Evidence map›Paper›PMID 24890832›Full record

ReviewCold Spring Harbor perspectives in medicine2014

MYC activation is a hallmark of cancer initiation and maintenance.

Meital Gabay, Yulin Li, Dean W Felsher

Open access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 533 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
533citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

533 citing papers in PubMed, 2 syntheses or guidelines pooled it, 842 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. A Phase I/II Open-Label Study of Molibresib for the Treatment of Relapsed/Refractory Hematologic Malignancies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Trial
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473 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Meital GabayDivision of Oncology, Departments of Medicine and Pathology, Stanford University School of Medicine, Stanford, California 94305.
Yulin LiDivision of Oncology, Departments of Medicine and Pathology, Stanford University School of Medicine, Stanford, California 94305.
Dean W FelsherDivision of Oncology, Departments of Medicine and Pathology, Stanford University School of Medicine, Stanford, California 94305.
Stanford University · US

Funding

TRIGGERING CELL DEATH IN B CELL LYMPHOMAP01CA034233 · NCI · STANFORD UNIVERSITY · PI FELSHER, DEAN W · 1985 to 2010
$19.5M
Small Animal ImagingP50CA114747 · NCI · STANFORD UNIVERSITY · PI RAO, JIANGHONG · 2005 to 2014
$18.2M
MYC's Role in the Initiation and Maintenance of CancerR01CA089305 · NCI · STANFORD UNIVERSITY · PI FELSHER, DEAN W · 2001 to 2011
$3.7M
Modeling and Predicting Therapeutic Resistance of CancerU01CA188383 · NCI · STANFORD UNIVERSITY · PI FELSHER, DEAN W, GAMBHIR, SANJIV S · 2014 to 2018
$3.2M
Computational Modeling of Cancer BiologyU56CA112973 · NCI · STANFORD UNIVERSITY · PI PLEVRITIS, SYLVIA KATINA · 2004 to 2009
$2.9M
Mechanisms by which Oncogene Inactivation Elicits Tumor Cell DeathR01CA170378 · NCI · STANFORD UNIVERSITY · PI FELSHER, DEAN W · 2012 to 2015
$2.1M
Molecular and Cellular Basis of Oncogene AddictionR01CA105102 · NCI · STANFORD UNIVERSITY · PI FELSHER, DEAN W · 2004 to 2010
$2.0M
NCI NIH HHS P01 CA034233NCI NIH HHS P01CA034233NCI NIH HHS P50 CA114747NCI NIH HHS P50CA114747NCI NIH HHS R01 CA089305NCI NIH HHS R01 CA105102NCI NIH HHS R01CA105102NCI NIH HHS R01 CA170378NCI NIH HHS R01CA17037801NCI NIH HHS R01CA89305NCI NIH HHS U01 CA188383NCI NIH HHS U56 CA112973NCI NIH HHS U56CA112973
6 · The paper itself

Abstract

The MYC proto-oncogene has been implicated in the pathogenesis of most types of human tumors. MYC activation alone in many normal cells is restrained from causing tumorigenesis through multiple genetic and epigenetically controlled checkpoint mechanisms, including proliferative arrest, apoptosis, and cellular senescence. When pathologically activated in a permissive epigenetic and/or genetic context, MYC bypasses these mechanisms, enforcing many of the "hallmark" features of cancer, including relentless tumor growth associated with DNA replication and transcription, cellular proliferation and growth, protein synthesis, and altered cellular metabolism. MYC mandates tumor cell fate, by inducing stemness and blocking cellular senescence and differentiation. Additionally, MYC orchestrates changes in the tumor microenvironment, including the activation of angiogenesis and suppression of the host immune response. Provocatively, brief or even partial suppression of MYC back to its physiological levels of activation can result in the restoration of intrinsic checkpoint mechanisms, resulting in acute and sustained tumor regression, associated with tumor cells undergoing proliferative arrest, differentiation, senescence, and apoptosis, as well as remodeling of the tumor microenvironment, recruitment of an immune response, and shutdown of angiogenesis. Hence, tumors appear to be "addicted" to MYC because of both tumor cell-intrinsic, cell-autonomous and host-dependent, immune cell-dependent mechanisms. Both the trajectory and persistence of many human cancers require sustained MYC activation. Multiscale mathematical modeling may be useful to predict when tumors will be addicted to MYC. MYC is a hallmark molecular feature of both the initiation and maintenance of tumorigenesis.

Indexed as

Genes, mycBiomarkers, TumorCarcinogenesisCell Transformation, NeoplasticEpigenesis, GeneticGene Expression Regulation, NeoplasticHumansNeoplasmsProto-Oncogene MasProto-Oncogene Proteins c-mycTumor MicroenvironmentBiomarkers, TumorMAS1 protein, humanMYC protein, humanProto-Oncogene MasProto-Oncogene Proteins c-myc

Identifiers

PMID24890832
PMCPMC4031954
OpenAlexW2162723598

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.