Evidence map›Paper›PMID 20139980›Full record

ArticleNature genetics2010

Identification of DOK genes as lung tumor suppressors.

Alice H Berger, Masaru Niki, Alessandro Morotti, Barry S Taylor, Nicholas D Socci, Agnes Viale, Cameron Brennan, Janos Szoke, Noriko Motoi, Paul B Rothman and 4 more

Open access · greenAbstract read
In one paragraph

Article in Nature genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
4.8field-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

71 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
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  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Expression and clinical significance of DOK3 in renal clear cell carcinoma.The Journal of international medical research · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Frontiers in oncology · 2022
    Article
  17. Review
  18. Article
  19. Article
  20. Article

11 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

14 authors at 5 institutions in 1 country.

Alice H BergerCancer Genetics Program, Beth Israel Deaconess Cancer Center, Departments of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Masaru Niki
Alessandro Morotti
Barry S Taylor
Nicholas D Socci
Agnes Viale
Cameron Brennan
Janos Szoke
Noriko Motoi
Paul B Rothman
Julie Teruya-Feldstein
William L Gerald
Marc Ladanyi
Pier Paolo Pandolfi
Memorial Sloan Kettering Cancer Center · USKettering University · USBeth Israel Deaconess Medical Center · USCancer Genetics (United States) · USUniversity of Iowa · US

Funding

The Role of Focal Oncogene Amplifications in Lung CancerP01CA129243 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI Piro Lito · 2007 to 2026
$31.2M
SELECTIVE THERAPY OF CHRONIC MYELOID LEUKEMIAP01CA064593 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI CLARKSON, BAYARD D · 1994 to 2007
$7.5M
Role of DOK family proteins in lung tumor suppressionR01CA142787 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI PANDOLFI, PIER PAOLO · 2010 to 2014
$1.7M
Role of DOK Proteins in Lung CancerR01CA132591 · NCI · UNIVERSITY OF IOWA · PI NIKI, MASARU · 2008 to 2012
$1.4M
NCI NIH HHS CA-129243NCI NIH HHS CA-64593NCI NIH HHS P01 CA064593NCI NIH HHS P01 CA129243NCI NIH HHS R01 CA132591NCI NIH HHS R01 CA142787
6 · The paper itself

Abstract

Genome-wide analyses of human lung adenocarcinoma have identified regions of consistent copy-number gain or loss, but in many cases the oncogenes and tumor suppressors presumed to reside in these loci remain to be determined. Here we identify the downstream of tyrosine kinase (Dok) family members Dok1, Dok2 and Dok3 as lung tumor suppressors. Single, double or triple compound loss of these genes in mice results in lung cancer, with penetrance and latency dependent on the number of lost Dok alleles. Cancer development is preceded by an aberrant expansion and signaling profile of alveolar type II cells and bronchioalveolar stem cells. In human lung adenocarcinoma, we identify DOK2 as a target of copy-number loss and mRNA downregulation and find that DOK2 suppresses lung cancer cell proliferation in vitro and in vivo. Given the genomic localization of DOK2, we propose it as an 8p21.3 haploinsufficient human lung tumor suppressor.

Indexed as

Adaptor Proteins, Signal TransducingAdenocarcinomaAnimalsCell ProliferationDNA-Binding ProteinsGene Expression Regulation, NeoplasticGenes, Tumor SuppressorGenetic Predisposition to DiseaseHumansLung NeoplasmsMiceMice, KnockoutMice, NudePhosphoproteinsRNA-Binding ProteinsTransplantation, HeterologousAdaptor Proteins, Signal TransducingDNA-Binding ProteinsDok1 protein, mouseDok2 protein, mouseDok3 protein, mousePhosphoproteinsRNA-Binding Proteins

Identifiers

PMID20139980
PMCPMC2956443
OpenAlexW1999906037

What OpenQuestion holds

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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.