Xinhua News Agency, Xi'an, September 18 (Reporter Yan Juan) The reporter learned from the National Joint Engineering Research Center for Biodiagnosis and Treatment of the Second Affiliated Hospital of Xi'an Jiaotong University that the team of Professor Kong Guangyao discovered a disease that can kill bone marrow proliferative tumors. A new strategy for cells may bring good news to the treatment of patients with this type of myeloid leukemia.
Professor Kong Guangyao's team recently published an online publication in the leukemia authoritative journal Leukemia entitled "Lowering the Notch signaling pathway in myeloproliferative tumors to counteract the activation of ERK signaling pathways and oxidative phosphorylation by KrasG12D mutants" Research results. This study shows that, unlike acute myeloid leukemia, the Notch signaling pathway plays a major role in oncogenes in myeloproliferative neoplasms. Further mechanistic studies have shown that inhibition of Notch signaling pathway can inhibit the activation of ERK signaling pathway and also inhibit oxidative phosphorylation of leukemia cells. More importantly, simultaneous inhibition of ERK signaling pathway and oxidative phosphorylation has a better targeted killing effect on leukemia cells, which may be a new strategy for targeted therapy of myeloproliferative tumors.
According to reports, leukemia ranks 6th (male) and 8th (female) among the malignant tumor mortality rates in China, ranking first among children and adults under 35 years old. Kong Guangyao said that myeloproliferative neoplasms are a type of malignant hematological tumor originating from hematopoietic stem cells, and there is currently no effective targeted therapy strategy. The researchers found that the Notch signaling pathway is involved in the development of multiple tumors, but its role in different tumors has significant tissue specificity and environmental dependence. Previous studies have shown that the Notch signaling pathway has the role of a tumor suppressor gene in acute myeloid leukemia.
Source: Xinhuanet
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