Lookup NU author(s): Dr Hannah Gautrey,
Dr Alison Tyson-Capper
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
Overexpression of human epidermal growth-factor receptor (HER-2) occurs in 20-30% of breast cancers and confers survival and proliferative advantages on the tumour cells making HER-2 an ideal therapeutic target for drugs like Herceptin. Continued delineation of tumour biology has identified splice variants of HER-2, with contrasting roles in tumour cell biology. For example, the splice variant 16HER2 (results from exon 16 skipping) increases transformation of cancer cells and is associated with treatment resistance; conversely, Herstatin (results from intron 8 retention) and p100 (results from intron 15 retention) inhibit tumour cell proliferation. This review focuses on the potential clinical implications of the expression and coexistence of HER-2 splice variants in cancer cells in relation to breast cancer progression and drug resistance. ‘Individualised’ strategies currently guide breast cancer management; in accordance, HER-2 splice variants may prove valuable as future prognostic and predictive factors, as well as potential therapeutic targets.
Author(s): Jackson C, Browell D, Gautrey H, Tyson-Capper AJ
Publication type: Review
Publication status: Published
Journal: International Journal of Cell Biology
Print publication date: 13/06/2013
ISSN (print): 1687-8876
ISSN (electronic): 1687-8884
Notes: Special Issue: Alternative Splicing: Role in Cancer Development and Progression.