Evidence map›Paper›PMID 24706787›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

T helper 17 cells play a critical pathogenic role in lung cancer.

Seon Hee Chang, Seyedeh Golsar Mirabolfathinejad, Harshadadevi Katta, Amber M Cumpian, Lei Gong, Mauricio S Caetano, Seyed Javad Moghaddam, Chen Dong

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 207 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
207citing papers in PubMed, 3 pooled it
13.3field-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

207 citing papers in PubMed, 3 syntheses or guidelines pooled it, 322 citations in OpenAlex.

  1. Pooled it
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  6. Review
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  17. The role and mechanisms of the HIF-1 signaling pathway in LC-COPD.Journal of cancer research and clinical oncology · 2025
    Review
  18. Review
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147 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 1 institution in 1 country.

Seon Hee ChangDepartments of Immunology and Pulmonary Medicine, Center for Inflammation and Cancer, The University of Texas MD Anderson Cancer Center, Houston, TX 77054.
Seyedeh Golsar Mirabolfathinejad
Harshadadevi Katta
Amber M Cumpian
Lei Gong
Mauricio S Caetano
Seyed Javad Moghaddam
Chen Dong
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
NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Lung cancer development is associated with extensive pulmonary inflammation. In addition, the linkage between chronic obstructive pulmonary disease (COPD) and lung cancer has been demonstrated in population-based studies. IL-17-producing CD4 helper T cells (Th17 cells) play a critical role in promoting chronic tissue inflammation. Although Th17 cells are found in human COPD and lung cancer, their role is not understood. We have thus used a mouse model of lung cancer, in which an oncogenic form of K-ras (K-ras(G12D)), frequently found in human lung cancer, is restrictedly expressed in lung epithelial cells [via Clara cell secretory protein (CCSP(cre))]. In this model, Th17 and Treg but not Th1 cells were found enriched at the tumor tissues. When CCSP(cre)/K-ras(G12D) mice were weekly challenged with a lysate of nontypeable Haemophilus influenza (NTHi), which induces COPD-type inflammation and accelerates the tumor growth, they showed greatly enhanced Th17 cell infiltration in the lung tissues. Lack of IL-17, but not IL-17F, resulted in a significant reduction in lung tumor numbers in CCSP(cre)/K-ras(G12D) mice and also those treated with NTHi. Absence of IL-17 not only resulted in reduction of tumor cell proliferation and angiogenesis, but also decreased the expression of proinflammatory mediators and reduced recruitment of myeloid cells. Depletion of Gr-1(+)CD11b(+) myeloid cells in CCSP(cre)/K-ras(G12D) mice suppressed tumor growth in lung, indicating Gr-1(+)CD11b(+) myeloid cells recruited by IL-17 play a protumor role. Taken together, our data demonstrate a critical role for Th17 cell-mediated inflammation in lung tumorigenesis and suggest a novel way for prevention and treatment of this disease.

Indexed as

AnimalsDNA PrimersFlow CytometryGenes, rasHaemophilus influenzaeImmunohistochemistryLung NeoplasmsMiceMice, Mutant StrainsMutationMyeloid CellsPneumoniaPulmonary Disease, Chronic ObstructiveReal-Time Polymerase Chain ReactionTh17 CellsUteroglobinDNA PrimersScgb1a1 protein, mouseUteroglobininterleukin 17lung adenocarcinoma

Identifiers

PMID24706787
PMCPMC3992670
OpenAlexW2053968039

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.