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1、·56·大肠肛门病外科杂志2001年第7卷第2期ture.Ann-Chir,1999,53(10):1029-1032.obstructionoftheleftcolon.DisColonRectum,1998,7CamunezF,EchenagusiaA,SimoG,etal.Malignantcol-41:28-32.orectalobstructiontreatedbymeansofself-expanding13V.NaraynsinghR,RampaulD,MaharajT,etmetallicstents:e
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6、obstructionoftotalcolectomyinemergencytreatmentofocclusivecan-theleftcolonforcancer.AmSurg,2000,66(7):619-ceroftheleftcolon.AnnChir,1999,53(10):1019-622.1022.12HsuTC.One-stageresectionandanastomosisforacute(收稿日期:2001-04-11)APC基因与结直肠肿瘤广西医科大学第一附属医院大肠肛门病外科530021梁君林综
7、述高枫唐宗江审校“正常结直肠上皮-腺瘤性息肉-侵袭性癌”病针分析,确定DP2.5基因即为APC基因。理转变是一个多步骤、多基因参与的过程,涉及到癌2APC基因及APC蛋白的结构基因的激活和抑癌基因的失活。APC基因(adeno-matouspolyposiscoligene)的改变不仅可引起家族性APC基因位于染色体5q21,其cDNA克隆序列腺瘤性息肉病(familialadenomatouspolyposis,分析显示1个8538个核苷酸组成的开放阅读框[4]FAP),而且参与散发性结直肠肿瘤的形成。近年随架,含15
8、个外显子,其中15外显子最大,为[3]着分子生物学技术的提高,APC基因在结直肠肿瘤6571bp,占该基因编码区的77%。“突变密集区”[5]发生发展中的机理研究得到不断深入。(mutationclusterregion,MCR)位于该外显子内。该阅读框架5'端含有1个甲硫氨酸密码子,其上游1APC基因的定位、发现9