Evidence map›Paper›PMID 24120666›Full record

ArticleMolecular cell2013

The Mre11 complex suppresses oncogene-driven breast tumorigenesis and metastasis.

Gaorav P Gupta, Katelynd Vanness, Afsar Barlas, Katia O Manova-Todorova, Yong H Wen, John H J Petrini

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

37 citing papers in PubMed, 48 citations in OpenAlex.

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  20. Nbn-Mre11 interaction is required for tumor suppression and genomic integrity.Proceedings of the National Academy of Sciences of the United States of America · 2019
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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

6 authors at 1 institution in 1 country.

Gaorav P GuptaMolecular Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA; Department of Radiation Oncology, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.
Katelynd Vanness
Afsar Barlas
Katia O Manova-Todorova
Yong H Wen
John H J Petrini
Memorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
ROLES OF MRELL AND RAD50 IN THE DNA DAMAGE RESPONSER01GM056888 · NIGMS · UNIVERSITY OF WISCONSIN MADISON · PI PETRINI, JOHN HJ · 1998 to 2019
$8.6M
Regulation of the DNA damage response by the Mre11 complexR37GM059413 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI PETRINI, JOHN HJ · 2012 to 2020
$5.2M
The Mre11 complex: linking recombination to checkpointsR01GM059413 · NIGMS · UNIVERSITY OF WISCONSIN MADISON · PI PETRINI, JOHN HJ · 1999 to 2011
$5.2M
FASEB SRC on Genetic Recombination and Genome RearrangementsR13CA162528 · NCI · FEDERATION OF AMER SOC FOR EXPER BIOLOGY · PI PETRINI, JOHN HJ · 2011 to 2011
$5k
NCI NIH HHS P30 CA008748NCI NIH HHS R13 CA162528NIGMS NIH HHS GM59413NIGMS NIH HHS R01 GM056888NIGMS NIH HHS R01 GM059413NIGMS NIH HHS R37 GM059413
6 · The paper itself

Abstract

The DNA damage response (DDR) is activated by oncogenic stress, but the mechanisms by which this occurs, and the particular DDR functions that constitute barriers to tumorigenesis, remain unclear. We established a mouse model of sporadic oncogene-driven breast tumorigenesis in a series of mutant mouse strains with specific DDR deficiencies to reveal a role for the Mre11 complex in the response to oncogene activation. We demonstrate that an Mre11-mediated DDR restrains mammary hyperplasia by effecting an oncogene-induced G2 arrest. Impairment of Mre11 complex functions promotes the progression of mammary hyperplasias into invasive and metastatic breast cancers, which are often associated with secondary inactivation of the Ink4a-Arf (CDKN2a) locus. These findings provide insight into the mechanism of DDR engagement by activated oncogenes and highlight genetic interactions between the DDR and Ink4a-Arf pathways in suppression of oncogene-driven tumorigenesis and metastasis.

Indexed as

CarcinogenesisOncogenesAnimalsBreast NeoplasmsCyclin-Dependent Kinase Inhibitor p16DNA-Binding ProteinsDNA DamageFemaleGene Expression Regulation, NeoplasticHumansHyperplasiaMammary Glands, AnimalMiceMRE11 Homologue ProteinNeoplasm MetastasisCdkn2a protein, mouseCyclin-Dependent Kinase Inhibitor p16DNA-Binding ProteinsMRE11 Homologue ProteinMRE11 protein, human

Identifiers

PMID24120666
PMCPMC3902959
OpenAlexW2013338142

What OpenQuestion holds

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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.