High-grade serous ovarian carcinoma (HGSOC) is the most common type of epithelial ovarian cancer. The majority of cases are diagnosed at advanced stages, when intraperitoneal (IP) spread has already occurred. Despite significant surgical and chemotherapeutic advances in HGSOC treatment over the past decades, survival rates with HGSOC have only modestly improved.
View Article and Find Full Text PDFChimeric antigen receptor (CAR) T-cell therapy has shown remarkable successes in fighting B-cell leukemias/lymphomas. Promising response rates are reported in patients treated with B-cell maturation antigen (BCMA) CAR T cells for multiple myeloma. However, responses appear to be nondurable, highlighting the need to expand the repertoire of multiple myeloma-specific targets for immunotherapy and to generate new CAR T cells.
View Article and Find Full Text PDFSelective autophagy is essential for maintaining cellular homeostasis under different growth conditions. Huntingtin, mutated versions of which have been implicated in Huntington disease, is now shown to act as a scaffold protein that couples the induction of autophagy and the selective recruitment of cargo into autophagosomes.
View Article and Find Full Text PDFTwo papers by McEwan et al. (McEwan et al., 2015a, 2015b) identify interactions of PLEKHM1 with autophagosome-associated Atg8 proteins and Salmonella typhimurium effector, SifA, linking autophagy and the Salmonella-containing vacuole (SCV) to the endolysosomal Rab7/HOPS-regulated tethering machinery.
View Article and Find Full Text PDFIn this issue of Molecular Cell, Ito et al. (2013) identify 8-nitro-cGMP as a new autophagy inducer mediating the clearance of invading bacteria in a mechanism that depends on protein S-guanylation and Lys63-linked ubiquitination. This study reveals an additional link between the innate immune response and autophagy.
View Article and Find Full Text PDFAutophagy is an evolutionarily-conserved catabolic process initiated by the engulfment of cytosolic components in a crescent-shaped structure, called the phagophore, that expands and fuses to form a closed double-membrane vesicle, the autophagosome. Autophagosomes are subsequently targeted to the lysosome/vacuole with which they fuse to degrade their content. The formation of the autophagosome is carried out by a set of autophagy-related proteins (Atg), highly conserved from yeast to mammals.
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