Evidence map›Paper›PMID 23274911›Full record

ArticleCancer discovery2013

Mutant N-RAS protects colorectal cancer cells from stress-induced apoptosis and contributes to cancer development and progression.

Yufang Wang, Sérgia Velho, Efsevia Vakiani, Shouyong Peng, Adam J Bass, Gerald C Chu, Jessica Gierut, James M Bugni, Channing J Der, Mark Philips and 2 more

Open access · greenAbstract read
In one paragraph

Article in Cancer discovery, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Detection ofOncology research · 2026
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  10. MicroRNA in adenoid cystic carcinoma (Review).International journal of oncology · 2023
    Review
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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

12 authors at 6 institutions in 1 country.

Yufang WangMolecular Pathology Unit, Center for Cancer Research and Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Charlestown 02129 , USA.
Sérgia Velho
Efsevia Vakiani
Shouyong Peng
Adam J Bass
Gerald C Chu
Jessica Gierut
James M Bugni
Channing J Der
Mark Philips
David B Solit
Kevin M Haigis
Brigham and Women's Hospital · USNew York University · USUniversity of North Carolina at Chapel Hill · USCenter for Cancer Research · USCenter for Systems Biology · USUNC Lineberger Comprehensive Cancer Center

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG · 1991 to 2026
$35.3M
Tumor Cell Networks CenterU54CA112967 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LAUFFENBURGER, DOUGLAS A · 2004 to 2015
$26.2M
Regulation of K-Ras by a Farnesyl-electrostatic SwitchR01CA116034 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI PHILIPS, MARK REID · 2005 to 2017
$3.4M
Isoprenylcysteine Carboxyl Methyltransferase (ICMT) as a Target in NRAS Driven Melanoma - Resubmission - 1R01CA163489 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI PHILIPS, MARK REID · 2012 to 2020
$2.8M
Genetic and genomic analysis of Ras signaling in colorectal cancer progressionK01CA118425 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI HAIGIS, KEVIN · 2006 to 2010
$781k
NCI NIH HHS CA118425NCI NIH HHS K01 CA118425NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA116034NCI NIH HHS R01 CA163489NCI NIH HHS U54 CA112967NIDDK NIH HHS DK043351NIDDK NIH HHS P30 DK043351
6 · The paper itself

Abstract

N-RAS is one member of a family of oncoproteins that are commonly mutated in cancer. Activating mutations in NRAS occur in a subset of colorectal cancers, but little is known about how the mutant protein contributes to the onset and progression of the disease. Using genetically engineered mice, we find that mutant N-RAS strongly promotes tumorigenesis in the context of inflammation. The protumorigenic nature of mutant N-RAS is related to its antiapoptotic function, which is mediated by activation of a noncanonical mitogen-activated protein kinase pathway that signals through STAT3. As a result, inhibition of MAP-ERK kinase selectively induces apoptosis in autochthonous colonic tumors expressing mutant N-RAS. The translational significance of this finding is highlighted by our observation that NRAS mutation correlates with a less favorable clinical outcome for patients with colorectal cancer. These data show for the first time the important role that N-RAS plays in colorectal cancer.

Indexed as

AnimalsApoptosisCell Line, TumorColitisColorectal NeoplasmsDisease ProgressionExtracellular Signal-Regulated MAP KinasesGenes, rasGTP PhosphohydrolasesHumansMAP Kinase Signaling SystemMembrane ProteinsMiceProto-Oncogene Proteins c-rafras ProteinsSignal TransductionExtracellular Signal-Regulated MAP KinasesGTP PhosphohydrolasesMembrane ProteinsNRAS protein, humanProto-Oncogene Proteins c-rafras ProteinsSTAT3 protein, humanStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID23274911
PMCPMC3595397
OpenAlexW2165092724

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.