Evidence map›Paper›PMID 25897424›Full record

ReviewOncoscience2015

HER2 and uPAR cooperativity contribute to metastatic phenotype of HER2-positive breast cancer.

Vineesh Indira Chandran, Serenella Eppenberger-Castori, Thejaswini Venkatesh, Kara Lea Vine, Marie Ranson

Open access · diamondAbstract readReview
In one paragraph

Review in Oncoscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Prognostic Significance of Microvessel Density in Invasive Ductal Carcinoma of Breast.International journal of hematology-oncology and stem cell research · 2023
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Pharmaceutics · 2020
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
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

5 authors at 3 institutions in 2 countries.

Vineesh Indira ChandranDepartment of Clinical Sciences, Section of Oncology and Pathology, Lund University, Lund, Sweden.
Serenella Eppenberger-CastoriInstitute for Pathology, Department of Molecular Pathology, Schoenbeinstrasse, Basel, Switzerland.
Thejaswini VenkateshNitte University Centre for Science Education and Research (NUCSER), K. S. Hegde Medical Academy, Nitte University, Deralakatte, Mangalore, Karnataka, India.
Kara Lea VineSchool of Biological Sciences, University of Wollongong, Wollongong, NSW, Australia ; Centre for Medical & Molecular Bioscience, University of Wollongong, Wollongong, NSW, Australia ; Illawarra Health and Medical Research Institute, University of Wollongong, Wollongong, NSW, Australia.
Marie RansonSchool of Biological Sciences, University of Wollongong, Wollongong, NSW, Australia ; Centre for Medical & Molecular Bioscience, University of Wollongong, Wollongong, NSW, Australia ; Illawarra Health and Medical Research Institute, University of Wollongong, Wollongong, NSW, Australia.
Illawarra Health and Medical Research Institute · AULund University · SEUniversity of Wollongong · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human epidermal growth factor receptor type 2 (HER2)-positive breast carcinoma is highly aggressive and mostly metastatic in nature though curable/manageable in part by molecular targeted therapy. Recent evidence suggests a subtype of cells within HER2-positive breast tumors that concomitantly expresses the urokinase plasminogen activator receptor (uPAR) with inherent stem cell/mesenchymal-like properties promoting tumor cell motility and a metastatic phenotype. This HER-positive/uPAR-positive subtype may be partially responsible for the failure of HER2-targeted treatment strategies. Herein we discuss and substantiate the cumulative preclinical and clinical evidence on HER2-uPAR cooperativity in terms of gene co-amplification and/or mRNA/protein co-overexpression. We then propose a regulatory signaling model that we hypothesize to maintain upregulation and cooperativity between HER2 and uPAR in aggressive breast cancer. An improved understanding of the HER2/uPAR interaction in breast cancer will provide critical biomolecular information that may help better predict disease course and response to therapy.

Indexed as

co-amplificationco-overexpressioncorrelationHER2/ERBB2HER2-positive breast canceruPAR/PLAUR

Identifiers

PMID25897424
PMCPMC4394126
OpenAlexW2137398417

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.