ErbB-2 nuclear function in breast cancer growth, metastasis and resistance to therapy.


Approximately 15-20% of breast cancers (BC) show either membrane overexpression of ErbB-2 (MErbB-2), a member of the ErbBs family of receptor tyrosine kinases, or ERBB2 gene amplification. Until the development of MErbB-2-targeted therapies, this BC subtype, called ErbB-2-positive, was associated with increased metastatic potential and poor prognosis. Although these therapies have significantly improved overall survival and cure rates, resistance to available drugs is still a major clinical issue. In its classical mechanism, MErbB-2 activates downstream signaling cascades, which transduce its effects in BC. The fact that ErbB-2 is also present in the nucleus of BC cells was discovered over twenty years ago. Also, compelling evidence revealed a non-canonical function of nuclear ErbB-2 as a transcriptional regulator. As a deeper understanding of nuclear ErbB-2 actions would be crucial to the disclosure of its role as a biomarker and a target of therapy in BC, we will here review its function in BC, in particular, its role in growth, metastatic spreading and response to currently available MErbB-2-positive BC therapies.

Citations per Year

Citation Velocity: 16

Averaging 16 citations per year over the last 2 years.

Learn more about how we calculate this metric in our FAQ.

Cite this paper

@article{Elizalde2016ErbB2NF, title={ErbB-2 nuclear function in breast cancer growth, metastasis and resistance to therapy.}, author={Patricia V. Elizalde and Rosal{\'i}a I Cordo Russo and Maria F Chervo and Roxana Schillaci}, journal={Endocrine-related cancer}, year={2016}, volume={23 12}, pages={T243-T257} }