摘要
目的探讨食管癌组织中脑源性神经营养因子(BDNF)、酪氨酸蛋白激酶受体B(TrkB)、增殖细胞核抗原(Ki-67)和肿瘤抑制基因p63蛋白的表达水平及临床意义。方法回顾性分析2018年7月至2021年4月惠州市第三人民医院收治的84例食管癌患者的临床资料。采用免疫组织化学两步法检测癌组织及癌旁正常组织的BDNF、Trk B、Ki-67和p63阳性表达水平,采用单因素分析法分析食管癌组织中BDNF、Trk B、Ki-67、p63蛋白阳性表达水平与临床特征的关系。结果食管癌组织中BDNF、Trk B、Ki-67、p63蛋白阳性表达率分别为73.81%、86.90%、75.00%、84.52%,明显高于癌旁正常组织的9.52%、15.48%、47.62%、27.38%,差异均有统计学意义(P<0.05);低分化、有淋巴结转移、TNMⅢ~Ⅳ期、深层浸润食管癌组织中的BDNF阳性表达率分别为96.15%、91.89%、94.00%、84.91%,明显高于高分化、无淋巴结转移、TNMⅠ~Ⅱ期、浅层浸润的55.88%、59.57%、44.12%、54.84%,低分化、有淋巴结转移、TNMⅢ~Ⅳ期、深层浸润食管癌组织中的Trk B阳性表达率分别为96.15%、100.00%、98.00%、94.34%,明显高于高分化、无淋巴结转移、TNMⅠ~Ⅱ期、浅层浸润的76.47%、76.60%、70.59%、74.19%,差异均有统计学意义(P<0.05);深层浸润食管癌组织中的Ki-67阳性表达率为84.91%,明显高于浅层浸润的58.06%,差异有统计学意义(P<0.05);有淋巴结转移食管癌组织中的p63的阳性表达率为94.59%,明显高于无淋巴结转移的76.60%,差异有统计学意义(P<0.05);BDNF阳性表达与Trk B、Ki-67、p63阳性表达均呈正相关(r=0.415、0.397、0.496,P<0.05)。结论食管癌组织中BDNF、Trk B、Ki-67、p63蛋白的阳性表达水平均较高,且BDNF和Trk B与肿瘤分化度、淋巴结转移、TNM分期、浸润深度相关,Ki-67与浸润深度相关,p63与淋巴结转移相关,它们可能参与了食管癌的产生、发展。
Objective To study the expression levels of brain-derived neurotrophic factor(BDNF),tyrosine protein kinase receptor B(TrkB),proliferating cell nuclear antigen(Ki-67),and tumor suppressor gene p63(p63)protein in esophageal cancer tissues and their clinical significance.Methods The clinical data of 84 patients with esophageal cancer treated in Huizhou Third People’s Hospital from July 2018 to April 2021 were retrospectively analyzed.The two-step immunohistochemistry method was used to detect the positive expression levels of BDNF,Trk B,Ki-67,and p63 in cancer tissues and normal tissues adjacent to cancer,and single factor analysis method was used to analyze the relationship between the positive expression level of BDNF,Trk B,Ki-67,p63 protein and clinical characteristics in esophageal cancer tissue.Results In esophageal cancer tissues,the positive expression rates of BDNF,Trk B,Ki-67,and p63 were 73.81%,86.90%,75.00%,and 84.52%,respectively,which were significantly higher than 9.52%,15.48%,47.62%,and 27.38%of normal tissues adjacent to cancer(P<0.05);the positive expression rates of BDNF in esophageal cancer tissue with poorly differentiation,lymph node metastasis,TNMⅢ-Ⅳ,and deep infiltration were 96.15%,91.89%,94.00%,and 84.91%,which were significantly higher than 55.88%,59.57%,44.12%,54.84%in esophageal cancer tissue with well differentiation,non-lymph node metastasis,TNMⅠ~Ⅱ,superficial infiltration.The positive expression rates of Trk B in esophageal cancer tissue with poorly differentiation,lymph node metastasis,TNMⅢ-Ⅳ,and deep infiltration were 96.15%,100.00%,98.00%,94.34%,significantly higher than 76.47%,76.60%,70.59%,74.19%in esophageal cancer tissue with well-differentiation,no lymph node metastasis,TNM stageⅠ-Ⅱ,superficial invasion(P<0.05).The positive expression rate of Ki-67 inesophageal cancer tissuewith deep infiltration was 84.91%,which was significantly higher than 58.06%in inesophageal cancer tissue with superficial infiltration(P<0.05).The positive expression rate of p63 in esophageal cancer tissue with lymph node metastasis was 94.59%,which was significantly higher than 76.60%in esophageal cancer tissue without lymph node metastasis(P<0.05).The positive expression of BDNF was positively correlated with the positive expression of Trk B,Ki-67,and p63(r=0.415,0.397,0.496,P<0.05).Conclusion The positive expression levels of BDNF,Trk B,Ki-67,and p63 protein in esophageal cancer tissues are relatively high,and BDNF and Trk B are related to tumor differentiation,lymph node metastasis,TNM staging,and depth of invasion.Ki-67 is related to depth of invasion,and p63 is related to lymph node metastasis,which may be both involved in the generation and development of esophageal cancer.
作者
赵震
胡惠军
古彩红
ZHAO Zhen;HU Hui-jun;GU Cai-hong(Department of Pathology,Huizhou Third People's Hospital,Huizhou 516000,Guangdong,CHINA)
出处
《海南医学》
CAS
2021年第24期3141-3144,共4页
Hainan Medical Journal
基金
广东省惠州市科技计划项目(编号:2020Y251)。
关键词
食管癌
脑源性神经营养因子
酪氨酸蛋白激酶受体B
增殖细胞核抗原
肿瘤抑制基因p63
病理
Esophageal cancer
Brain-derived neurotrophic factor
Protein tyrosine kinase receptor B
Proliferating cell nuclear antigen
Tumor suppressor gene p63
Pathology