Abstract
TO THE EDITOR: Dave et al 1 have recently shown that, in a cohort of patients with locally advanced human epidermal growth factor receptor 2 (HER2) -positive breast cancer who were under- going neoadjuvant therapy, the presence of activating mutations of phosphoinositol-3 (PI3) kinase (PIK3CA) or low phosphatase and tensin homolog (PTEN) conferred resistance to trastuzumab (T)- including regimens, and at the same time this molecular scenario predicted for response to lapatinib (L). T is the main anti-HER2-targeted therapy to demonstrate clinical efficacy in the treatment of early and advanced HER2- positive breast cancer in women. The efficacy of T seems to be exclusively related to the overexpression of HER2 protein or am- plification of the HER2 gene. In the first-line treatment of meta- static breast cancer, overall response rate to T alone or in combination with antiblastic agents ranged from 24% to 60%; the majority of patients experienced disease progression within 12 months from the start of therapy as a result of acquired resistance to the monoclonal antibody. 2
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