Evidence map›Paper›PMID 25099679›Full record

ArticleNature communications2014

Recurrent ESR1-CCDC170 rearrangements in an aggressive subset of oestrogen receptor-positive breast cancers.

Jamunarani Veeraraghavan, Ying Tan, Xi-Xi Cao, Jin Ah Kim, Xian Wang, Gary C Chamness, Sourindra N Maiti, Laurence J N Cooper, Dean P Edwards, Alejandro Contreras and 4 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 3 pooled it
5.8field-weighted citation impact, top 3% 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

102 citing papers in PubMed, 3 syntheses or guidelines pooled it, 148 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Characteristics of fusion genes in breast cancer.Cancer cell international · 2026
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. ESR1 fusions in breast cancer: functions, mechanisms and therapeutic opportunities.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2026
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Pathogenesis of Endometriosis and Endometriosis-Associated Cancers.International journal of molecular sciences · 2024
    Review
  17. Review
  18. Review
  19. Article
  20. Article

42 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 3 institutions in 1 country.

Jamunarani Veeraraghavan1] Lester &Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas 77030, USA [2] Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas 77030, USA [3] Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA [4].
Ying Tan1] Lester &Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas 77030, USA [2] Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas 77030, USA [3] Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA [4].
Xi-Xi Cao1] Lester &Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas 77030, USA [2] Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas 77030, USA [3] Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA [4].
Jin Ah Kim1] Lester &Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas 77030, USA [2] Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas 77030, USA [3] Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA.
Xian Wang1] Lester &Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas 77030, USA [2] Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas 77030, USA [3] Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA.
Gary C Chamness1] Lester &Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas 77030, USA [2] Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas 77030, USA [3] Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA.
Sourindra N MaitiDivision of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Laurence J N CooperDivision of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Dean P Edwards1] Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA [2] Department of Pathology &Immunology, Baylor College of Medicine, Houston, Texas 77030, USA.
Alejandro ContrerasDepartment of Pathology &Immunology, Baylor College of Medicine, Houston, Texas 77030, USA.
Susan G Hilsenbeck1] Lester &Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas 77030, USA [2] Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas 77030, USA [3] Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA.
Eric C Chang1] Lester &Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas 77030, USA [2] Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas 77030, USA [3] Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA.
Rachel Schiff1] Lester &Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas 77030, USA [2] Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas 77030, USA [3] Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA [4] Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA.
Xiao-Song Wang1] Lester &Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas 77030, USA [2] Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas 77030, USA [3] Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA [4] Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA.
Baylor College of Medicine · USChildren's Cancer Center · USThe 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
Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
CHARACTERIZATION OF RECURRENT ADJACENT GENE TRANSLOCATIONS IN BREAST CANCERR01CA183976 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WANG, XIAOSONG · 2014 to 2019
$1.6M
ACQUISITION OF A CIRCULAR DICHROISM SPECTROMETER SYSTEMS10RR002950 · NCRR · EMORY UNIVERSITY · PI WILKINSON, KEITH D · 1986 to 1986
–
NCI NIH HHS CA183976NCI NIH HHS P30 CA016672NCI NIH HHS P30 CA125123NCI NIH HHS R01 CA183976NCRR NIH HHS S10RR02950PHS HHS P30-125123PHS HHS P30-125123-06
6 · The paper itself

Abstract

Characterizing the genetic alterations leading to the more aggressive forms of oestrogen receptor-positive (ER+) breast cancers is of critical significance in breast cancer management. Here we identify recurrent rearrangements between the oestrogen receptor gene ESR1 and its neighbour CCDC170, which are enriched in the more aggressive and endocrine-resistant luminal B tumours, through large-scale analyses of breast cancer transcriptome and copy number alterations. Further screening of 200 ER+ breast cancers identifies eight ESR1-CCDC170-positive tumours. These fusions encode amino-terminally truncated CCDC170 proteins (ΔCCDC170). When introduced into ER+ breast cancer cells, ΔCCDC170 leads to markedly increased cell motility and anchorage-independent growth, reduced endocrine sensitivity and enhanced xenograft tumour formation. Mechanistic studies suggest that ΔCCDC170 engages Gab1 signalosome to potentiate growth factor signalling and enhance cell motility. Together, this study identifies neoplastic ESR1-CCDC170 fusions in a more aggressive subset of ER+ breast cancer, which suggests a new concept of ER pathobiology in breast cancer.

Indexed as

Gene Expression Regulation, NeoplasticGene RearrangementAdaptor Proteins, Signal TransducingAnimalsBreast NeoplasmsCarrier ProteinsCell Line, TumorCell MovementCell ProliferationCell SeparationEstrogen Receptor alphaFemaleFlow CytometryGene Expression ProfilingHumansIntercellular Signaling Peptides and ProteinsAdaptor Proteins, Signal TransducingCarrier ProteinsCCDC170 protein, humanESR1 protein, humanEstrogen Receptor alphaGAB1 protein, humanIntercellular Signaling Peptides and ProteinsKi-67 AntigenRNA, Small Interfering

Identifiers

PMID25099679
PMCPMC4130357
OpenAlexW2025784247

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.