春7-围手术期处理+肿瘤2015-丁克峰.ppt

* * * * 上图中三条曲线代表了三种不同的治疗方法，从图中我们可以看出治愈性治疗（肝转移灶切除）的生存时间姑息性治疗不治疗。所以对于结直肠癌肝转移患者应该尽量行肝转移灶切除从而延长时间生存。 参考文献： Eric Van Cutsem, et al. EJC 2006;42:2212-2221 * * * * Most human CRCs arise from large-bowel adenomas (adenomatous polyps) that are dysplastic but nonmalignant. Adenomatous polyps form in the colon when normal mechanisms regulating epithelial renewal are disrupted. As a result of apoptosis and exfoliation, surface cells lining the intestine are continuously lost into the bowel lumen and must be continuously replaced. Typically, proliferation occurs at the crypt base. As cells move toward the luminal surface, they cease proliferating and terminally differentiate. This ordered process is disrupted as adenomas increase in size, become dysplastic, and attain invasive potential. CRCs develop from intermediate precancerous precursors. Early carcinomas are seen within large adenomatous polyps. Adenomas and carcinomas are found in similar distributions throughout the large bowel. Adenomas are observed 10 to 15 years prior to the onset of cancer in both sporadic and familial cases. Specific genetic changes are believed to drive the transformation from normal colonic epithelium to invasive cancer. The molecular basis for CRC is a multistep process in which each accumulated genetic event confers a selective growth advantage to the colonic epithelial cell. Germline mutations underlie the common inherited syndromes (eg, APC, HNPCC), whereas sporadic cancers result from the stepwise accumulation of multiple somatic mutations. Mutations in the APC gene, a feature common to both inherited and sporadic tumors, occur early in the process; mutations of the p53 suppressor gene generally occur late. References Lynch HP, Hoops TC. The genetic pathogenesis of colorectal cancer. Hematol Oncol Clin North Am. 2002;16:775-810; Tejpar S, Van Cutsem E. Molecular and genetic defects in colorectal tumorigenesis. Best Pract Res Clin Gastroenterol. 2002;16:171-185. * * * III型酪氨酸激酶受体 细胞