散发性结直肠癌等位基因杂合缺失的精细定位研究
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摘要
目的：结直肠癌是临床上常见的消化道肿瘤，随着人们生活水平的提高，近二十年来我国的结直肠癌发病率呈持续上升趋势。大多数结直肠癌因为没有明显的遗传背景而被称为散发性结直肠癌，占整个结直肠肿瘤的80％—90％。散发性结直肠癌变这一个多基因参与、多步骤发生的过程被奉为上皮性肿瘤发生的模板。已有的研究显示，结直肠癌的发生、发展已经形成了较为复杂的分子通路。尽管如此，目前全面的分子发生、调控机制仍不十分清楚，只有当我们真正认识了结直肠癌的发生机制，才能实现该病的早期诊断、提高诊治效果。目前认为结直肠癌发生包括以下几种机制：原癌基因的激活、肿瘤抑制基因的失活、错配修复基因的突变等。一般认为4-5个基因的失活才能导致恶性表型的出现。Knudson通过对家族性和散发性视网膜母细胞瘤的研究，提出了著名的“二次打击”假说，典型的第二次打击往往是整条染色体或其中较大片断的缺失，而且均可表现为杂合缺失，缺失区域内往往含有肿瘤抑制基因，因而可以通过检测肿瘤组织基因组中的杂合缺失位点来作为寻找肿瘤抑制基因的线索。肿瘤抑制基因的杂合缺失(LOH)被认为是结直肠癌形成的关键通路之一。大肠癌课题组先前应用400个微卫星标记物进行了83例散发性结直肠癌的全基因组杂合缺失的扫描，发现了一些高频LOH位点和与肿瘤分期、分化相关的微卫星位点。本研究拟通过对全基因组杂合缺失扫描后发现的6个高频LOH微卫星位点以及3个与结直肠癌分期、分化相关微卫星位点的杂合缺失精细定位分析，以期缩小候选散发性结直肠癌相关基因的筛查范围，为后期发现及验证相关基因奠定基础。
方法：研究对象为上海第一人民医院院普外科2年间经手术治疗的83例散发性结直肠癌患者，其中男性40例，女性43例，中位年龄66岁。依据
Background & Objective: Colorectal cancer is one of the leading causes of cancer-associated death in western countries. In England and Wales, it is the second most common cancer in women and the third most common in men; the same trend occours in China in recent years. In the carcinogenesis of colorectal cancer, the concept of adenoma-carcinoma sequence is widely accepted. In this pathway, polypoid adenoma develops into early polypoid cancer and then progresses to advanced cancer.
Colorectal cancer is characterized by genomic instability, the accumulation of multiple genetic alterations, and allelic imbalance throughout the genome. Loss of heterozygosity (LOH) is a common form of allelic imbalance, and the detection of LOH has been used to identify genomic regions that harbor tumor suppressor genes and to characterize different tumor types, pathological stages and progression. Global patterns of LOH can be discerned by allelotyping of tumors with polymorphic genetic markers. Identification of molecular markers associated with colorectal adenoma may uncover critical events involved in the initiation and progression of colorectal cancer. Inactivation of tumor suppressor genes is one of the major events involved in carcinogenesis and the most common representation is loss of heterozygosity (LOH). So, We made refined deletion mapping on 6 high LOH luci and 3 LOH luci involved in tumor stage and differentiation to make further study conveniently.
方法：研究对象为上海第一人民医院院普外科2年间经手术治疗的83例散发性结直肠癌患者，其中男性40例，女性43例，中位年龄66岁。依据
Background & Objective: Colorectal cancer is one of the leading causes of cancer-associated death in western countries. In England and Wales, it is the second most common cancer in women and the third most common in men; the same trend occours in China in recent years. In the carcinogenesis of colorectal cancer, the concept of adenoma-carcinoma sequence is widely accepted. In this pathway, polypoid adenoma develops into early polypoid cancer and then progresses to advanced cancer.
Colorectal cancer is characterized by genomic instability, the accumulation of multiple genetic alterations, and allelic imbalance throughout the genome. Loss of heterozygosity (LOH) is a common form of allelic imbalance, and the detection of LOH has been used to identify genomic regions that harbor tumor suppressor genes and to characterize different tumor types, pathological stages and progression. Global patterns of LOH can be discerned by allelotyping of tumors with polymorphic genetic markers. Identification of molecular markers associated with colorectal adenoma may uncover critical events involved in the initiation and progression of colorectal cancer. Inactivation of tumor suppressor genes is one of the major events involved in carcinogenesis and the most common representation is loss of heterozygosity (LOH). So, We made refined deletion mapping on 6 high LOH luci and 3 LOH luci involved in tumor stage and differentiation to make further study conveniently.
引文
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