PPM1D/Wip1 is amplified, overexpressed, and mutated in human non-Hodgkin's lymphomas.

Background: Wip1, is a p53-dependent Ser/Thr phosphatase involved in the timely termination of DDR. The PPM1D gene encoding Wip1 is deregulated and thus gained an oncogene character in common human solid tumors and cell lines. This study assessed the oncogenic potential of the PPM1D gene in human non- Hodgkin's lymphomas (NHL), the most common hematological malignancy worldwide.

Effects of bone marrow-derived mesenchymal stem cells on doxorubicin-induced liver injury in rats.

Doxorubicin (DOX) is a potent chemotherapeutic agent and has toxic effects on various organs, including the liver. In the current study, we aimed to investigate the effects of bone-marrow-derived mesenchymal stem cell (BM-MSC) administration on DOX-induced hepatotoxicity in rats. 24 Wistar-albino rats were divided into three groups: Control, DOX, and DOX+MSC.

Oncogenic WIP1 phosphatase attenuates the DNA damage response and sensitizes p53 mutant Jurkat cells to apoptosis.

Wild-type (wt) p53-induced phosphatase 1 (Wip1), encoded by the protein phosphatase, Mg/Mn dependent 1D (PPM1D) gene, is a serine/threonine phosphatase induced upon genotoxic stress in a p53-dependent manner. Wip1/PPM1D is frequently overexpressed, amplified and mutated in human solid tumors harboring wt p53 and is thus currently recognized as an oncogene. Oncogenic Wip1 dampens cellular stress responses, such as cell cycle checkpoints, apoptosis and senescence, and consequently increases resistance to anticancer therapeutics.