.05)。子宫内膜癌组织中C-erb B-2、突变型p53与Ki-67阳性表达呈正相关(r=0.589,P=0.000;r=0.780,P=0.000),而C-erb B-2与突变型p53在子宫内膜癌中的阳性表达无相关性(r=0.148,P=0.258)。结论联合检测C-erb B-2、突变型p53、Ki-67对评价子宫内膜癌的发生、发展、恶性程度及预后更具有临床价值。
Objective To detect the expressions of human epidermal growth factor- 2( C- erb B- 2),mutant P53,and Ki- 67 in early endometrial adenocarcinoma,explore the relationships with clinicopathological parameters. Methods Immunohistochemical method was used to detect the expressions of C- erb B- 2,mutant P53,and Ki- 67 proteins in 15 cases with endometrial hyperplasia,15 cases with atypical endometrial hyperplasia,and 60 cases with endometrial carcinoma. Results The positive expression rates of C- erb B- 2,mutant P53,and Ki- 67 in endometrial carcinoma were 33. 33%,35. 00%,and 75. 00%,respectively. The positive expression rate of C- erb B-2 in endometrial carcinoma was statistically significantly higher than those in endometrial hyperplasia and atypical endometrial hyperplasia( χ~2= 7. 292,P < 0. 05). The positive expression rates of mutant P53 and Ki- 67 in endometrial carcinoma were statistically significantly higher than those in endometrial hyperplasia and atypical endometrial hyperplasia( χ~2= 23. 627,P < 0. 05). There was no statistically significant difference between endometrial hyperplasia and atypical endometrial hyperplasia( χ~2= 4. 647,P > 0. 05). The positive expression rate of C- erb B- 2 in endometrial carcinoma increased gradually with surgical- pathological staging,histological grading,and depth of myometrial invasion,but there was no statistically significant difference( χ~2= 0. 313,P > 0. 05). There was no statistically significant difference in the expression rate of mutant P53 between stage Ⅰ endometrial carcinoma and stage Ⅱ endometrial carcinoma( χ~2= 0. 659,P >0. 05). There was statistically significant difference between G1 endometrial carcinoma and G3 endometrial carcinoma( χ~2= 12. 290,P =0. 001). The positive expression rates of mutant P53 increased gradually with depth of myometrial invasion,but there was no statistically significant difference( χ~2= 3. 956,P > 0. 05). The positive expression rates of mutant Ki- 67 increased gradually with depth of myometrial invasion,and there was statistically significant difference( χ~2= 19. 622,P < 0. 05). In endometrial carcinoma,the positive expression rates of C- erb B- 2 and mutant P53 were positively correlated with positive expression rate of Ki- 67( r = 0. 589,P = 0. 000; r = 0. 780,P =0. 000). There was no correlation between positive expression rate of C- erb B- 2 and positive expression rate of mutant P53 in endometrial carcinoma( r = 0. 148,P = 0. 258). Conclusion Joint detection of C- erb B- 2,mutant P53,and Ki- 67 has clinical value in evaluating occurrence,development,malignant degree,and prognosis of endometrial carcinoma.
Objective To detect the expressions of human epidermal growth factor- 2( C- erb B- 2),mutant P53,and Ki- 67 in early endometrial adenocarcinoma,explore the relationships with clinicopathological parameters. Methods Immunohistochemical method was used to detect the expressions of C- erb B- 2,mutant P53,and Ki- 67 proteins in 15 cases with endometrial hyperplasia,15 cases with atypical endometrial hyperplasia,and 60 cases with endometrial carcinoma. Results The positive expression rates of C- erb B- 2,mutant P53,and Ki- 67 in endometrial carcinoma were 33. 33%,35. 00%,and 75. 00%,respectively. The positive expression rate of C- erb B-2 in endometrial carcinoma was statistically significantly higher than those in endometrial hyperplasia and atypical endometrial hyperplasia( χ~2= 7. 292,P < 0. 05). The positive expression rates of mutant P53 and Ki- 67 in endometrial carcinoma were statistically significantly higher than those in endometrial hyperplasia and atypical endometrial hyperplasia( χ~2= 23. 627,P < 0. 05). There was no statistically significant difference between endometrial hyperplasia and atypical endometrial hyperplasia( χ~2= 4. 647,P > 0. 05). The positive expression rate of C- erb B- 2 in endometrial carcinoma increased gradually with surgical- pathological staging,histological grading,and depth of myometrial invasion,but there was no statistically significant difference( χ~2= 0. 313,P > 0. 05). There was no statistically significant difference in the expression rate of mutant P53 between stage Ⅰ endometrial carcinoma and stage Ⅱ endometrial carcinoma( χ~2= 0. 659,P >0. 05). There was statistically significant difference between G1 endometrial carcinoma and G3 endometrial carcinoma( χ~2= 12. 290,P =0. 001). The positive expression rates of mutant P53 increased gradually with depth of myometrial invasion,but there was no statistically significant difference( χ~2= 3. 956,P > 0. 05). The positive expression rates of mutant Ki- 67 increased gradually with depth of myometrial invasion,and there was statistically significant difference( χ~2= 19. 622,P < 0. 05). In endometrial carcinoma,the positive expression rates of C- erb B- 2 and mutant P53 were positively correlated with positive expression rate of Ki- 67( r = 0. 589,P = 0. 000; r = 0. 780,P =0. 000). There was no correlation between positive expression rate of C- erb B- 2 and positive expression rate of mutant P53 in endometrial carcinoma( r = 0. 148,P = 0. 258). Conclusion Joint detection of C- erb B- 2,mutant P53,and Ki- 67 has clinical value in evaluating occurrence,development,malignant degree,and prognosis of endometrial carcinoma.
引文
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[9]Alkushi A,Kbel M,Kalloger SE,et al.High-grade endometrial carcinoma:serous and grade 3 endometrioid carcinomas have different immunophenotypes and outcomes[J].Int J Gynecol Pathol,2010,29(4):343-350.
[10]Athanassiadou P,Petrakakou E,Liossi A,et al.Prognostic significance of p53,bcl-2 and EGFR in carcinoma of the endometrium[J].Acta Cytol,2011,43(6):1039-1044.
[11]Apostolou G,Apostolou N,Biteli M,et al.Utility of Ki-67,p53,Bcl-2,and Cox-2 biomarkers for low-grade endometrial cancer and disordered proliferative/benign hyperplastic endometrium by imprint cytology[J].Diagn Cytopathol,2014,42(2):134-142.
[12]Apostolou G,Apostolou N,Nikolaidou C,et al.Cytodiagnosis of endometrial carcinoma and hyperplasia on imprint smears with additional immunocytochemistry using Ki-67 and p53 biomarkers[J].Cytopathology,2014,25(2):86-94.
[13]Chakravarty D,Gupta N,Goda JS,et al.Steroid receptors,HER2/neu and Ki-67,in endometrioid type of endometrial carcinoma:Correlation with conventional histomorphological features of prognosis[J].Acta Histochem,2010,112(4):355-363.
[14]Clarke BA,Gilks CB.Endometrial carcinoma:controversies in histopathological assessment of grade and tumour cell type[J].J Clin Pathol,2010,63(5):410-415.
[15]Smith LH,Leiserowitz G,Xing G,et al.Short-term Femara(letrozole)treatment and suppression of Ki-67 expression in postmenopausal endometrial carcinoma[J].Open J Obstet Gynecol,2013,3(3):347-351.
[2]Sopel M,Kasprzyk I,Berdowska I.Maspin and C-erb B-2 expression in correlation with microvessel density in invasive ductal breast cancer[J].Folia Histochem Cytobiol,2011,43(2):109-108.
[3]Suthipintawong C,Wejaranayang C,Vipupinyo C.Prognostic significance of ER,PR,Ki-67,C-erb B-2,and p53 in endometrial carcinoma[J].J Med Assoc Thai,2008,91(12):1779.
[4]Konecny G,Santos L,Winterhoff B,et al.HER2 gene amplification and EGFR expression in a large cohort of surgically staged patients with nonendometrioid(type II)endometrial cancer[J].Br J Cancer,2009,100(1):89-95.
[5]Lin CK,Lin WL,Chen FL,et al.Assessing the impact of polysomy-17 on HER2 status and the correlations of HER2 status with prognostic variables(ER,PR,p53,Ki-67)in epithelial ovarian cancer:a tissue microarray study using immunohistochemistry and fluorescent in situ hybridization[J].Int J Gynecol Pathol,2011,30(4):372-379.
[6]Gadducci A,Guerrieri ME,Greco C.Tissue biomarkers as prognostic variables of cervical cancer[J].Crit Rev Oncol Hematol,2013,86(2):104-129.
[7]Concer Genome Atlas Research Netucrk,Kandoth C,Schultz N,et al.Integrated genomic characterization of endometrial carcinoma[J].Nature,2013,497(7447):67-73.
[8]Catasus L,Gallardo A,Cuatrecasas M,et al.Concomitant PI3KAKT and p53 alterations in endometrial carcinomas are associated with poor prognosis[J].Mod Pathol,2009,22(4):522-529.
[9]Alkushi A,Kbel M,Kalloger SE,et al.High-grade endometrial carcinoma:serous and grade 3 endometrioid carcinomas have different immunophenotypes and outcomes[J].Int J Gynecol Pathol,2010,29(4):343-350.
[10]Athanassiadou P,Petrakakou E,Liossi A,et al.Prognostic significance of p53,bcl-2 and EGFR in carcinoma of the endometrium[J].Acta Cytol,2011,43(6):1039-1044.
[11]Apostolou G,Apostolou N,Biteli M,et al.Utility of Ki-67,p53,Bcl-2,and Cox-2 biomarkers for low-grade endometrial cancer and disordered proliferative/benign hyperplastic endometrium by imprint cytology[J].Diagn Cytopathol,2014,42(2):134-142.
[12]Apostolou G,Apostolou N,Nikolaidou C,et al.Cytodiagnosis of endometrial carcinoma and hyperplasia on imprint smears with additional immunocytochemistry using Ki-67 and p53 biomarkers[J].Cytopathology,2014,25(2):86-94.
[13]Chakravarty D,Gupta N,Goda JS,et al.Steroid receptors,HER2/neu and Ki-67,in endometrioid type of endometrial carcinoma:Correlation with conventional histomorphological features of prognosis[J].Acta Histochem,2010,112(4):355-363.
[14]Clarke BA,Gilks CB.Endometrial carcinoma:controversies in histopathological assessment of grade and tumour cell type[J].J Clin Pathol,2010,63(5):410-415.
[15]Smith LH,Leiserowitz G,Xing G,et al.Short-term Femara(letrozole)treatment and suppression of Ki-67 expression in postmenopausal endometrial carcinoma[J].Open J Obstet Gynecol,2013,3(3):347-351.