Rac inhibition as a novel therapeutic strategy for EGFR/HER2 targeted therapy resistant breast cancer.

ABSTRACT:

Background

Even though targeted therapies are available for cancers expressing oncogenic epidermal growth receptor (EGFR) and (or) human EGFR2 (HER2), acquired or intrinsic resistance often confounds therapy success. Common mechanisms of therapy resistance involve activating receptor point mutations and (or) upregulation of signaling downstream of EGFR/HER2 to Akt and (or) mitogen activated protein kinase (MAPK) pathways. However, additional pathways of resistance may exist thus, confounding successful therapy.

Methods

To determine novel mechanisms of EGFR/HER2 therapy resistance in breast cancer, gefitinib or lapatinib resistant variants were created from SKBR3 breast cancer cells. Syngenic therapy sensitive and resistant SKBR3 variants were characterized for mechanisms of

SUBMITTER: Borrero-Garcia LD 

PROVIDER: S-EPMC8170972 | biostudies-literature | 2021 Jun

REPOSITORIES: biostudies-literature