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作者早期的研究工作显示:Dukes分期,淋巴和/或毛细血管微浸润,肿瘤的大体形态和种族四个病理因素与结肠直肠癌根治术后五年生存率有关.同时作者还观察到ras原癌基因的过度表达与肿瘤的高度恶性行为和预后差有关.一般认为表现为等位基因缺失的肿瘤抑制基因失活(如杂合性等位基因丢失),至少部分地与恶性肿瘤的发展和其它生物学行为有关.结肠直肠癌中最频繁的杂合性等位基因缺失位点被定位在第5号染色体长臂(5q),第17号染色体短臂(17p)和第18号染色体长臂上(18q).这些可能是以下基因的位点,家族性结肠息肉病基因(APC)、p~(53)基因和结肠癌缺失基因(DCC).作者还研究了第8号染色体短臂(8p)的杂合性等位基因缺失,该处可能含有两个肿瘤抑制基因.为了阐明等位基因缺失作为潜在性预后因素的价值,现在报告:5q、8p、17p和18q上杂合性等位基因丢失与Dukes分期和微浸润之间的关系.
The author’s earlier research showed that: Dukes stage, lymphatic and / or capillary microinvasion, the tumor’s gross morphology and race four pathological factors and the five-year survival rate after radical resection of colorectal cancer is also related to the same time the author also observed ras cancer Overexpression of a gene is associated with a high degree of malignant behavior and poor prognosis of the tumor. It is generally believed that the loss of tumor suppressor gene (such as loss of heterozygosity allele) manifests as allele deletion, at least in part with the development of malignancy and other Biological behavior is involved. The most frequent heterozygous allele deletion sites in colorectal cancer are located on chromosome 5 long arm (5q), chromosome 17 short arm (17p) and chromosome 18 long arm Upper (18q). These may be the locus of the following genes, familial colon polyposis gene (APC), p53 gene and colon cancer deletion gene (DCC). The authors also studied the short arm of chromosome 8 ( Loss of heterozygous alleles at 8p) may contain two tumor suppressor genes. To elucidate the value of allele deletion as a potential prognostic factor, heterozygosity at 5q, 8p, 17p, and 18q is now reported. Loss of gene and Dukes staging and The relationship between the infiltration.