Evidence map›Paper›PMID 19755392›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2009

Lung cancer in never smokers: molecular profiles and therapeutic implications.

Charles M Rudin, Erika Avila-Tang, Curtis C Harris, James G Herman, Fred R Hirsch, William Pao, Ann G Schwartz, Kirsi H Vahakangas, Jonathan M Samet

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
11.9field-weighted citation impact, top 1% 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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 167 citations in OpenAlex.

  1. Pooled it
  2. Article
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  5. Article
  6. Review
  7. Article
  8. Review
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  10. Review
  11. Article
  12. Article
  13. Squamous Cell Carcinoma in Never Smokers: An Insight into SMARCB1 Loss.International journal of molecular sciences · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

14 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 5 institutions in 2 countries.

Charles M RudinJohns Hopkins University School of Medicine, David H. Koch Cancer Research Building, Room 544, 1550 Orleans Street, Baltimore, MD 21231, USA. rudin@jhmi.edu
Erika Avila-Tang
Curtis C Harris
James G Herman
Fred R Hirsch
William Pao
Ann G Schwartz
Kirsi H Vahakangas
Jonathan M Samet
Memorial Sloan Kettering Cancer Center · USNational Cancer Institute · USUniversity of Colorado Denver · USUniversity of Eastern Finland · FIWayne State University · US

Funding

Molecular Epidemiology of Human Lung CancerZIABC005480 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HARRIS, CURTIS · 2009 to 2012
$3.0M
Molecular Epidemiology of Human Lung CancerZ01BC005480 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HARRIS, CURTIS · 1996 to 2008
$2.3M
Intramural NIH HHS ZIA BC005480
6 · The paper itself

Abstract

The majority of lung cancers are caused by long term exposure to the several classes of carcinogens present in tobacco smoke. Although a significant fraction of lung cancers in never smokers may also be attributable to tobacco, many such cancers arise in the absence of detectable tobacco exposure, and may follow a very different cellular and molecular pathway of malignant transformation. Recent studies summarized here suggest that lung cancers arising in never smokers have a distinct natural history, profile of oncogenic mutations, and response to targeted therapy. The majority of molecular analyses of lung cancer have focused on genetic profiling of pathways responsible for metabolism of primary tobacco carcinogens. Limited research has been conducted evaluating familial aggregation and genetic linkage of lung cancer, particularly among never smokers in whom such associations might be expected to be strongest. Data emerging over the past several years show that lung cancers in never smokers are much more likely to carry activating mutations of the epidermal growth factor receptor (EGFR), a key oncogenic factor and direct therapeutic target of several newer anticancer drugs. EGFR mutant lung cancers may represent a distinct class of lung cancers, enriched in the never-smoking population, and less clearly linked to direct tobacco carcinogenesis. These insights followed initial testing and demonstration of efficacy of EGFR-targeted drugs. Focused analysis of molecular carcinogenesis in lung cancers in never smokers is needed, and may provide additional biologic insight with therapeutic implications for lung cancers in both ever smokers and never smokers.

Indexed as

Genetic Predisposition to DiseaseBiomarkers, TumorEnvironmental ExposureErbB ReceptorsGenome-Wide Association StudyHumansLung NeoplasmsMolecular EpidemiologyBiomarkers, TumorErbB Receptors

Identifiers

PMID19755392
PMCPMC2950319
OpenAlexW2012248028

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.