ArticleCancer gene therapy2001
Adenovirus-mediated wt-p16 reintroduction induces cell cycle arrest or apoptosis in pancreatic cancer.
Article in Cancer gene therapy, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 37 citations in OpenAlex.
- Cyclooxygenase-2 Influences Response to Cotargeting of MEK and CDK4/6 in a Subpopulation of Pancreatic Cancers.Molecular cancer therapeutics · 2018Article
- Increased p16 and p53 protein expression predicts poor prognosis in mucosal melanoma.Oncotarget · 2017Article
- Molecular Drivers of Pancreatic Cancer Pathogenesis: Looking Inward to Move Forward.International journal of molecular sciences · 2017Review
- CDK4/6 inhibitors have potent activity in combination with pathway selective therapeutic agents in models of pancreatic cancer.Oncotarget · 2014Article
- p16(Ink4a) overexpression in cancer: a tumor suppressor gene associated with senescence and high-grade tumors.Oncogene · 2011Review
- Article
- Co-regulation of p16INK4A and migratory genes in culture conditions that lead to premature senescence in human keratinocytes.The Journal of investigative dermatology · 2005Article
- Identification and functional significance of genes regulated by structurally different histone deacetylase inhibitors.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Is there a role for staging laparoscopy in patients with locally advanced, unresectable pancreatic adenocarcinoma?Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2004Article
- p16(Ink4a) interferes with Abelson virus transformation by enhancing apoptosis.Journal of virology · 2004Article
- Effects of p16 gene on biological behaviours in hepatocellular carcinoma cells.World journal of gastroenterology · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic cancer has long carried poor prognosis. The development of new therapeutic approaches is particularly urgent. Inactivation of the tumor-suppressor gene p16(INK4a/CDKN2), a specific inhibitor of the cyclin-dependent kinases CDK4 and CDK6, is the most common genetic alteration in human pancreatic cancer, making it an ideal target for gene replacement. Here we transfected tumor cells using a recombinant adenovirus containing the wt-p16 cDNA (Ad5RSV-p16). The overexpression of p16 decreased cell proliferation in all four human pancreatic tumor cell lines (NP-9, NP-18, NP-29, and NP-31). However, G1 arrest and senescence were observed in only three. In contrast, the fourth (NP-18) showed a significant increase in apoptosis. This differential behavior may be related to the differences found in the expression level of E2F-1. Experiments on subcutaneous pancreatic xenografts demonstrated the effectiveness of p16 in the inhibition of pancreatic tumor growth in vivo. Taken together, our results indicate that approaches involving p16 replacement are promising in pancreatic cancer treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.