Evidence map›Paper›PMID 19017734›Full record

ArticleProceedings of the American Thoracic Society2008

Smoking and lung cancer: the role of inflammation.

Tonya Walser, Xiaoyan Cui, Jane Yanagawa, Jay M Lee, Eileen Heinrich, Gina Lee, Sherven Sharma, Steven M Dubinett

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the American Thoracic Society, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 191 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
191citing papers in PubMed, 8 pooled it
4.3field-weighted citation impact, top 5% 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

191 citing papers in PubMed, 8 syntheses or guidelines pooled it, 383 citations in OpenAlex.

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  7. Association between serum copper levels and lung cancer risk: A meta-analysis.The Journal of international medical research · 2018
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131 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

8 authors at 4 institutions in 1 country.

Tonya WalserLung Cancer Research Program, Division of Pulmonary and Critical Care Medicine, 37-131 CHS, 10833 Le Conte Avenue, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1690, USA.
Xiaoyan Cui
Jane Yanagawa
Jay M Lee
Eileen Heinrich
Gina Lee
Sherven Sharma
Steven M Dubinett
University of California, Los Angeles · USPulmonary and Critical Care Associates · USVA Greater Los Angeles Healthcare System · USUCLA Jonsson Comprehensive Cancer Center

Funding

Gene Modified Dendritic Cell Therapy in Lung CancerK23CA131577 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LEE, JAY M · 2009 to 2013
$660k
6 · The paper itself

Abstract

Worldwide over 1 million people die due to lung cancer each year. It is estimated that cigarette smoking explains almost 90% of lung cancer risk in men and 70 to 80% in women. Clinically evident lung cancers have multiple genetic and epigenetic abnormalities. These abnormalities may result in activation of oncogenes and inactivation of tumor-suppressor genes. Chronic inflammation, which is known to promote cancer, may result both from smoking and from genetic abnormalities. These mediators in turn may be responsible for increased macrophage recruitment, delayed neutrophil clearance, and increase in reactive oxygen species (ROS). Thus, the pulmonary environment presents a unique milieu in which lung carcinogenesis proceeds in complicity with the host cellular network. The pulmonary diseases that are associated with the greatest risk for lung cancer are characterized by abundant and deregulated inflammation. Pulmonary disorders such as chronic obstructive pulmonary disease (COPD)/emphysema are characterized by profound abnormalities in inflammatory and fibrotic pathways. The cytokines and growth factors aberrantly produced in COPD and the developing tumor microenvironment have been found to have deleterious properties that simultaneously pave the way for both epithelial-mesenchymal transition (EMT) and destruction of specific host cell-mediated immune responses. Full definition of these pathways will afford the opportunity to intervene in specific inflammatory events mediating lung tumorigenesis and resistance to therapy.

Indexed as

FemaleHumansInflammationLung NeoplasmsMaleSmoking

Identifiers

PMID19017734
PMCPMC4080902
OpenAlexW1969574651

What OpenQuestion holds

Textmetadata
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.