Evidence map›Paper›PMID 21947652›Full record

ArticleBreast cancer research and treatment2012

The rearranged during transfection/papillary thyroid carcinoma tyrosine kinase is an estrogen-dependent gene required for the growth of estrogen receptor positive breast cancer cells.

Chunyu Wang, Julie Ann Mayer, Abhijit Mazumdar, Powel H Brown

Abstract read
In one paragraph

Article in Breast cancer research and treatment, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Review
  7. Review
  8. [Research Progress of Fusion Genes RET in Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2021
    Review
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  14. Article
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  18. Inhibition of RET increases the efficacy of antiestrogen and is a novel treatment strategy for luminal breast cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014
    Article
  19. Article
  20. Review
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

4 authors at 1 institution in 1 country.

Chunyu WangDepartment of Clinical Cancer Prevention, The University of Texas M D Anderson Cancer Center, Houston, TX 77030, USA.
Julie Ann Mayer
Abhijit Mazumdar
Powel H Brown
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Targeting AP-1 / ER Crosstalk for the Prevention and Treatment of Breast CancerR01CA123246 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BROWN, POWEL H · 2007 to 2011
$1.4M
NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA123246NCI NIH HHS R01-CA123246
6 · The paper itself

Abstract

The rearranged during transfection/papillary thyroid carcinoma (RET/PTC) tyrosine kinase is an oncogene implicated in the tumorigenesis of thyroid cancer. Recent studies by us and others have shown that RET/PTC kinase expression is induced by estrogen in breast cancer cells. Due to the critical involvement of estrogen-regulated genes in the pathogenesis of breast cancer, we investigated the expression, regulation, and function of RET/PTC kinase in breast cancer cells. We found that RET/PTC kinase expression correlates with estrogen receptor (ER) expression in breast cancer cells and tumor specimens, and that RET/PTC kinase expression is associated with a poor prognosis in ER-positive breast cancer patients. We found that estrogen rapidly induces RET/PTC kinase expression in an ER-dependent manner in breast cancer cells and that this induction is through a transcriptional regulatory mechanism. Using reporter assays, small interfering RNA (siRNA) assays, and chromatin immunoprecipitation (ChIP) assays, we demonstrated the necessity of crosstalk between ER and the forkhead box A1 (FOXA1) transcription factor in regulating RET/PTC kinase expression. In functional studies, increased expression of RET/PTC kinase induced by estrogen stimulation resulted in elevated phosphorylation of multiple downstream kinase signaling pathways. Conversely, knockdown of RET/PTC expression was associated with the inhibition of these same kinase signaling pathways, and, in fact, decreased the stimulatory effect of estrogen on the proliferation of ER-positive breast cancer cells. These results demonstrate a novel pathway of ER and FOXA1 transcription factor crosstalk in regulating RET/PTC kinase expression, and demonstrate that RET/PTC kinase is a critical regulator for the proliferation of ER-positive breast cancer cells. Taken together, our study suggests that RET/PTC kinase may serve as a novel prognostic biomarker and therapeutic target for prevention and treatment of ER-positive breast cancer.

Indexed as

Base SequenceBinding SitesBreast NeoplasmsCell Line, TumorCell ProliferationEnhancer Elements, GeneticEstrogensFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGene OrderHepatocyte Nuclear Factor 3-alphaHumansProtein BindingProto-Oncogene Proteins c-retReceptors, EstrogenEstrogensFOXA1 protein, humanHepatocyte Nuclear Factor 3-alphaProto-Oncogene Proteins c-retReceptors, EstrogenRET protein, human

Identifiers

PMID21947652
PMCPMC3424514
OpenAlexW2136111590

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.