Release date: 2016-12-06 T cell acute lymphoblastic leukemia is an aggressive, malignant blood disease with a high recurrence rate in children with acute lymphoblastic leukemia. Although most T-ALL patients carry a NOTCH1 activating mutation, scientists are still less aware of other collaborative genetic events that accelerate leukemia and promote disease progression. In a new study, researchers from Baylor College of Medicine in the United States found that gene expression of the transcription factor KLF4 was inhibited by DNA methylation in children with T-ALL. They observed that KLF4 deletion in the mouse model accelerated the induction of T-ALL by NOTCH1, enhanced the conversion of leukemia cells from G1 to S, and promoted the expansion of leukemia stem cells. By studying the mechanism, the researchers found that KLF4 can inhibit the expression of kinase MAP2K7. In mouse models and children with T-ALL, KLF4 deletion leads to activation of MAP2K7 and downstream effectors JNK and ATF2. In addition, the researchers have developed a targeted therapeutic strategy that found that JNK inhibitors can inhibit the expansion of leukemia cells in cell-derived and patient-derived tumor xenograft models. Collectively, these data reveal a novel function of KLF4 in regulating the MAP2K7 signaling pathway in T-ALL cells, targeting this pathway or clearing leukemia stem cells in T-ALL patients. The relevant research results were published in the international academic journal Leukemia. Source: Bio Valley Veterinary Drugs: refers to substances (including medicated feed additives) used to prevent, treat, diagnose animal diseases or purposefully regulate animal physiological functions.
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