Evidence map›Paper›PMID 28652369›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Quantitative proteomics identify Tenascin-C as a promoter of lung cancer progression and contributor to a signature prognostic of patient survival.

Vasilena Gocheva, Alexandra Naba, Arjun Bhutkar, Talia Guardia, Kathryn M Miller, Carman Man-Chung Li, Talya L Dayton, Francisco J Sanchez-Rivera, Caroline Kim-Kiselak, Noor Jailkhani and 4 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 2 pooled it
7.1field-weighted citation impact, top 2% 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

95 citing papers in PubMed, 2 syntheses or guidelines pooled it, 147 citations in OpenAlex.

  1. Pooled it
  2. Prognostic Role of Tenascin-C for Cancer Outcome: A Meta-Analysis.Technology in cancer research & treatment · 2019
    Pooled it
  3. Article
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  7. Review
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  9. Cell-Instructive Biomaterials with Native-Like Biochemical Complexity.Annual review of biomedical engineering · 2025
    Review
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  19. Article
  20. Shaping Oncogenic Microenvironments: Contribution of Fibronectin.Frontiers in cell and developmental biology · 2024
    Review

35 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 1 institution in 1 country.

Vasilena GochevaDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Alexandra NabaDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139; anaba@uic.edu tjacks@mit.edu.
Arjun BhutkarDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Talia GuardiaDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Kathryn M MillerDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Carman Man-Chung LiDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Talya L DaytonDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Francisco J Sanchez-RiveraDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Caroline Kim-KiselakDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Noor JailkhaniDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Monte M WinslowDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Amanda Del RosarioDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Richard O HynesDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Tyler JacksDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139; anaba@uic.edu tjacks@mit.edu.
Massachusetts Institute of Technology · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
Tumor-Stroma Interacions in the Tumor MicroenvironmentU54CA126515 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI WEINBERG, ROBERT A · 2006 to 2010
$6.5M
The Extracellular Matrix in Tumor Progression and MetastasisU54CA163109 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI WEINBERG, ROBERT A · 2011 to 2015
$3.7M
Howard Hughes Medical InstituteNCI NIH HHS P30 CA014051NCI NIH HHS U54 CA126515NCI NIH HHS U54 CA163109
6 · The paper itself

Abstract

The extracellular microenvironment is an integral component of normal and diseased tissues that is poorly understood owing to its complexity. To investigate the contribution of the microenvironment to lung fibrosis and adenocarcinoma progression, two pathologies characterized by excessive stromal expansion, we used mouse models to characterize the extracellular matrix (ECM) composition of normal lung, fibrotic lung, lung tumors, and metastases. Using quantitative proteomics, we identified and assayed the abundance of 113 ECM proteins, which revealed robust ECM protein signatures unique to fibrosis, primary tumors, or metastases. These analyses indicated significantly increased abundance of several S100 proteins, including Fibronectin and Tenascin-C (Tnc), in primary lung tumors and associated lymph node metastases compared with normal tissue. We further showed that Tnc expression is repressed by the transcription factor Nkx2-1, a well-established suppressor of metastatic progression. We found that increasing the levels of Tnc, via CRISPR-mediated transcriptional activation of the endogenous gene, enhanced the metastatic dissemination of lung adenocarcinoma cells. Interrogation of human cancer gene expression data revealed that high

Indexed as

AdenocarcinomaAnimalsAnnexin A2CRISPR-Cas SystemsDisease ProgressionExtracellular MatrixFemaleGene Expression Regulation, NeoplasticHumansLung NeoplasmsMaleMiceMice, Inbred C57BLMultivariate AnalysisNeoplasm MetastasisPrognosisAnnexin A2NKX2-1 protein, humanS100A11 protein, humanS100 Calcium Binding Protein A10S100 ProteinsTenascinThyroid Nuclear Factor 1extracellular matrixlung cancerquantitative proteomicsTenascin-Ctumor microenvironment

Identifiers

PMID28652369
PMCPMC5514763
OpenAlexW2691615730

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.