| First Author | Sha X | Year | 2018 |
| Journal | Oncotarget | Volume | 9 |
| Issue | 70 | Pages | 33360-33367 |
| PubMed ID | 30279966 | Mgi Jnum | J:294740 |
| Mgi Id | MGI:6458259 | Doi | 10.18632/oncotarget.26076 |
| Citation | Sha X, et al. (2018) Loss of Gadd45b accelerates BCR-ABL-driven CML. Oncotarget 9(70):33360-33367 |
| abstractText | Gadd45b is a member of Gadd45 stress sensor protein family that also includes Gadd45a & Gadd45g. To investigate the effect of Gadd45b in bcr-abl oncogene driven chronic myeloid leukemia (CML) development, syngeneic wild type lethally irradiated mice were reconstituted with either wild type or Gadd45b null myeloid progenitors transduced with a retroviral vector expressing BCR-ABL. Loss of Gadd45b was observed to accelerate BCR-ABL driven CML development with shortened median mouse survival time. BCR-ABL Gadd45b deficient CML progenitors exhibited increased proliferation and decreased apoptosis, associated with hyper-activation of c-Jun NH2-terminal kinase and Stat5. These results provide novel evidence that gadd45b, like gadd45a, functions as a suppressor of BCR-ABL driven leukemia, albeit via a different mechanism. |
