Evidence map›Paper›PMID 32345725›Full record

ArticleScience signaling2020

Regulation of the error-prone DNA polymerase Polκ by oncogenic signaling and its contribution to drug resistance.

Kelsey Temprine, Nathaniel R Campbell, Richard Huang, Erin M Langdon, Theresa Simon-Vermot, Krisha Mehta, Averill Clapp, Mollie Chipman, Richard M White

Open access · greenAbstract read
In one paragraph

Article in Science signaling, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 39 citations in OpenAlex.

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  11. Polymorphisms of DNA Repair Genes in Thyroid Cancer.International journal of molecular sciences · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Kelsey TemprineCancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.ORCID 0000-0002-1322-6450
Nathaniel R CampbellCancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.ORCID 0000-0002-0355-0708
Richard HuangCancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.ORCID 0000-0001-8739-0571
Erin M LangdonUniversity of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA.ORCID 0000-0002-9324-6215
Theresa Simon-VermotCancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.ORCID 0000-0002-2814-2903
Krisha MehtaDivision of General Internal Medicine, Department of Medicine, Weill Cornell Medical College, New York, NY 10065, USA.
Averill ClappUniversity of Chicago, Chicago, IL 60637, USA.ORCID 0000-0002-5854-4428
Mollie ChipmanCancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.ORCID 0000-0002-8266-8367
Richard M WhiteCancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. whiter@mskcc.org.ORCID 0000-0001-9099-9169
Memorial Sloan Kettering Cancer Center · USCornell University · USUniversity of Chicago · USUniversity of North Carolina at Chapel Hill · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
Evolutionary dynamics of melanoma metastasisDP2CA186572 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI WHITE, RICHARD MARK · 2013 to 2013
$2.7M
The role of melanocyte precursors in zebrafish pigmentation disordersK08AR055368 · NIAMS · SLOAN-KETTERING INST CAN RESEARCH · PI WHITE, RICHARD MARK · 2009 to 2013
$635k
Dissecting the Ecology of Metastasis in a Zebrafish Model: Trade-Offs of Size and Diversity in Circulating Tumor Cell ClustersF30CA220954 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CAMPBELL, NATHANIEL R · 2018 to 2021
$194k
Investigating the Role of Polymerase kappa in Melanoma Heterogeneity and Drug ResistanceF31CA200341 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI TEMPRINE, KELSEY · 2015 to 2017
$83k
NCI NIH HHS DP2 CA186572NCI NIH HHS F30 CA220954NCI NIH HHS F31 CA200341NCI NIH HHS P30 CA008748NIAMS NIH HHS K08 AR055368NIGMS NIH HHS T32 GM007739
6 · The paper itself

Abstract

The DNA polymerase Polκ plays a key role in translesion synthesis, an error-prone replication mechanism. Polκ is overexpressed in various tumor types. Here, we found that melanoma and lung and breast cancer cells experiencing stress from oncogene inhibition up-regulated the expression of Polκ and shifted its localization from the cytoplasm to the nucleus. This effect was phenocopied by inhibition of the kinase mTOR, by induction of ER stress, or by glucose deprivation. In unstressed cells, Polκ is continually transported out of the nucleus by exportin-1. Inhibiting exportin-1 or overexpressing Polκ increased the abundance of nuclear-localized Polκ, particularly in response to the BRAF

Indexed as

Drug Resistance, NeoplasmSignal TransductionCell Line, TumorDNA-Directed DNA PolymeraseHumansMelanomaNeoplasm ProteinsY-Family DNA PolymerasesDNA-Directed DNA PolymeraseNeoplasm ProteinsPOLK protein, humanY-Family DNA Polymerases

Identifiers

PMID32345725
PMCPMC7428051
OpenAlexW3018422753

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.