Mitochondrial dynamics, a new therapeutic target for Triple Negative Breast Cancer.

Triple Negative Breast Cancer (TNBC) is an aggressive tumour with patients survival rarely exceeding five years. TNBC tumours are larger in size, more chemoresistant, highly proliferative and usually more enriched in stem and immune cells comparing to other breast cancer subtypes. Functionally, these changes are dependent on a high-quality mitochondrial pool.

HDAC6 Degradation Inhibits the Growth of High-Grade Serous Ovarian Cancer Cells.

Histone deacetylase 6 (HDAC6) is a unique histone deacetylating enzyme that resides in the cell cytoplasm and is linked to the modulation of several key cancer related responses, including cell proliferation and migration. The promising anti-cancer response of the first-generation HDAC6 catalytic inhibitors continues to be assessed in clinical trials, although its role in high grade serous ovarian cancer is unclear. This study investigated HDAC6 tumor expression by immunohistochemistry in high-grade serous ovarian cancer (HGSOC) tissue samples and a meta-analysis of HDAC6 gene expression in ovarian cancer from publicly available data.

Frequency, impact and a preclinical study of novel gene family mutations in HER2-positive breast cancer.

Background: Somatic mutations in the genes (epidermal growth factor receptor: ) promote oncogenesis and lapatinib resistance in metastatic HER2+ (human epidermal growth factor-like receptor 2) breast cancer . Our study aimed to determine the frequency of mutations in four genes: and and to investigate whether these mutations affect cellular behaviour and therapy response and outcomes after adjuvant trastuzumab-based therapy in clinical samples.

Methods: We performed Agena MassArray analysis of 227 HER2+ breast cancer samples to identify the type and frequency of family mutations.

Protein and chemotherapy profiling of extracellular vesicles harvested from therapeutic induced senescent triple negative breast cancer cells.

Triple negative breast cancer (TNBC) is an aggressive subtype with relatively poor clinical outcomes and limited treatment options. Chemotherapy, while killing cancer cells, can result in the generation of highly chemoresistant therapeutic induced senescent (TIS) cells that potentially form stem cell niches resulting in metastases. Intriguingly, senescent cells release significantly more extracellular vesicles (EVs) than non-senescent cells.

The fate of chemoresistance in triple negative breast cancer (TNBC).

Background: Treatment options for women presenting with triple negative breast cancer (TNBC) are limited due to the lack of a therapeutic target and as a result, are managed with standard chemotherapy such as paclitaxel (Taxol®). Following chemotherapy, the ideal tumour response is apoptotic cell death. Post-chemotherapy, cells can maintain viability by undergoing viable cellular responses such as cellular senescence, generating secretomes which can directly enhance the malignant phenotype.