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人类胰腺癌表现出一致的遗传学改变,包括Ki-ras基因突变(>80％),P~(53)基因突发(50-70％)和P(16)基因突变或纯合型缺失(>85％)。等位基因型资料表明附加肿瘤抑制基因在其它区域的存在,最显著地位于18q,约有90％的胰腺癌显示出这一区带的杂合性丢失(LOH)。为了证明候补肿癌抑制基因在18q,作者对纯合型缺失的集中部位进行了胰腺癌嵌板分析,25/84的肿瘤在18q21·1在纯合型缺失,这一位点不包括DCC基因(一个结直肠癌候补肿瘤抑制基因),包括DPC_4基因,6/27例胰腺癌存在着DPC_4潜在的、不活动的突变,它们在18q 21·1没有纯合型缺失,这些作者所希望找到的肿瘤抑制基因的突变结果证明DPC4基因作为一种候补肿瘤抑制基因,与胰腺癌的发生有密切关系。
Human pancreatic cancer showed consistent genetic changes including Ki-ras mutations (>80%), P53 mutations (50-70%) and P(16) mutations or homozygous deletions ( >85%). Allelic data indicate that additional tumor suppressor genes are present in other regions, most prominently at 18q, and approximately 90% of pancreatic cancers show loss of heterozygosity (LOH) in this region. In order to prove that the candidate tumor suppressor gene is 18q, the authors performed a pancreatic cancer panel analysis on the site of homozygous deletion, and the 25/84 tumor was absent on homozygous 18q21·1. This site did not include the DCC gene. (One colorectal cancer candidate tumor suppressor gene), including DPC_4 gene, 6/27 pancreatic cancers have potential, inactive mutations in DPC_4, they have no homozygous deletion in 18q 21·1, these authors hope to find Mutation of tumor suppressor genes demonstrated that DPC4 gene as a candidate tumor suppressor gene is closely related to the occurrence of pancreatic cancer.