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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-β (TGF-β)-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.
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“SMAD4 is a tumor suppressor gene, and reported results about the prognostic value of SMAD4 have been inconsistent39,60–62.”
From Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma (2024) · cites this paper as [60]
In the citing paper
“SMAD4 is a tumor suppressor gene, and reported results about the prognostic value of SMAD4 have been inconsistent39,60–62.”
From Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma (2024) · cites this paper as [60]
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Self-citation
Metadata
- Authors
- Hahn, S. A., Schutte, M., Shamsul Hoque, A. T. M., Moskaluk, C. A., da Costa, L. T., Rozenblum, E., Weinstein, C. L., Fischer, A., Yeo, C. J., Hruban, R. H., & Kern, S. E.
- Affiliations
- Johns Hopkins University (US)
- S. A. Hahn, M. Schutte, A. T. M. S. Hoque, C. A. Moskaluk, E. Rozenblum, C. L. Weinstein, A. Fischer, R. H. Hruban, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
- L. T. da Costa, Graduate Program in Human Genetics and Molecular Biology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
- Corresponding author
- Kern, Scott E.
- ORCID
- Venue
- Science
- Published
- 1996-01-19
- Volume
- 271
- Issue
- 5247
- Pages
- 350-353
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2100522747
- Cited by
- 2,337
- References
- 25
- Citations by year
- 2026: 20 · 2025: 21 · 2024: 29 · 2023: 26 · 2022: 31 · 2021: 41 · 2020: 33 · 2019: 44 · 2018: 41 · 2017: 46 · 2016: 55 · 2015: 59 · 2014: 71 · 2013: 64 · 2012: 67
- FWCI
- 70.80
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (P50CA062924, CA 62924)
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- SMAD4, tumor suppressor, pancreatic cancer, homozygous deletion, loss of heterozygosity, TGF-beta signaling, loss-of-function mutations, candidate gene identification
- MeSH terms
- Alleles, Amino Acid Sequence, Animals, Base Sequence, Cell Division, Chromosome Mapping, Chromosomes, Human, Pair 18, DNA-Binding Proteins, Genetic Markers, Humans, Molecular Sequence Data, Mutation, Neoplasm Transplantation, Pancreatic Neoplasms, Proteins, Transplantation, Heterologous, Tumor Cells, Cultured, Signal Transduction, Trans-Activators, Gene Expression, Genes, Tumor Suppressor, Transforming Growth Factor beta, Gene Deletion, Mice, Smad4 Protein
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