PPM1D Mutations Drive Clonal Hematopoiesis in Response to Cytotoxic Chemotherapy - Hsu, Joanne I.; Dayaram, Tajhal; Tovy, Ayala; De Braekeleer, Etienne; Jeong, Mira; Wang, Feng; Zhang, Jianhua; Heffernan, Timothy P.; Gera, Sonal; Kovacs, Jeffrey J.; Marszalek, Joseph R.; Bristow, Christopher; et al. (Cell stem cell, 2018)
Keywords: Aged; Animals; Antineoplastic Agents - chemistry; Antineoplastic Agents - pharmacology; Cell Proliferation - drug effects; CHIP; cisplatin; Cisplatin - chemistry; Cisplatin - pharmacology; clonal hematopoiesis; Clone Cells - drug effects; DNA damage response; doxorubicin; Doxorubicin - chemistry; Doxorubicin - pharmacology; Drug Screening Assays, Antitumor; etoposide; Female; HEK293 Cells; Hematopoiesis - drug effects; Hematopoiesis - genetics; Humans; Leukemia, Myeloid, Acute - drug therapy; Leukemia, Myeloid, Acute - metabolism; Leukemia, Myeloid, Acute - pathology; Male; Mice; Mice, Inbred C57BL; Mice, Inbred NOD; Middle Aged; Mutation; Neoplasms, Experimental - drug therapy; Neoplasms, Experimental - metabolism; Neoplasms, Experimental - pathology; PPM1D; Protein Phosphatase 2C - genetics; Protein Phosphatase 2C - metabolism; t-AML; t-MDS; topoisomerase inhibitors; clonal hematopoiesis; CHIP; topoisomerase inhibitors; DNA damage response; etoposide; t-MDS; doxorubicin; PPM1D; cisplatin; t-AML