癌变
生物
基因
癌症研究
突变
抑癌基因
胰腺癌
癌基因
癌症
抑制器
遗传学
细胞周期
作者
Ester Rozenblum,Mieke Schutte,Michael Goggins,Stephan A. Hahn,SarahLena Panzer,Marianna Zahurak,Steven N. Goodman,Taylor A. Sohn,Ralph H. Hruban,Charles J. Yeo,Scott E. Kern
出处
期刊:PubMed
日期:1997-05-01
卷期号:57 (9): 1731-4
被引量:684
摘要
During tumorigenesis, positive selection is exerted upon those tumor cells that alter rate-limiting regulatory pathways. A corollary of this principle is that mutation of one gene abrogates the need for alteration of another gene in the same pathway and also that the coexistence in a single tumor of mutations in different genes implies their involvement in distinct tumor-suppressive pathways. We studied 42 pancreatic adenocarcinomas for genetic alterations in the K-ras oncogene and the p16, p53, and DPC4 tumor suppressor genes. All of them had the K-ras gene mutated. Thirty-eight % of the tumors had four altered genes, another 38% had three altered genes, 15% had two altered genes, and 8% of the tumors had one altered gene. Interestingly, we noted a high concordance of DPC4 and p16 inactivations (P = 0.007), suggesting that the genetic inactivation of p16 increases the selective advantage of subsequent mutation in DPC4. No statistically significant association was identified between the alteration of these cancer genes and pathological or clinical parameters. This type of multigenic analysis in human tumors may serve to substantiate experimental tumor models and thus increase our understanding of the truly physiologically relevant tumor-suppressive pathways that are abrogated during human tumorigenesis.
科研通智能强力驱动
Strongly Powered by AbleSci AI