[Etiology of colorectal cancer].

G.E.N Pub Date : 1994-10-01
M Matos Villalobos
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Abstract

Colorectal cancer affect the 15% of general population in developed countries. Cancer is a multistep process in which multiple genetic alterations must usually occur in several years. The premalignant step consists of one or multiple aberrant crypts due to hyperproliferation of cells and its shift from the deep third of the crypt to its surface. It has been suggested that abnormality in the APC gene is responsible for this. Furthermore, there exists DNA hypometilation, activation of the gene K-ras and ornithine decarboxylase activity. There is also a loss of MCC gene, that seems to interact with the APC gene. Entire alterations described make possible the Class I adenoma formation. This adenoma, needs the loss of the DCC gene (late stage in the carcinogenesis process), to become a Class II adenoma. The following alteration is deleted and mutation of the p53 gene. There is also an activation of the c-myc oncogene. These two genes are important mechanisms for the conversion of a benign adenoma to a malignant one, adenoma with in situ carcinoma or Class III adenoma. This type of adenoma becomes carcinoma and metastatic stage, throughout inactivation of several tumor suppressor genes. Besides the hereditary APC alteration and other acquired genetic changes as described above there are other associated genetics, antigenics, and enzymes that have an important role in the adenoma-carcinoma sequence. Several carcinogenic factors have been described which also contribute in the adenoma and carcinoma formation: ulcerative colitis, acromegaly, familial history of colonic neoplasia, certain professions, smoking and drinking, consumption of red or processed meat, etc.(ABSTRACT TRUNCATED AT 250 WORDS)

【结直肠癌病因学】。
结直肠癌影响着发达国家15%的总人口。癌症是一个多步骤的过程,在这个过程中,多种基因的改变通常必须在几年内发生。癌前阶段由一个或多个异常隐窝组成,这是由于细胞的过度增殖以及它从隐窝的深三分之一转移到其表面。有人认为APC基因的异常是造成这种情况的原因。此外,还存在DNA降低、K-ras基因活化和鸟氨酸脱羧酶活性。还有MCC基因的缺失,这似乎与APC基因相互作用。所描述的全部改变使I类腺瘤的形成成为可能。这种腺瘤,需要DCC基因的缺失(癌变过程的晚期),才能成为II类腺瘤。以下是p53基因的缺失和突变。还有c-myc癌基因的激活。这两个基因是良性腺瘤向恶性腺瘤转化的重要机制,腺瘤伴原位癌或III类腺瘤。这种类型的腺瘤通过几种肿瘤抑制基因的失活而成为癌和转移期。除了上述遗传性APC改变和其他获得性遗传改变外,还有其他相关遗传学、抗原性和酶在腺瘤-癌序列中起重要作用。一些致癌因素也有助于腺瘤和癌的形成:溃疡性结肠炎、肢端肥大症、结肠瘤的家族史、某些职业、吸烟和饮酒、食用红肉或加工肉等。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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