Evidence map›Paper›PMID 22675468›Full record

ArticlePloS one2012

Functional characterization of CLPTM1L as a lung cancer risk candidate gene in the 5p15.33 locus.

Michael A James, Weidong Wen, Yian Wang, Lauren A Byers, John V Heymach, Kevin R Coombes, Luc Girard, John Minna, Ming You

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 9 pooled it
5.4field-weighted citation impact, top 3% 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

75 citing papers in PubMed, 9 syntheses or guidelines pooled it, 102 citations in OpenAlex.

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  7. Cleft lip and palate transmembrane protein 1 rs31489 polymorphism is associated with lung cancer risk: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
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15 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

9 authors at 4 institutions in 1 country.

Michael A JamesMCW Cancer Center, Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
Weidong Wen
Yian Wang
Lauren A Byers
John V Heymach
Kevin R Coombes
Luc Girard
John Minna
Ming You
The University of Texas MD Anderson Cancer Center · USMedical College of Wisconsin · USThe University of Texas Southwestern Medical Center · USWashington University in St. Louis · US

Funding

Washington University Center for Cellular ImagingP30CA091842 · NCI · WASHINGTON UNIVERSITY · PI TIMOTHY J. EBERLEIN · 2001 to 2026
$128.0M
UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GIBBONS, DON LYNN · 1996 to 2024
$57.4M
Transdisciplinary Research in Cancer of the Lung (TRICL)U19CA148127 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI AMOS, CHRISTOPHER I., LE MARCHAND, LOIC · 2010 to 2014
$10.9M
NCI NIH HHS P30 CA091842NCI NIH HHS #P30 CA91842NCI NIH HHS P50 CA070907NCI NIH HHS U19 CA148127NCI NIH HHS U19CA148127
6 · The paper itself

Abstract

Cleft Lip and Palate Transmembrane Protein 1-Like (CLPTM1L), resides in a region of chromosome 5 for which copy number gain has been found to be the most frequent genetic event in the early stages of non-small cell lung cancer (NSCLC). This locus has been found by multiple genome wide association studies to be associated with lung cancer in both smokers and non-smokers. CLPTM1L has been identified as an overexpressed protein in human ovarian tumor cell lines that are resistant to cisplatin, which is the only insight thus far into the function of CLPTM1L. Here we find CLPTM1L expression to be increased in lung adenocarcinomas compared to matched normal lung tissues and in lung tumor cell lines by mechanisms not exclusive to copy number gain. Upon loss of CLPTM1L accumulation in lung tumor cells, cisplatin and camptothecin induced apoptosis were increased in direct proportion to the level of CLPTM1L knockdown. Bcl-xL accumulation was significantly decreased upon loss of CLPTM1L. Expression of exogenous Bcl-xL abolished sensitization to apoptotic killing with CLPTM1L knockdown. These results demonstrate that CLPTM1L, an overexpressed protein in lung tumor cells, protects from genotoxic stress induced apoptosis through regulation of Bcl-xL. Thus, this study implicates anti-apoptotic CLPTM1L function as a potential mechanism of susceptibility to lung tumorigenesis and resistance to chemotherapy.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseaseAdenocarcinomaAdenocarcinoma of LungApoptosisbcl-X ProteinCell Line, TumorChromosomes, Human, Pair 5DNA DamageDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticGenetic LociHumansLung NeoplasmsMembrane ProteinsMutagensbcl-X ProteinCLPTM1L protein, humanMembrane ProteinsMutagensNeoplasm Proteins

Identifiers

PMID22675468
PMCPMC3366984
OpenAlexW2076953184

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.