Evidence map›Paper›PMID 24890125›Full record

ArticleThe Journal of pathology2014

Loss of the novel tumour suppressor and polarity gene Trim62 (Dear1) synergizes with oncogenic Ras in invasive lung cancer.

Alfonso Quintás-Cardama, Sean M Post, Luisa M Solis, Shunbin Xiong, Peirong Yang, Nanyue Chen, Ignacio I Wistuba, Ann M Killary, Guillermina Lozano

Open access · greenAbstract read
In one paragraph

Article in The Journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

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  13. Association ofBreast cancer : basic and clinical research · 2020
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  18. Downregulation of TRIM21 contributes to hepatocellular carcinoma carcinogenesis and indicates poor prognosis of cancers.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    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

9 authors at 1 institution in 1 country.

Alfonso Quintás-CardamaDepartment of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA; Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Sean M Post
Luisa M Solis
Shunbin Xiong
Peirong Yang
Nanyue Chen
Ignacio I Wistuba
Ann M Killary
Guillermina Lozano
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
TRANSCRIPTIONAL REGULATION OF WT-1P01CA034936 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI STRONG, LOUISE C · 1985 to 2010
$26.4M
Role of p53 Missense Mutations on Tumorigenesis in VivoR01CA082577 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LOZANO, GUILLERMINA · 1999 to 2024
$7.3M
NCI NIH HHS CA016672NCI NIH HHS CA82577NCI NIH HHS P01 CA034936NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA082577
6 · The paper itself

Abstract

Deregulation of cell polarity proteins has been linked to the processes of invasion and metastasis. TRIM62 is a regulator of cell polarity and a tumour suppressor in breast cancer. Here, we demonstrate that human non-small cell lung cancer lesions show a step-wise loss of TRIM62 levels during disease progression, which was associated with poor clinical outcomes. To directly examine the role of Trim62 in development of lung cancer, we deleted Trim62 in a mutant K-Ras mouse model of lung cancer. In this context, haploinsufficiency of Trim62 synergized with a K-RasG12D mutation to promote invasiveness and disrupt three-dimensional morphogenesis, both of which are associated with epithelial-mesenchymal transitions. Re-expression of Trim62 reverted these phenotypes in tumour cell lines. Thus, Trim62 loss cooperates with K-Ras mutation in tumourigenesis and metastasis in vivo, indicating that decreased levels of TRIM62 may play an important role in the evolution of lung cancer.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCarcinoma, Non-Small-Cell LungCell Transformation, NeoplasticEpithelial-Mesenchymal TransitionFemaleGenes, rasHumansLungLung NeoplasmsMiceMice, Inbred BALB CMice, Inbred C57BLMutationReceptors, AngiotensinReceptors, EndothelinDear1 protein, mouseReceptors, AngiotensinReceptors, EndothelinTRIM62 protein, humanTripartite Motif ProteinsTumor Suppressor ProteinsUbiquitin-Protein LigasesanoikisEMTmetastasismouse models

Identifiers

PMID24890125
PMCPMC4138305
OpenAlexW1966025845

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.