Evidence map›Paper›PMID 36018850›Full record

ArticlePloS one2022

S146L in MYC is a context-dependent activating substitution in cancer development.

John W Hinds, Edmond J Feris, Owen M Wilkins, Luke T Deary, Xiaofeng Wang, Michael D Cole

Abstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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

1 citing paper in PubMed.

  1. MYC Point Mutations in Cancer: A Reboot and a Sequel.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Review
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.

John W HindsDepartment of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth College, Hanover, New Hampshire, Unites States of America.
Edmond J FerisDepartment of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth College, Hanover, New Hampshire, Unites States of America.ORCID 0000-0001-9649-2844
Owen M WilkinsCenter for Quantitative Biology (CQB), Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire, Unites States of America.
Luke T DearyDepartment of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth College, Hanover, New Hampshire, Unites States of America.
Xiaofeng WangDepartment of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth College, Hanover, New Hampshire, Unites States of America.
Michael D ColeDepartment of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth College, Hanover, New Hampshire, Unites States of America.ORCID 0000-0002-3421-5451

Funding

Translational Engineering in Cancer (TEC)P30CA023108 · NCI · DARTMOUTH COLLEGE · PI Steven D Leach · 1985 to 2026
$91.3M
Zhao - Proj 2P20GM130454 · NIGMS · DARTMOUTH COLLEGE · PI Chengxiang Qiu · 2019 to 2026
$27.2M
FUNCTION OF THE C-MYC ONCOGENER01CA055248 · NCI · PRINCETON UNIVERSITY · PI COLE, MICHAEL DAVID · 1992 to 2020
$8.6M
NCI NIH HHS P30 CA023108NCI NIH HHS R01 CA055248NIGMS NIH HHS P20 GM130454
6 · The paper itself

Abstract

MYC is one of the most dysregulated oncogenes and is thought to be fundamental to tumor formation and/or maintenance in many cancer types. This dominant pro-tumor activity makes MYC an attractive target for cancer therapy. However, MYC is a transcription factor lacking enzymatic activity, and the structure of one of its two domains is unknown e.g., its transactivation domain. Consequently, few direct MYC-targeting therapies have been developed, and none have been successful in the clinic. Nevertheless, significant effort has been devoted to understanding the mechanisms of oncogenic MYC activity with the objective of uncovering novel vulnerabilities of MYC-dependent cancers. These extensive investigations have revealed in detail how MYC translocation, amplification, and other upstream perturbations contribute to MYC activity in cancer. However, missense mutations of the MYC gene have remained relatively understudied for their potential role in MYC-mediated oncogenesis. While the function of several low-frequency mutations in MYC have been described, our understanding of other equally or more frequent mutations is incomplete. Herein, we define the function of a recurrent missense mutation in MYC resulting in the substitution S146L. This mutation enhances the interaction between MYC and its cofactor TRRAP and may enhance oncogenic MYC activity in certain cellular contexts.

Indexed as

NeoplasmsProto-Oncogene Proteins c-mycHumansProto-Oncogene Proteins c-myc

Identifiers

PMID36018850
PMCPMC9417018

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Registered trials

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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.