Loss of HER2 in breast cancer: biological mechanisms and technical pitfalls.
HER2 downregulation
HER2 loss
breast cancer
clonal selection
subtype switch
technical pitfalls
tumor heterogeneity
Journal
Cancer drug resistance (Alhambra, Calif.)
ISSN: 2578-532X
Titre abrégé: Cancer Drug Resist
Pays: United States
ID NLM: 101738710
Informations de publication
Date de publication:
2022
2022
Historique:
received:
18
04
2022
revised:
18
06
2022
accepted:
10
08
2022
entrez:
11
1
2023
pubmed:
12
1
2023
medline:
12
1
2023
Statut:
epublish
Résumé
Loss of HER2 in previously HER2-positive breast tumors is not rare, occurring in up to 50% of breast cancers; however, clinical research and practice underestimate this issue. Many studies have reported the loss of HER2 after neoadjuvant therapy and at metastatic relapse and identified clinicopathological variables more frequently associated with this event. Nevertheless, the biological mechanisms underlying HER2 loss are still poorly understood. HER2 downregulation, intratumoral heterogeneity, clonal selection, and true subtype switch have been suggested as potential causes of HER2 loss, but translational studies specifically investigating the biology behind HER2 loss are virtually absent. On the other side, technical pitfalls may justify HER2 loss in some of these samples. The best treatment strategy for patients with HER2 loss is currently unknown. Considering the prevalence of this phenomenon and its apparent correlation with worse outcomes, we believe that correlative studies specifically addressing HER2 loss are warranted.
Identifiants
pubmed: 36627895
doi: 10.20517/cdr.2022.55
pmc: PMC9771738
doi:
Types de publication
Journal Article
Langues
eng
Pagination
971-980Subventions
Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States
Informations de copyright
© The Author(s) 2022.
Déclaration de conflit d'intérêts
Curigliano G received honoraria for consulting/advisory role/speaker bureau and/or travel funding from Roche, Lilly, Bristol-Myers Squibb, Pfizer, Novartis, and Seagen; Criscitiello C received honoraria for consulting/advisory role/speaker bureau from Novartis, Eli-Lilly, Pfizer, MSD, Seagen and Roche; Fusco N from Merck Sharp and Dohme (MSD), Boehringer Ingelheim, Novartis, AstraZeneca, and Daiichi Sankyo. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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