ArticleDNA repair2012
The human gastric cancer-associated DNA polymerase β variant D160N is a mutator that induces cellular transformation.
Article in DNA repair, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Harnessing DNA polymerase beta defect enhances synthetic lethality and treatment response in gastric cancer cells: implication for immunotherapy.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2025Review
- Aberrant DNA polymerase beta expression is associated with dysregulated tumor immune microenvironment and its prognostic value in gastric cancer.Clinical and experimental medicine · 2024Article
- Role of Base Excision Repair in Innate Immune Cells and Its Relevance for Cancer Therapy.Biomedicines · 2022Review
- The Role of Natural Polymorphic Variants of DNA Polymerase β in DNA Repair.International journal of molecular sciences · 2022Review
- Single molecule glycosylase studies with engineered 8-oxoguanine DNA damage sites show functional defects of a MUTYH polyposis variant.Nucleic acids research · 2019Article
- DNA Polymerase β Cancer-Associated Variant I260M Exhibits Nonspecific Selectivity toward the β-γ Bridging Group of the Incoming dNTP.Biochemistry · 2017Article
- A Change in the Rate-Determining Step of Polymerization by the K289M DNA Polymerase β Cancer-Associated Variant.Biochemistry · 2017Article
- Base Excision Repair Variants in Cancer.Methods in enzymology · 2017Article
- A Point Mutation in DNA Polymerase β (POLB) Gene Is Associated with Increased Progesterone Receptor (PR) Expression and Intraperitoneal Metastasis in Gastric Cancer.Journal of Cancer · 2016Article
- The K167I variant of DNA polymerase β that is found in Esophageal Carcinoma patients impairs polymerase activity and BER.Scientific reports · 2015Article
- Base excision repair: a critical player in many games.DNA repair · 2014Review
- The S229L colon tumor-associated variant of DNA polymerase β induces cellular transformation as a result of decreased polymerization efficiency.The Journal of biological chemistry · 2014Article
- Irreversible inhibition of DNA polymerase β by small-molecule mimics of a DNA lesion.Journal of the American Chemical Society · 2014Article
- Cellular roles of DNA polymerase beta.The Yale journal of biology and medicine · 2013Review
- DNA polymerase β promoter mutations and transcriptional activity in esophageal squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Article
- Colon cancer-associated DNA polymerase β variant induces genomic instability and cellular transformation.The Journal of biological chemistry · 2012Article
- The E288K colon tumor variant of DNA polymerase β is a sequence specific mutator.Biochemistry · 2012Article
- Transcriptional profiling reveals elevated Sox2 in DNA polymerase ß null mouse embryonic fibroblasts.American journal of cancer research · 2012Article
- Genome instability caused by a germline mutation in the human DNA repair gene POLB.PLoS genetics · 2012Article
- Tumor-specific microsatellite instability: do distinct mechanisms underlie the MSI-L and EMAST phenotypes?Mutation researchReview
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Approximately 30% of human tumors sequenced to date harbor mutations in the POLB gene that are not present in matched normal tissue. Many mutations give rise to enzymes that contain non-synonymous single amino acid substitutions, several of which have been found to have aberrant activity or fidelity and transform cells when expressed. The DNA Polymerase β (Pol β) variant Asp160Asn (D160N) was first identified in a gastric tumor. Expression of D160N in cells induces cellular transformation as measured by hyperproliferation, focus formation, anchorage-independent growth and invasion. Here, we show that D160N is an active mutator polymerase that induces complex mutations. Our data support the interpretation that complex mutagenesis is the underlying mechanism of the observed cellular phenotypes, all of which are linked to tumorigenesis or tumor progression.
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Registered trials
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.