leukemogenesis การใช้

• Besides glioma, OLIG2 is also involved in leukemogenesis.
• JDP2 induces cell cycle arrest through cyclin D, JDP2 downregulates p53 transcription, which promotes leukemogenesis.
• This list included 140 genes and included regulatory proteins for myelopoiesis and leukemogenesis ( e . g.
• This protein also interacts with rhombotin-2 which functions distinctly in erythropoiesis and in T-cell leukemogenesis.
• The protein encoded by this gene binds to the AML1-MTG8 complex and may be important in promoting leukemogenesis.
• A specific translocation event which causes a fusion between this gene and the NUP98 gene has been associated with myeloid leukemogenesis.
• The upstream ORF encodes a 13kDa protein that is a member of the TCL1 family; this protein may be involved in leukemogenesis.
• This inhibition can lead to cellular differentiation or apoptosis, and therefore any resistance to TGF-? is thought to contribute in some way to human leukemogenesis.
• This result shows that DNA methylation status is not an important regulator of survivin re-expression during leukemogenesis . suggesting that epigenetic mechanisms plays an indirect role on abnormal over-expression of survivin.
• The incidence for the GATA1 mutation in about 4 % of Down Syndrome patients, but less than 10 % of those with the mutation developed AMKL . This mutation is present in the fetus, suggesting an early role in leukemogenesis.
• An important pathophysiological mechanism of leukemogenesis in AML is the epigenetic induction of dedifferentiation by genetic mutations that alter the function of epigenetic enzymes, such as the DNA demethylase TET2 and the metabolic enzymes IDH1 and IDH2, which lead to the generation of a novel oncometabolite, " D "-2-hydroxyglutarate, which inhibits the activity of epigenetic enzymes such as TET2.
• PAK2-mediated phosphorylation of merlin at S518 modulates its tumor suppressor activity, c-Jun phosphorylation at T2, T8, T89, T93 and T286 contributes to the growth of growth factor-stimulated melanoma cells, Caspase-7 phosphorylation at S30, T173 and S239 inhibits apoptotic activity in breast cancer cells, and STAT5 phosphorylation at S779 modulates BCL-ABL-mediated leukemogenesis.