Evidence map›Paper›PMID 20215510›Full record

ArticleCancer research2010

LYN is a mediator of epithelial-mesenchymal transition and a target of dasatinib in breast cancer.

Yoon-La Choi, Melanie Bocanegra, Mi Jeong Kwon, Young Kee Shin, Seok Jin Nam, Jung-Hyun Yang, Jessica Kao, Andrew K Godwin, Jonathan R Pollack

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 2 pooled it
7.0field-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

89 citing papers in PubMed, 2 syntheses or guidelines pooled it, 152 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Perioperative COX-2 and β-Adrenergic Blockade Improves Metastatic Biomarkers in Breast Cancer Patients in a Phase-II Randomized Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
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  18. Identification of aFrontiers in cellular and infection microbiology · 2022
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29 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

9 authors at 4 institutions in 2 countries.

Yoon-La ChoiDepartment of Pathology and Division of Breast and Endocrine Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Melanie Bocanegra
Mi Jeong Kwon
Young Kee Shin
Seok Jin Nam
Jung-Hyun Yang
Jessica Kao
Andrew K Godwin
Jonathan R Pollack
Samsung Medical Center · KRSeoul National University · KRFox Chase Cancer Center · USSungkyunkwan University · KR

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
Fox Chase Clinical Epidemiology and Validation CenterU01CA113916 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI ENGSTROM, PAUL FREDERICK · 2005 to 2015
$8.6M
Role of Gene Amplification in Breast CancerR01CA097139 · NCI · STANFORD UNIVERSITY · PI POLLACK, JONATHAN R · 2003 to 2007
$1.6M
Characterizing an EMT signature in breast cancerF31CA130172 · NCI · STANFORD UNIVERSITY · PI BOCANEGRA, MELANIE · 2007 to 2007
$17k
NCI NIH HHS BC073467NCI NIH HHS CA09302NCI NIH HHS CA113916NCI NIH HHS CA130172NCI NIH HHS CA97139NCI NIH HHS F31 CA130172NCI NIH HHS N01 CN043309NCI NIH HHS N01-CN-43309NCI NIH HHS R01 CA097139NCI NIH HHS T32 CA009302NCI NIH HHS U01 CA113916
6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT), a switch of polarized epithelial cells to a migratory, fibroblastoid phenotype, is considered a key process driving tumor cell invasiveness and metastasis. Using breast cancer cell lines as a model system, we sought to discover gene expression signatures of EMT with clinical and mechanistic relevance. A supervised comparison of epithelial and mesenchymal breast cancer lines defined a 200-gene EMT signature that was prognostic across multiple breast cancer cohorts. The immunostaining of LYN, a top-ranked EMT signature gene and Src-family tyrosine kinase, was associated with significantly shorter overall survival (P = 0.02) and correlated with the basal-like ("triple-negative") phenotype. In mesenchymal breast cancer lines, RNAi-mediated knockdown of LYN inhibited cell migration and invasion, but not proliferation. Dasatinib, a dual-specificity tyrosine kinase inhibitor, also blocked invasion (but not proliferation) at nanomolar concentrations that inhibit LYN kinase activity, suggesting that LYN is a likely target and that invasion is a relevant end point for dasatinib therapy. Our findings define a prognostically relevant EMT signature in breast cancer and identify LYN as a mediator of invasion and a possible new therapeutic target (and theranostic marker for dasatinib response), with particular relevance to clinically aggressive basal-like breast cancer.

Indexed as

Breast NeoplasmsCell Line, TumorDasatinibEpithelial CellsFemaleGene Expression ProfilingHumansMesodermPrognosisProtein Kinase InhibitorsPyrimidinessrc-Family KinasesThiazolesDasatiniblyn protein-tyrosine kinaseProtein Kinase InhibitorsPyrimidinessrc-Family KinasesThiazoles

Identifiers

PMID20215510
PMCPMC2869247
OpenAlexW2121390608

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.