Heat Shock Proteins in Triple-Negative Breast Cancer (TNBC) Treatment

Abstract

Triple-negative breast cancer (TNBC) accounts for approximately 15 % of breast cancer diagnoses, and exhibits substantial overlap with basal-type and BRCA1-positive breast cancer. Large population based studies have identified a higher proportion of triple-negative breast tumors among premenopausal African American women, and a suggestion that increased parity, younger age at first term pregnancy, shorter duration of breast feeding, and elevated hip-to-waist ratio might be particular risk factors. In recent years, a greater understanding of the biology of this disease has led to the development of numerous and varied therapeutic approaches. Neoadjuvant trials using conventional cytotoxic agents such as cisplatin have demonstrated TNBC to be a relatively chemosensitive disease. Drugs developed to inhibit the angiogenic process may be particularly effective in TNBC. The molecular chaperone heat shock protein (HSP90) is required for the conformational maturation and stability of a variety of proteins in multiple pathways, such as epidermal growth factor receptor (EGFR), AKT, Raf, cdk4, etc. Therefore, an HSP90 inhibitor may show therapeutic benefit in TNBC by targeting multiple pathways. In terms of therapy, an increasingly rational drug development effort has resulted in agents against new molecular targets that are active against P. Kaur ( ) Assistant Professor,