Abstract: Disclosed is an assay for determining resistance in a target cell or tissue to a therapy associated with cellular stress using chemical microscopy and high-throughput single cell analysis to determine functional metabolic alteration, including determining metabolic reprogramming in a target cell or tissue to a therapy associated with cellular stress, and methods of using the assays.

Abstract: Disclosed is an assay for determining resistance in a target cell or tissue to a therapy associated with cellular stress using chemical microscopy and high-throughput single cell analysis to determine functional metabolic alteration, including determining metabolic reprogramming in a target cell or tissue to a therapy associated with cellular stress, and methods of using the assays.

Abstract: Disclosed is an assay for determining resistance in a target cell or tissue to a therapy associated with cellular stress using chemical microscopy and high-throughput single cell analysis to determine functional metabolic alteration, including determining metabolic reprogramming in a target cell or tissue to a therapy associated with cellular stress, and methods of using the assays.

Abstract: Disclosed is an assay for determining resistance in a target cell or tissue to a therapy associated with cellular stress using chemical microscopy and high-throughput single cell analysis to determine functional metabolic alteration, including determining metabolic reprogramming in a target cell or tissue to a therapy associated with cellular stress, and methods of using the assays.

Abstract: The present invention provides inhibitors of ALDH1A1 activity which have substantially no effect on either ALDH2 or ALDH3A1. Compositions and methods of use, as well as methods to treat cancer using the ALDH1A1 inhibitors, are also provided.

Abstract: Tissue transglutaminase-2 (TG2) is involved in Ca++-dependent aggregation and polymerization of proteins. TG2 is upregulated in epithelial ovarian cancer (EOC) cells as compared to normal ovarian epithelium. TG2 is also highly expressed in ovarian tumors and secreted in malignant ascites, but it is not detected in non-transformed ovarian epithelium. Furthermore, TG2 enhances EOC cell adhesion to fibronectin and haptotactic cell migration. This phenotype is preserved in-vivo, where the pattern of tumor dissemination in the peritoneal space is dependent on TG2 expression levels. TG2 knock down diminishes dissemination of tumors on the peritoneal surface and mesentery in an i.p. ovarian xenograft model. This phenotype is due to deficient ?1 integrin-fibronectin interaction, leading to weaker anchorage of cancer cells to the peritoneal matrix.