Evidence map›Paper›PMID 21406400›Full record

ArticleCancer research2011

Interaction between MYC and MCL1 in the genesis and outcome of non-small-cell lung cancer.

Thaddeus D Allen, Chang Qi Zhu, Kirk D Jones, Naoki Yanagawa, Ming-Sound Tsao, J Michael Bishop

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Pivotal Role of Fatty Acid Synthase in c-MYC Driven Hepatocarcinogenesis.International journal of molecular sciences · 2020
    Article
  6. Notch Transduction in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2020
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. IncreasedOncoTargets and therapy · 2019
    Article
  12. Article
  13. Frontiers in cell and developmental biology · 2017
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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 3 institutions in 2 countries.

Thaddeus D AllenG.W. Hooper Research Foundation, University of California, San Francisco, USA. Thaddeus.Allen@ucsf.edu
Chang Qi Zhu
Kirk D Jones
Naoki Yanagawa
Ming-Sound Tsao
J Michael Bishop
University of California, San Francisco · USUniversity of Toronto · CAOntario Institute for Cancer Research · CA

Funding

THE MOLECULAR ANALYSIS OF TUMOR VIRUSEST32CA009043 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BISHOP, J. MICHAEL · 1985 to 2009
$5.9M
NCI NIH HHS CA009043NCI NIH HHS T32 CA009043
6 · The paper itself

Abstract

MYC exerts both positive and negative functions in cancer cells, such that its procancerous effects are unmasked only after its anticancer effects are blocked. Here we used multiple mouse models of lung adenocarcinoma to identify genetic events that can cooperate with MYC activation to promote the genesis of non-small-cell lung cancer (NSCLC), the most common form of lung cancer in humans. MYC overexpression targeted to pulmonary alveolar cells was sufficient to induce lung adenomas and carcinomas. Tumorigenesis was assisted by either spontaneous mutations in Kras or experimental introduction of activated RAS, but investigations revealed that additional events were required to circumvent apoptosis, one of the most significant negative functions exerted by MYC. We determined that overexpression of the antiapoptotic protein MCL1 was sufficient to circumvent apoptosis in this setting. Previous clinical studies have indicated that prognosis of human NSCLC is not associated with MCL1, despite its overexpression in many NSCLCs. In reexamining the prognostic value in this setting, we found that MCL1 overexpression does correlate with poor patient survival, but only when accompanied by MYC overexpression. Our findings therefore produce a convergence of mouse and human results that explain how MCL1 can block an important negative consequence of MYC overexpression in both experimental models and clinical cases of NSCLC.

Indexed as

AgedAnimalsApoptosisBlotting, WesternCarcinoma, Non-Small-Cell LungCell ProliferationGene ExpressionHumansHyperplasiaImmunohistochemistryIn Situ Nick-End LabelingKaplan-Meier EstimateLung NeoplasmsMiceMice, TransgenicMiddle AgedMcl1 protein, mouseMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-mycras Proteins

Identifiers

PMID21406400
PMCPMC3076947
OpenAlexW2028662696

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.