Combined targeting EGFR and SRC as a potential novel therapeutic approach for the treatment of triple negative breast cancer.
Bcl2
EGFR
TNBC
afatinib
dasatinib
Journal
Therapeutic advances in medical oncology
ISSN: 1758-8340
Titre abrégé: Ther Adv Med Oncol
Pays: England
ID NLM: 101510808
Informations de publication
Date de publication:
2020
2020
Historique:
received:
28
03
2019
accepted:
06
12
2019
entrez:
18
2
2020
pubmed:
18
2
2020
medline:
18
2
2020
Statut:
epublish
Résumé
Triple negative breast cancer (TNBC) is an aggressive subtype of breast cancer with limited therapeutic options. Epidermal growth factor receptor (EGFR) has been shown to be over-expressed in TNBC and represents a rational treatment target. We examined single agent and combination effects for afatinib and dasatinib in TNBC. We then determined IC A total of 14 TNBC cell lines responded to afatinib with IC We demonstrate that afatinib combined with dasatinib has potential clinical activity in TNBC but warrants further preclinical investigation.
Sections du résumé
BACKGROUND
BACKGROUND
Triple negative breast cancer (TNBC) is an aggressive subtype of breast cancer with limited therapeutic options. Epidermal growth factor receptor (EGFR) has been shown to be over-expressed in TNBC and represents a rational treatment target.
METHODS
METHODS
We examined single agent and combination effects for afatinib and dasatinib in TNBC. We then determined IC
RESULTS
RESULTS
A total of 14 TNBC cell lines responded to afatinib with IC
CONCLUSIONS
CONCLUSIONS
We demonstrate that afatinib combined with dasatinib has potential clinical activity in TNBC but warrants further preclinical investigation.
Identifiants
pubmed: 32064003
doi: 10.1177/1758835919897546
pii: 10.1177_1758835919897546
pmc: PMC6987485
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1758835919897546Informations de copyright
© The Author(s), 2020.
Déclaration de conflit d'intérêts
Conflict of interest statement: Alexandra Canonici, John Crown and Norma O’Donovan received research funding from Boehringer Ingelheim (BI). Flavio Solca is a BI employee.
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