摘要
背景:胰岛素样生长因子(IGF)具有维持细胞正常增殖和分化的作用。多种脏器肿瘤存在IGFs过表达,IGFs与其受体IGF-R结合可促进肿瘤细胞增殖并可能加速肿瘤转移,提示IGFs/IGF-R可能在肿瘤的发生、发展中起有重要作用。目的:研究IGF及其受体在结肠癌中的表达及其与结肠癌生物学行为的相关性。方法:收集40例结肠癌患者的手术标本,以亲和免疫组化技术检测癌组织和远离癌灶的正常结肠黏膜组织IGF-ⅠR、IGF-Ⅱ的表达。分析IGF-ⅠR、IGF-Ⅱ的阳性程度与结肠癌Dukes分期的相关性。结果:结肠癌组织IGF-ⅠR、IGF-Ⅱ的表达均局限于细胞质,其表达阳性率分别为67.5%和55.0%,较正常结肠黏膜组织的32.5%和2.5%显著增高(P<0.01)。IGF-ⅠR的阳性程度与结肠癌Dukes分期之间存在相关性(P<0.05)。结论:结肠癌存在IGF-ⅠR、IGF-Ⅱ过表达,其中IGF-ⅠR的表达与结肠癌的生物学行为存在相关性。IGFs/IGF-ⅠR的检测可能对判断结肠癌患者的预后具有意义。
Background: Insulin-like growth factor (IGF) plays an important role in maintaining the proliferation and differentiation of normal cells, However, cancer cells of various organs might overexpress IGFs. Combined with its receptor (IGF-R), IGFs might stimulate proliferation and accelerate cancer metastasis. It has been suggested that IGFs/IGF-R might act as a crucial factor in the genesis and progression of cancer. Aims: To investigate the expression of IGF and IGF-R in colon cancer and its correlation with the biological behavior of colon cancer. Methods: Specimens of both cancerous lesion and distant normal mucosal tissue were collected from 40 patients with colon cancer. The expressions of IGF- ⅠR and IGF- Ⅱ were detected by affinity immunohistochemistry. Dukes staging and its relationship with the degree of positive expression of IGF- ⅠR, IGF- Ⅱ were further investigated. Results: The expressions of IGF- ⅠR and IGF- Ⅱ in cancerous tissues were confined to the cytoplasm, the positivity rates were significantly higher than those in the normal mucosal tissues (67.5% vs. 32.5% and 55.0% vs. 2,5%, P〈0.01). There was correlation between the expression level of IGF- ⅠR and Dukes staging of colon cancer (P〈0.05). Conclusions: There is overexpression of IGF- ⅠR and IGF- Ⅱ in colon cancer. Furthermore, there is correlation between IGF- ⅠR expression and the biological behavior of colon cancer. Detection of IGFs/IGF- ⅠR might be of significance for evaluating the prognosis of colon cancer.
出处
《胃肠病学》
2006年第3期139-142,共4页
Chinese Journal of Gastroenterology
基金
上海市重点学科建设项目(No.Y0205)资助