Evidence map›Paper›PMID 31519989›Full record

ReviewOncogene2020

ERBB3 mutations in cancer: biological aspects, prevalence and therapeutics.

Nicolas Kiavue, Luc Cabel, Samia Melaabi, Guillaume Bataillon, Celine Callens, Florence Lerebours, Jean-Yves Pierga, Francois-Clement Bidard

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
7.0field-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

70 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Increased ErbB2 Signaling Is an Early Adaptation to Androgen Signaling Inhibition and Persists in Castration-Resistant Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Unveiling the dynamics and therapeutic potential of mInternational journal of biological sciences · 2025
    Review
  14. Review
  15. HER4 is a high-affinity dimerization partner for all EGFR/HER/ErbB family proteins.Protein science : a publication of the Protein Society · 2024
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

10 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

8 authors at 3 institutions in 1 country.

Nicolas Kiavue *Department of Medical Oncology, Institut Curie, PSL Research University, Paris, France.
Luc Cabel *Department of Medical Oncology, Institut Curie, PSL Research University, Paris, France.
Samia MelaabiDepartment of Medical Oncology, Institut Curie, PSL Research University, Paris, France.
Guillaume BataillonDepartment of Medical Oncology, Institut Curie, PSL Research University, Paris, France.
Celine CallensDepartment of Medical Oncology, Institut Curie, PSL Research University, Paris, France.
Florence LereboursDepartment of Medical Oncology, Institut Curie, PSL Research University, Paris, France.
Jean-Yves PiergaDepartment of Medical Oncology, Institut Curie, PSL Research University, Paris, France.
Francois-Clement BidardDepartment of Medical Oncology, Institut Curie, PSL Research University, Paris, France. francois-clement.bidard@curie.fr.ORCID http://orcid.org/0000-0001-5932-8949
Université Paris Sciences et Lettres · FRUniversité de Versailles Saint-Quentin-en-Yvelines · FRDélégation Paris 5 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HER3, a member of the EGFR family of receptor tyrosine kinases coded by the ERBB3 gene, plays an important role in cancer, despite its lack of intrinsic kinase activity. As with genes coding for potential heterodimeric partners of HER3, EGFR, and HER2, oncogenic mutations of ERBB3 have been explored by several studies. In this review, we discuss the evidence presenting ERBB3 somatic mutations as potential tumoral drivers. We then show that ERBB3 mutations are not uncommon in many cancer types. Finally, we present the recent results of several studies evaluating different therapeutic approaches for treating patients with oncogenic ERBB3 mutations.

Indexed as

AnimalsAntibodies, MonoclonalAntineoplastic Combined Chemotherapy ProtocolsCarcinogenesisCell Line, TumorClinical Trials as TopicErb-b2 Receptor Tyrosine KinasesHumansMiceMolecular Targeted TherapyMutationNeoplasmsProgression-Free SurvivalProtein Kinase InhibitorsProtein MultimerizationReceptor, ErbB-3Antibodies, MonoclonalERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesERBB3 protein, humanProtein Kinase InhibitorsReceptor, ErbB-3

Identifiers

PMID31519989
OpenAlexW2972418031

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.