Miki Y, Nishisho I, Miyoshi Y, Utsunomiya J, Nakamura Y
Department of Biochemistry, Cancer Institute, Tokyo, Japan.
Genes Chromosomes Cancer. 1992 Jan;4(1):81-3. doi: 10.1002/gcc.2870040112.
Accumulation of genetic alterations in oncogenes and tumor suppressor genes causes the transformation of a normal cell into a malignant cell. Recently, Fearon and Vogelstein (Cell 61:759-767, 1990) reported on a model for the genetic pathway in development of colorectal neoplasia. To investigate genetic alterations in colorectal carcinomas, we examined allelic losses on some chromosomes in adenomas and carcinomas derived from patients with adenomatous polyposis coli (APC). We found evidence for an interstitial deletion of 5q. Loss of heterozygosity (LOH) of 5q around the APC locus was observed in both adenoma and carcinoma in one case. The fact that the same region of chromosome 5 was lost in five adenomas and one carcinoma derived from the same patient suggests that a somatic interstitial deletion may be caused not by random mechanisms but by a specific mechanism.
癌基因和肿瘤抑制基因中遗传改变的积累导致正常细胞转变为恶性细胞。最近，费伦和沃格尔斯坦（《细胞》61:759 - 767，1990年）报道了一种关于结直肠肿瘤发生的遗传途径模型。为了研究结直肠癌中的遗传改变，我们检测了来自家族性腺瘤性息肉病（APC）患者的腺瘤和癌组织中一些染色体上的等位基因缺失情况。我们发现了5号染色体间质缺失的证据。在一个病例的腺瘤和癌组织中均观察到APC基因座周围5号染色体的杂合性缺失（LOH）。来自同一患者的5个腺瘤和1个癌组织中5号染色体的相同区域均缺失，这一事实表明体细胞间质缺失可能不是由随机机制引起的，而是由一种特定机制导致的。
