DPC4, a candidate tumor suppressor gene at human chromosome 18q21.1
- PMID: 8553070
- DOI: 10.1126/science.271.5247.350
DPC4, a candidate tumor suppressor gene at human chromosome 18q21.1
Abstract
About 90 percent of human pancreatic carcinomas show allelic loss at chromosome 18q. To identify candidate tumor suppressor genes on 18q, a panel of pancreatic carcinomas were analyzed for convergent sites of homozygous deletion. Twenty-five of 84 tumors had homozygous deletions at 18q21.1, a site that excludes DCC (a candidate suppressor gene for colorectal cancer) and includes DPC4, a gene similar in sequence to a Drosophila melanogaster gene (Mad) implicated in a transforming growth factor-beta (TGF-beta)-like signaling pathway. Potentially inactivating mutations in DPC4 were identified in six of 27 pancreatic carcinomas that did not have homozygous deletions at 18q21.1. These results identify DPC4 as a candidate tumor suppressor gene whose inactivation may play a role in pancreatic and possibly other human cancers.
Comment in
-
New tumor suppressor found in pancreatic cancer.Science. 1996 Jan 19;271(5247):294. doi: 10.1126/science.271.5247.294. Science. 1996. PMID: 8553063 No abstract available.
Similar articles
-
The 18q21 region in colorectal and pancreatic cancer: independent loss of DCC and DPC4 expression.Biochim Biophys Acta. 2000 Oct 18;1502(2):283-96. doi: 10.1016/s0925-4439(00)00054-5. Biochim Biophys Acta. 2000. PMID: 11040453
-
Homozygous deletions inactivate DCC, but not MADH4/DPC4/SMAD4, in a subset of pancreatic and biliary cancers.Genes Chromosomes Cancer. 2000 Apr;27(4):353-7. Genes Chromosomes Cancer. 2000. PMID: 10719364
-
Inactivation of both alleles of the DPC4/SMAD4 gene in advanced colorectal cancers: identification of seven novel somatic mutations in tumors from Japanese patients.Mutat Res. 1999 Aug;406(2-4):71-7. doi: 10.1016/s1383-5726(99)00003-5. Mutat Res. 1999. PMID: 10479724
-
DPC4/SMAD4 gene alterations in human cancer, and their functional implications.Ann Oncol. 1999;10 Suppl 4:56-9. Ann Oncol. 1999. PMID: 10436786 Review.
-
Role of Smad4 (DPC4) inactivation in human cancer.Biochem Biophys Res Commun. 2003 Jul 11;306(4):799-804. doi: 10.1016/s0006-291x(03)01066-0. Biochem Biophys Res Commun. 2003. PMID: 12821112 Review.
Cited by
-
Transflip mutations produce deletions in pancreatic cancer.Genes Chromosomes Cancer. 2015 Aug;54(8):472-481. doi: 10.1002/gcc.22258. Epub 2015 May 29. Genes Chromosomes Cancer. 2015. PMID: 26031834 Free PMC article.
-
New targeted therapies in pancreatic cancer.World J Gastroenterol. 2015 May 28;21(20):6127-45. doi: 10.3748/wjg.v21.i20.6127. World J Gastroenterol. 2015. PMID: 26034349 Free PMC article. Review.
-
SMAD4 loss is associated with response to neoadjuvant chemotherapy plus hydroxychloroquine in patients with pancreatic adenocarcinoma.Clin Transl Sci. 2021 Sep;14(5):1822-1829. doi: 10.1111/cts.13029. Epub 2021 May 18. Clin Transl Sci. 2021. PMID: 34002944 Free PMC article. Clinical Trial.
-
Consequences of Mutations and Abnormal Expression of SMAD4 in Tumors and T Cells.Onco Targets Ther. 2021 Apr 13;14:2531-2540. doi: 10.2147/OTT.S297855. eCollection 2021. Onco Targets Ther. 2021. PMID: 33888990 Free PMC article. Review.
-
Study of Clinical Survival and Gene Expression in a Sample of Pancreatic Ductal Adenocarcinoma by Parsimony Phylogenetic Analysis.OMICS. 2016 Jul;20(7):442-7. doi: 10.1089/omi.2016.0059. OMICS. 2016. PMID: 27428255 Free PMC article.
Publication types
MeSH terms
Substances
Associated data
- Actions
- Actions
- Actions
- Actions
- Actions
- Actions
- Actions
- Actions
- Actions
- Actions
- Actions
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Molecular Biology Databases
Miscellaneous