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STAG1 has been identified as a hardwired genetic dependency of cancer cells harbouring mutations in the cohesin subunit and emerging major tumor suppressor STAG2 holds the promise for the development of selective therapeutics.

L-mimosine and dopamine protect against cisplatin-induced oto- and nephrotoxicity in zebrafish and human cell line models.

Proteomics and functional genomics coupled to an antibody discovery pipeline revealed the influence of oncogenic RAS signaling on the cell-surface proteome and resulted in the discovery of potential therapeutic targets for RAS-driven cancers.

The theory of Buffered Qualitative Stability uses the importance of biological robustness to explain many features of gene regulatory networks in a wide range of organisms, and has implications for diverse biological phenomena including the ability of bacteria and cancer cells to ‘loosen’ their robustness and hence evade treatment.

Goblet cells secrete mucins—which are key components of mucus—in a process that is regulated by calcium ions, which enter the goblet cells via a mechanism involving a channel protein called TRPM5.

A mathematical model shows that mutations that recur even modestly among cancer patients are cancer driving nucleotides that can be exhaustively identified to serve as targets of cancer therapy.

Computational and experimental analyses show that homoharringtonine may be repurposed as an agent for the treatment and prevention of liver cancer.

A large-scale RNA interference screen uncovers a new transcriptional regulatory program involving the histone H3 demethylase KDM3A, which mediates detachment-induced apoptosis (anoikis) in breast epithelial cells.

Circulating human primed innate lymphoid cell precursors have the potential to functionally induce adhesion molecules' expression in endothelial cells and possibly support the immune cells' infiltration into the tumor site.

GDC-0810 is a novel, orally bioavailable SERD that exhibits robust pre-clinical activity in models of ER+ breast cancer, including models of tamoxifen resistance, and those that express the ERα mutations, ER.Y537S and ER.D538G.