| Oncogenic properties of PPM1D located within a breast cancer amplification epicenter at 17q23. | breast, |
| ablation of gene confers resistance to breast tumors induced by certain oncogenes | breast, |
| Medulloblastomas overexpress the p53-inactivating oncogene WIP1/PPM1D. | medulloblastomas, |
| [Expression of proto-oncogene Wip1 in breast cancer and its clinical significance]. | breast, |
| Oncogenic phosphatase Wip1 is a novel prognostic marker for lung adenocarcinoma patient survival. | lung, |
| Expression and significance of the Wip1 proto-oncogene in colorectal cancer. | colorectal, |
| These findings suggest that PPMD1 has oncogenic properties in colon cancer and exhibit therapeutic implications in colon cancer treatment. | colorectal, |
| The p53-induced oncogenic phosphatase PPM1D interacts with uracil DNA glycosylase and suppresses base excision repair. | None |
| Reversal of the ATM/ATR-mediated DNA damage response by the oncogenic phosphatase PPM1D. | None |
| Chk2 kinase was regualted by the oncogenic Wip1 phosphatase. | None |
| Regulation of the antioncogenic Chk2 kinase by the oncogenic Wip1 phosphatase. | None |
| Arsenic trioxide augments Chk2/p53-mediated apoptosis by inhibiting oncogenic Wip1 phosphatase. | None |
| The estrogen receptor alpha pathway induces oncogenic Wip1 phosphatase gene expression. | None |
| Findings uncover Wip1 as a first in class recovery competence gene, and suggest that the principal function of Wip1 in cellular transformation is to retain proliferative capacity in the face of oncogene-induced stress. | None |
| Nuclear factor-kappaB (NF-kappaB) is a novel positive transcriptional regulator of the oncogenic Wip1 phosphatase | None |
| Oncogenic Wip1 phosphatase is inhibited by miR-16 in the DNA damage signaling pathway. | None |
| Our findings provide new insights into contributions by p53 and Wip1 in the in vivo oncogenesis of Tax-induced tumors in mice. | None |
| The WIP1 oncogene promotes progression and invasion of aggressive medulloblastoma variants. | None |