Evidence map›Paper›PMID 24654231›Full record

SynthesisCancer research2014

A meta-analysis of lung cancer gene expression identifies PTK7 as a survival gene in lung adenocarcinoma.

Ron Chen, Purvesh Khatri, Pawel K Mazur, Melanie Polin, Yanyan Zheng, Dedeepya Vaka, Chuong D Hoang, Joseph Shrager, Yue Xu, Silvestre Vicent and 2 more

Abstract readMeta-Analysis
In one paragraph

Synthesis in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 8 pooled it
7.4field-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

94 citing papers in PubMed, 8 syntheses or guidelines pooled it, 158 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. META-ANALYSIS OF CONTINUOUS PHENOTYPES IDENTIFIES A GENE SIGNATURE THAT CORRELATES WITH COPD DISEASE STATUS.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2017
    Pooled it
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  9. Targeting Adaptive and Innate Immune Responses with Covalent Aptamers.Journal of the American Chemical Society · 2026
    Article
  10. Article
  11. Adoptive cell therapies in thoracic malignancies: a comprehensive review.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  12. Article
  13. RUNX1 promotes NSCLC progression by ACP5/SMAD3-mediated M2 macrophage polarization.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  14. Article
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  18. Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024
    Review
  19. Structure-based investigation of a DNA aptamer targeting PTK7 reveals an intricate 3D fold guiding functional optimization.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  20. Review

34 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

12 authors at 3 institutions in 3 countries.

Ron ChenAuthors' Affiliations: Cancer Biology Program, Division of Hematology/Oncology, Department of Pediatrics; Center for Biomedical Informatics Research, Department of Medicine; Institute for Immunity, Transplant and Infection; Department of Cardiothoracic Surgery; and Division of Systems Medicine, Department of Pediatrics, Stanford University School of Medicine, Stanford, California.
Purvesh KhatriAuthors' Affiliations: Cancer Biology Program, Division of Hematology/Oncology, Department of Pediatrics; Center for Biomedical Informatics Research, Department of Medicine; Institute for Immunity, Transplant and Infection; Department of Cardiothoracic Surgery; and Division of Systems Medicine, Department of Pediatrics, Stanford University School of Medicine, Stanford, CaliforniaAuthors' Affiliations: Cancer Biology Program, Division of Hematology/Oncology, Department of Pediatrics; Center for Biomedical Informatics Research, Department of Medicine; Institute for Immunity, Transplant and Infection; Department of Cardiothoracic Surgery; and Division of Systems Medicine, Department of Pediatrics, Stanford University School of Medicine, Stanford, California.
Pawel K MazurAuthors' Affiliations: Cancer Biology Program, Division of Hematology/Oncology, Department of Pediatrics; Center for Biomedical Informatics Research, Department of Medicine; Institute for Immunity, Transplant and Infection; Department of Cardiothoracic Surgery; and Division of Systems Medicine, Department of Pediatrics, Stanford University School of Medicine, Stanford, California.
Melanie PolinAuthors' Affiliations: Cancer Biology Program, Division of Hematology/Oncology, Department of Pediatrics; Center for Biomedical Informatics Research, Department of Medicine; Institute for Immunity, Transplant and Infection; Department of Cardiothoracic Surgery; and Division of Systems Medicine, Department of Pediatrics, Stanford University School of Medicine, Stanford, California.
Yanyan ZhengAuthors' Affiliations: Cancer Biology Program, Division of Hematology/Oncology, Department of Pediatrics; Center for Biomedical Informatics Research, Department of Medicine; Institute for Immunity, Transplant and Infection; Department of Cardiothoracic Surgery; and Division of Systems Medicine, Department of Pediatrics, Stanford University School of Medicine, Stanford, California.
Dedeepya VakaAuthors' Affiliations: Cancer Biology Program, Division of Hematology/Oncology, Department of Pediatrics; Center for Biomedical Informatics Research, Department of Medicine; Institute for Immunity, Transplant and Infection; Department of Cardiothoracic Surgery; and Division of Systems Medicine, Department of Pediatrics, Stanford University School of Medicine, Stanford, California.
Chuong D HoangAuthors' Affiliations: Cancer Biology Program, Division of Hematology/Oncology, Department of Pediatrics; Center for Biomedical Informatics Research, Department of Medicine; Institute for Immunity, Transplant and Infection; Department of Cardiothoracic Surgery; and Division of Systems Medicine, Department of Pediatrics, Stanford University School of Medicine, Stanford, California.
Joseph ShragerAuthors' Affiliations: Cancer Biology Program, Division of Hematology/Oncology, Department of Pediatrics; Center for Biomedical Informatics Research, Department of Medicine; Institute for Immunity, Transplant and Infection; Department of Cardiothoracic Surgery; and Division of Systems Medicine, Department of Pediatrics, Stanford University School of Medicine, Stanford, California.
Yue XuAuthors' Affiliations: Cancer Biology Program, Division of Hematology/Oncology, Department of Pediatrics; Center for Biomedical Informatics Research, Department of Medicine; Institute for Immunity, Transplant and Infection; Department of Cardiothoracic Surgery; and Division of Systems Medicine, Department of Pediatrics, Stanford University School of Medicine, Stanford, California.
Silvestre VicentAuthors' Affiliations: Cancer Biology Program, Division of Hematology/Oncology, Department of Pediatrics; Center for Biomedical Informatics Research, Department of Medicine; Institute for Immunity, Transplant and Infection; Department of Cardiothoracic Surgery; and Division of Systems Medicine, Department of Pediatrics, Stanford University School of Medicine, Stanford, California.
Atul J ButteAuthors' Affiliations: Cancer Biology Program, Division of Hematology/Oncology, Department of Pediatrics; Center for Biomedical Informatics Research, Department of Medicine; Institute for Immunity, Transplant and Infection; Department of Cardiothoracic Surgery; and Division of Systems Medicine, Department of Pediatrics, Stanford University School of Medicine, Stanford, California ascor@stanford.edu abutte@stanford.edu.
E Alejandro Sweet-CorderoAuthors' Affiliations: Cancer Biology Program, Division of Hematology/Oncology, Department of Pediatrics; Center for Biomedical Informatics Research, Department of Medicine; Institute for Immunity, Transplant and Infection; Department of Cardiothoracic Surgery; and Division of Systems Medicine, Department of Pediatrics, Stanford University School of Medicine, Stanford, California ascor@stanford.edu abutte@stanford.edu.
Institute of Infection and Immunity · CAStanford University · USTranslational Research Informatics Center (Japan) · JP

Funding

Translational Oncology Research Program (Project-005)P30CA124435 · NCI · STANFORD UNIVERSITY · PI Melinda L. Telli · 2007 to 2026
$71.4M
Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
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
NCI NIH HHS R01 CA138256NCI NIH HHS T32 CA009302NCI NIH HHS T32 CA128583
6 · The paper itself

Abstract

Lung cancer remains the most common cause of cancer-related death worldwide and it continues to lack effective treatment. The increasingly large and diverse public databases of lung cancer gene expression constitute a rich source of candidate oncogenic drivers and therapeutic targets. To define novel targets for lung adenocarcinoma, we conducted a large-scale meta-analysis of genes specifically overexpressed in adenocarcinoma. We identified an 11-gene signature that was overexpressed consistently in adenocarcinoma specimens relative to normal lung tissue. Six genes in this signature were specifically overexpressed in adenocarcinoma relative to other subtypes of non-small cell lung cancer (NSCLC). Among these genes was the little studied protein tyrosine kinase PTK7. Immunohistochemical analysis confirmed that PTK7 is highly expressed in primary adenocarcinoma patient samples. RNA interference-mediated attenuation of PTK7 decreased cell viability and increased apoptosis in a subset of adenocarcinoma cell lines. Further, loss of PTK7 activated the MKK7-JNK stress response pathway and impaired tumor growth in xenotransplantation assays. Our work defines PTK7 as a highly and specifically expressed gene in adenocarcinoma and a potential therapeutic target in this subset of NSCLC.

Indexed as

AdenocarcinomaAdenocarcinoma of LungAnimalsCell Adhesion MoleculesCell Line, TumorGene ExpressionGene Expression ProfilingHeterograftsHumansLung NeoplasmsMice, Inbred NODMice, SCIDReceptor Protein-Tyrosine KinasesCell Adhesion MoleculesPTK7 protein, humanReceptor Protein-Tyrosine Kinases

Identifiers

PMID24654231
PMCPMC4084668
OpenAlexW2100743480

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.