Evidence map›Paper›PMID 22962265›Full record

SynthesisCancer research2012

Cross-species functional analysis of cancer-associated fibroblasts identifies a critical role for CLCF1 and IL-6 in non-small cell lung cancer in vivo.

Silvestre Vicent, Leanne C Sayles, Dedeepya Vaka, Purvesh Khatri, Olivier Gevaert, Ron Chen, Yanyan Zheng, Anna K Gillespie, Nicole Clarke, Yue Xu and 5 more

Open access · bronzeAbstract readMeta-Analysis
In one paragraph

Synthesis in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

78 citing papers in PubMed, 123 citations in OpenAlex.

  1. Cytokines and cancer-associated fibroblasts.Journal of hematology & oncology · 2026
    Review
  2. Article
  3. Review
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  5. Targeting Lung Cancer Metabolism: Therapeutic Opportunities and Challenges.Advances in experimental medicine and biology · 2026
    Review
  6. Review
  7. Article
  8. Review
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18 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

15 authors at 1 institution in 1 country.

Silvestre VicentAutCancer Biology Program, Division of Hematology/Oncology, Department of Pediatrics, Stanford University School of Medicine, Stanford, California 94305, USA.
Leanne C Sayles
Dedeepya Vaka
Purvesh Khatri
Olivier Gevaert
Ron Chen
Yanyan Zheng
Anna K Gillespie
Nicole Clarke
Yue Xu
Joseph Shrager
Chuong D Hoang
Sylvia Plevritis
Atul J Butte
E Alejandro Sweet-Cordero
Stanford University · US

Funding

Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
MODELING THE ROLE OF PROGRESSION IN FOLLICULAR LYMPHOMAU54CA149145 · NCI · STANFORD UNIVERSITY · PI PLEVRITIS, SYLVIA KATINA · 2010 to 2014
$12.1M
Research Training in Childhood CancerT32CA128583 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Eric Alejandro Sweet-Cordero · 2007 to 2026
$6.0M
Comparative functional genomics for lung cancer gene discoveryR01CA138256 · NCI · STANFORD UNIVERSITY · PI BUTTE, ATUL J, SAGE, JULIEN · 2008 to 2012
$2.8M
Mechanisms of chemotherapy response and tumor re-initiation in lung cancerR01CA157510 · NCI · STANFORD UNIVERSITY · PI SWEET-CORDERO, ERIC ALEJANDRO · 2011 to 2015
$1.7M
NCI NIH HHS 1R01CA138256-01NCI NIH HHS R01 CA138256NCI NIH HHS R01 CA157510NCI NIH HHS T32 CA128583NCI NIH HHS U54 CA149145
6 · The paper itself

Abstract

Cancer-associated fibroblasts (CAF) have been reported to support tumor progression by a variety of mechanisms. However, their role in the progression of non-small cell lung cancer (NSCLC) remains poorly defined. In addition, the extent to which specific proteins secreted by CAFs contribute directly to tumor growth is unclear. To study the role of CAFs in NSCLCs, a cross-species functional characterization of mouse and human lung CAFs was conducted. CAFs supported the growth of lung cancer cells in vivo by secretion of soluble factors that directly stimulate the growth of tumor cells. Gene expression analysis comparing normal mouse lung fibroblasts and mouse lung CAFs identified multiple genes that correlate with the CAF phenotype. A gene signature of secreted genes upregulated in CAFs was an independent marker of poor survival in patients with NSCLC. This secreted gene signature was upregulated in normal lung fibroblasts after long-term exposure to tumor cells, showing that lung fibroblasts are "educated" by tumor cells to acquire a CAF-like phenotype. Functional studies identified important roles for CLCF1-CNTFR and interleukin (IL)-6-IL-6R signaling in promoting growth of NSCLCs. This study identifies novel soluble factors contributing to the CAF protumorigenic phenotype in NSCLCs and suggests new avenues for the development of therapeutic strategies.

Indexed as

AdenocarcinomaAnimalsCarcinoma, Non-Small-Cell LungCell Growth ProcessesCell Line, TumorFibroblastsHumansInterleukin-6Lung NeoplasmsMiceSpecies SpecificityStromal CellsTransplantation, HeterologousInterleukin-6

Identifiers

PMID22962265
PMCPMC3856949
OpenAlexW2115843698

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.