Evidence map›Paper›PMID 33144509›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

Rev7 loss alters cisplatin response and increases drug efficacy in chemotherapy-resistant lung cancer.

Faye-Marie Vassel, Ke Bian, Graham C Walker, Michael T Hemann

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Faye-Marie VasselDepartment of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139.ORCID 0000-0002-5721-6473
Ke BianDepartment of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139.ORCID 0000-0002-1268-2382
Graham C WalkerDepartment of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139; gwalker@mit.edu hemann@mit.edu.ORCID 0000-0001-7243-8261
Michael T HemannDepartment of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139; gwalker@mit.edu hemann@mit.edu.ORCID 0000-0001-6776-2163
Massachusetts Institute of Technology · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
PRE-DOCTORAL TRAINING IN THE BIOLOGICAL SCIENCEST32GM007287 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI BELL, STEPHEN P., KEATING, AMY E · 1985 to 2019
$40.8M
TOXICOLOGY CORE UNITP30ES002109 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LEVINE, STUART S · 1985 to 2020
$25.6M
TRAINING GRANTS IN ENVIROMENTAL TOXICOLOGYT32ES007020 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI ESSIGMANN, JOHN M · 1985 to 2024
$13.1M
Mechanism of Eukaryotic Environmental MutagenesisR35ES028303 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI WALKER, GRAHAM C · 2017 to 2024
$4.2M
Mechanism of Eukaryotic Environmental MutagenesisR01ES015818 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI WALKER, GRAHAM C · 2007 to 2016
$3.8M
RNA-Binding Proteins as Molecular Integrators that Control the Response of HGSOC to Ant-Cancer TherapiesR01CA226898 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI BURGE, CHRISTOPHER B, HEMANN, MICHAEL · 2019 to 2023
$2.7M
Identifying and targeting evolutionary trajectories in cancerR01CA233477 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI HEMANN, MICHAEL · 2019 to 2023
$1.7M
NCI NIH HHS P30 CA014051NCI NIH HHS R01 CA226898NCI NIH HHS R01 CA233477NIEHS NIH HHS P30 ES002109NIEHS NIH HHS R01 ES015818NIEHS NIH HHS R35 ES028303NIEHS NIH HHS T32 ES007020NIGMS NIH HHS T32 GM007287
6 · The paper itself

Abstract

Cisplatin is a standard of care for lung cancer, yet platinum therapy rarely results in substantial tumor regression or a dramatic extension in patient survival. Here, we examined whether targeting Rev7 (also referred to as Mad2B, Mad2L2, and FANCV), a component of the translesion synthesis (TLS) machinery, could potentiate the action of cisplatin in non-small cell lung cancer (NSCLC) treatment. Rev7 loss led to an enhanced tumor cell sensitivity to cisplatin and dramatically improved chemotherapeutic response in a highly drug-resistant mouse model of NSCLC. While cisplatin monotherapy resulted in tumor cell apoptosis, Rev7 deletion promoted a cisplatin-induced senescence phenotype. Moreover, Rev7 deficiency promoted greater cisplatin sensitivity than that previously shown following targeting of other Pol ζ-proteins, suggesting that Pol ζ-dependent and -independent roles of Rev7 are relevant to cisplatin response. Thus, targeting Rev7 may represent a unique strategy for altering and enhancing chemotherapeutic response.

Indexed as

AnimalsApoptosisCarcinoma, Non-Small-Cell LungCell Line, TumorCisplatinDNA-Binding ProteinsDNA DamageDNA-Directed DNA PolymeraseDNA RepairDrug Resistance, NeoplasmHumansLung NeoplasmsMad2 ProteinsMiceMutagenesisTumor Cells, CulturedCisplatinDNA-Binding ProteinsDNA-Directed DNA PolymeraseMAD2L2 protein, humanMad2l2 protein, mouseMad2 Proteinschemotherapycisplatinlung cancerRev7translesion synthesis

Identifiers

PMID33144509
PMCPMC7682549
OpenAlexW3095757372

What OpenQuestion holds

Textmetadata
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.