Evidence map›Paper›PMID 24056965›Full record

ArticleOncogene2014

c-Myc and Her2 cooperate to drive a stem-like phenotype with poor prognosis in breast cancer.

R Nair, D L Roden, W S Teo, A McFarland, S Junankar, S Ye, A Nguyen, J Yang, I Nikolic, M Hui and 16 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
6.6field-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

63 citing papers in PubMed, 92 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. SNAI2 Attenuated the Stem-like Phenotype by Reducing the Expansion of EPCAMInternational journal of molecular sciences · 2023
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

3 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

26 authors at 10 institutions in 2 countries.

R NairCancer Research Division, The Kinghorn Cancer Centre and Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, NSW, Australia.
D L RodenCancer Research Division, The Kinghorn Cancer Centre and Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, NSW, Australia.
W S Teo1] Cancer Research Division, The Kinghorn Cancer Centre and Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, NSW, Australia [2] St Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia.
A McFarlandCancer Research Division, The Kinghorn Cancer Centre and Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, NSW, Australia.
S Junankar1] Cancer Research Division, The Kinghorn Cancer Centre and Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, NSW, Australia [2] St Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia.
S Ye1] Cancer Research Division, The Kinghorn Cancer Centre and Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, NSW, Australia [2] St Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia.
A NguyenCancer Research Division, The Kinghorn Cancer Centre and Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, NSW, Australia.
J YangCancer Research Division, The Kinghorn Cancer Centre and Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, NSW, Australia.
I NikolicCancer Research Division, The Kinghorn Cancer Centre and Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, NSW, Australia.
M HuiCancer Research Division, The Kinghorn Cancer Centre and Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, NSW, Australia.
A Morey1] St Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia [2] Department of Anatomical Pathology, Sydpath, St Vincent's Hospital, Darlinghurst, NSW, Australia.
J ShahSchool of Medical Sciences, University of New South Wales, Camperdown, NSW, Australia.
A D Pfefferle1] Department of Pathology and Laboratory Medicine, Chapel Hill, NC, USA [2] Lineberger Comprehensive Cancer Center, Chapel Hill, NC, USA.
J Usary1] Lineberger Comprehensive Cancer Center, Chapel Hill, NC, USA [2] Department of Genetics, University of North Carolina, Chapel Hill, NC, USA.
C SelingerDepartment of Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital, Camperdown, NSW, Australia.
L A Baker1] Cancer Research Division, The Kinghorn Cancer Centre and Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, NSW, Australia [2] School of Biotechnology and Biomolecular Sciences, University of New South Wales, NSW, Australia.
N ArmstrongSchool of Mathematics and Statistics, The University of Sydney, Sydney, NSW, Australia.
M J Cowley1] Cancer Research Division, The Kinghorn Cancer Centre and Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, NSW, Australia [2] Peter Wills Bioinformatics Centre, Garvan Institute of Medical Research, Darlinghurst, NSW, Australia.
M J Naylor1] Cancer Research Division, The Kinghorn Cancer Centre and Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, NSW, Australia [2] St Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia [3] Discipline of Physiology and Bosch Institute, School of Medical Sciences, University of Sydney, Sydney, NSW, Australia.
C J Ormandy1] Cancer Research Division, The Kinghorn Cancer Centre and Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, NSW, Australia [2] St Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia.
S R LakhaniThe University of Queensland, UQ Centre for Clinical Research, School of Medicine and Pathology Queensland, The Royal Brisbane and Women's Hospital, Herston, Brisbane, QLD, Australia.
J I HerschkowitzDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA.
C M Perou1] Department of Pathology and Laboratory Medicine, Chapel Hill, NC, USA [2] Lineberger Comprehensive Cancer Center, Chapel Hill, NC, USA [3] Department of Genetics, University of North Carolina, Chapel Hill, NC, USA.
W Kaplan1] St Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia [2] Peter Wills Bioinformatics Centre, Garvan Institute of Medical Research, Darlinghurst, NSW, Australia.
S A O'Toole1] Cancer Research Division, The Kinghorn Cancer Centre and Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, NSW, Australia [2] St Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia [3] Department of Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital, Camperdown, NSW, Australia [4] Sydney Medical School, University of Sydney, Sydney, NSW, Australia.
A Swarbrick1] Cancer Research Division, The Kinghorn Cancer Centre and Cancer Research Program Garvan Institute of Medical Research, Darlinghurst, NSW, Australia [2] St Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia.
Garvan Institute of Medical Research · AUSt Vincent's Clinic · AUThe Kinghorn Cancer Centre · AUUniversity of North Carolina at Chapel Hill · USUNSW Sydney · AUBaylor College of Medicine · USRoyal Prince Alfred Hospital · AUUNC Lineberger Comprehensive Cancer CenterUniversity of Queensland · AUUniversity of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The HER2 (ERBB2) and MYC genes are commonly amplified in breast cancer, yet little is known about their molecular and clinical interaction. Using a novel chimeric mammary transgenic approach and in vitro models, we demonstrate markedly increased self-renewal and tumour-propagating capability of cells transformed with Her2 and c-Myc. Coexpression of both oncoproteins in cultured cells led to the activation of a c-Myc transcriptional signature and acquisition of a self-renewing phenotype independent of an epithelial-mesenchymal transition programme or regulation of conventional cancer stem cell markers. Instead, Her2 and c-Myc cooperated to induce the expression of lipoprotein lipase, which was required for proliferation and self-renewal in vitro. HER2 and MYC were frequently coamplified in breast cancer, associated with aggressive clinical behaviour and poor outcome. Lastly, we show that in HER2(+) breast cancer patients receiving adjuvant chemotherapy (but not targeted anti-Her2 therapy), MYC amplification is associated with a poor outcome. These findings demonstrate the importance of molecular and cellular context in oncogenic transformation and acquisition of a malignant stem-like phenotype and have diagnostic and therapeutic consequences for the clinical management of HER2(+) breast cancer.

Indexed as

AdultAgedAged, 80 and overAnimalsBreast NeoplasmsCarcinoma, Ductal, BreastCell Line, TumorCell ProliferationErb-b2 Receptor Tyrosine KinasesFemaleGene ExpressionHumansMiceMiddle AgedMultivariate AnalysisNeoplasm TransplantationERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesMYC protein, humanProto-Oncogene Proteins c-myc

Identifiers

PMID24056965
OpenAlexW1974784117

What OpenQuestion holds

Textmetadata
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.