TNBC

NOTCH3 inactivation increases Triple Negative Breast Cancer sensitivity to gefitinib by promoting EGFR tyrosine dephosphorylation and its intracellular arrest.

Triple-negative breast cancer (TNBC) accounts for about 15-20% of breast cancers and represents the most aggressive subtype (1). To date, no molecularly targeted agents are approved for TNBC, leading to the conventional chemotherapy the role of primary option for systemic treatment. Therefore, effective therapeutic strategies for TNBC are urgently needed.

Notch signaling activation as a hallmark for triple-negative breast cancer subtype

Triple-negative breast cancer (TNBC) is a subgroup of 15%-20% of diagnosed breast cancer patients. It is generally considered to be the most difficult breast cancer subtype to deal with, due to the lack of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), which usually direct targeted therapies. In this scenario, the current treatments of TNBC-affected patients rely on tumor excision and conventional chemotherapy. As a result, the prognosis is overall poor.

NOTCH3 inactivation increases triple negative breast cancer sensitivity to gefitinib by promoting EGFR tyrosine dephosphorylation and its intracellular arrest.

Notch dysregulation has been implicated in numerous tumors, including triple-negative breast cancer (TNBC), which is the breast cancer subtype with the worst clinical outcome. However, the importance of individual receptors in TNBC and their specific mechanism of action remain to be elucidated, even if recent findings suggested a specific role of activated-Notch3 in a subset of TNBCs.

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