Evidence map›Paper›PMID 31737566›Full record

ReviewFrontiers in oncology2019

Deciphering HER2 Breast Cancer Disease: Biological and Clinical Implications.

Ana Godoy-Ortiz, Alfonso Sanchez-Muñoz, Maria Rosario Chica Parrado, Martina Álvarez, Nuria Ribelles, Antonio Rueda Dominguez, Emilio Alba

Abstract readReview
In one paragraph

Review in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

54 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
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  13. Multi-parametric MRI radiomics predicts different HER2 expression in breast cancer.Cancer imaging : the official publication of the International Cancer Imaging Society · 2025
    Article
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  20. Non-Coding RNAs in Breast Cancer: Diagnostic and Therapeutic Implications.International journal of molecular sciences · 2024
    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

7 authors.

Ana Godoy-OrtizUnidad de Gestión Clínica Intercentros de Oncología Medica, Hospitales Universitarios Regional y Virgen de la Victoria de Málaga, Málaga, Spain.
Alfonso Sanchez-MuñozUnidad de Gestión Clínica Intercentros de Oncología Medica, Hospitales Universitarios Regional y Virgen de la Victoria de Málaga, Málaga, Spain.
Maria Rosario Chica ParradoLaboratorio de Biología Molecular del Centro de Investigaciones Médico-Sanitarias de Málaga (CIMES), Instituto de Investigación Biomédica de Málaga (IBIMA), Universidad de Málaga (UMA), Málaga, Spain.
Martina ÁlvarezLaboratorio de Biología Molecular del Centro de Investigaciones Médico-Sanitarias de Málaga (CIMES), Instituto de Investigación Biomédica de Málaga (IBIMA), Universidad de Málaga (UMA), Málaga, Spain.
Nuria RibellesUnidad de Gestión Clínica Intercentros de Oncología Medica, Hospitales Universitarios Regional y Virgen de la Victoria de Málaga, Málaga, Spain.
Antonio Rueda DominguezUnidad de Gestión Clínica Intercentros de Oncología Medica, Hospitales Universitarios Regional y Virgen de la Victoria de Málaga, Málaga, Spain.
Emilio AlbaUnidad de Gestión Clínica Intercentros de Oncología Medica, Hospitales Universitarios Regional y Virgen de la Victoria de Málaga, Málaga, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The main obstacle for designing effective treatment approaches in breast cancer is the extensive and the characteristic heterogeneity of this tumor. The vast majority of critical genomic changes occurs during breast cancer progression, creating a significant variability within primary tumors as well as between the primary breast cancer and their metastases, a hypothesis have already demonstrated in retrospective studies (1). A clear example of this is the HER2-positive breast cancer. In these tumors, we can find all of the transcriptional subtypes of breast cancer, even the basal like or luminal A subtypes. Although the HER2-enriched is the most representative transcriptional subtype in the HER2-positive breast cancer, we can find it too in breast cancers with HER2-negative status. This intrinsic subtype shows a high expression of the HER2 and is associated with proliferation-related genes clusters, among other features. Therefore, two hypotheses can be suggested. First, the HER2 amplification can be a well-defined driver event present in all of the intrinsic subtypes, and not a subtype marker isolated. Secondly, HER2-enriched subtype can have a distinctive transcriptional landscape independent of HER2 amplification. In this review, we present an extensive revision about the last highlights and advances in clinical and genomic settings of the HER2-positive breast cancer and the HER2-enriched subtype, in an attempt to improving the knowledge of the underlying biology of both entities and to explaining the intrinsic heterogeneity of HER2-positive breast cancers.

Indexed as

breast cancerHER2-enrichedHER2-positiveheterogeneityintrinsic subtypemolecular

Identifiers

PMID31737566
PMCPMC6828840

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Registered trials

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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.