Su G H, Bansal R, Murphy K M, Montgomery E, Yeo C J, Hruban R H, Kern S E
Department of Oncology, Pathology, and Surgery, The Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA.
Proc Natl Acad Sci U S A. 2001 Mar 13;98(6):3254-7. doi: 10.1073/pnas.051484398.
DPC4 is known to mediate signals initiated by type beta transforming growth factor (TGFbeta) as well as by other TGFbeta superfamily ligands such as activin and BMP (bone morphogenic proteins), but mutational surveys of such non-TGFbeta receptors have been negative to date. Here we describe the gene structure and novel somatic mutations of the activin type I receptor, ACVR1B, in pancreatic cancer. ACVR1B has not been described previously as a mutated tumor-suppressor gene.
已知DPC4可介导由β型转化生长因子（TGFβ）以及其他TGFβ超家族配体（如激活素和骨形态发生蛋白（BMP））引发的信号，但迄今为止，对这类非TGFβ受体的突变研究均为阴性。在此，我们描述了胰腺癌中激活素I型受体ACVR1B的基因结构和新的体细胞突变。ACVR1B此前尚未被描述为一种突变的肿瘤抑制基因。
