AKT and EZH2 inhibitors kill TNBCs by hijacking mechanisms of involution - Schade, Amy E.; Perurena, Naiara; Yang, Yoona; Rodriguez, Carrie L.; Krishnan, Anjana; Gardner, Alycia; Loi, Patrick; Xu, Yilin; Nguyen, Van T. M.; Mastellone, G. M.; Pilla, Natalie F.; Watanabe, Marina; et al. (Nature (London), 2024)
Keywords: 1-Phosphatidylinositol 3-kinase; 13/106; 13/2; 13/51; 13/89; 13/95; 14/63; 38/39; 38/90; 631/67/1059/602; 631/67/1347; 631/67/395; AKT protein; AKT1 protein; Animals; Antineoplastic Agents - administration & dosage; Antineoplastic Agents - pharmacology; Antineoplastic Agents - therapeutic use; Breast cancer; Cancer therapies; Cell culture; Cell death; Cell Death - drug effects; Cell differentiation; Cell Differentiation - drug effects; Cell Line, Tumor; Chemotherapy; Cytotoxicity; Deregulation; Drug Synergism; Drug Therapy, Combination; Enhancer of Zeste Homolog 2 Protein - antagonists & inhibitors; Enhancer of Zeste Homolog 2 Protein - metabolism; Epigenetics; Female; Genes; Histone methyltransferase; Humanities and Social Sciences; Humans; Immunotherapy; Inhibitors; Machine Learning; Mammary gland; Mammary glands; Mice; multidisciplinary; Mutation; Organ Specificity; Pharmacology; Protein Kinase Inhibitors - administration & dosage; Protein Kinase Inhibitors - pharmacology; Protein Kinase Inhibitors - therapeutic use; Proto-Oncogene Proteins c-akt - antagonists & inhibitors; Proto-Oncogene Proteins c-akt - metabolism; Regression analysis; Science; Science (multidisciplinary); Stem cells; Synergism; Therapeutic targets; Triple Negative Breast Neoplasms - drug therapy; Triple Negative Breast Neoplasms - metabolism; Triple Negative Breast Neoplasms - pathology; Tumors; Xenograft Model Antitumor Assays