Leukemia: The combination of the drug quizatini in combination with dasatinyni may be effective in the treatment of acute myeloid leukemia.

August 7, 2020 // -- Tyrosine kinases are proteases in cells that perform a variety of functions, including cell signaling, growth, and division, but sometimes they become overactive and help cancer Cell survival and reproduction, tyrosine kinase inhibitors (TKI) can help treat patients with specific acute myeloid leukemias, thereby blocking the activity of overactive tyrosine kinases in their bodies and ultimately blocking or slowing the growth of cancer cells.
Photo Source: Wikipedia Recently, in a study published in the international journal Leukemia, scientists from the Huntsman Cancer Institute and others found that special factors produced by bone marrow-supporting cells may help leukemia cells survive under the drug quizartinib, a tyrosine attack. Enzyme inhibitors, which close the replaceable survival path of cancer cells when they bind to another TKI called dasatinib, could be more effective in promoting leukemia cell death, and the results may help researchers develop new therapies to treat AML patients with the FRT3 gene mutation.
AML is a blood cancer that affects white blood cells in the patient's body, and about 30% of AML patients carry mutations in the tyrosine kinase gene called FRT3, which expresses proteins located on the surface of blood cells and binds to special molecules called FL outside the cell, normally when associated with FL When combined, the FLT3 receptors can be activated and cell growth promoted; however, mutations in the FLT3 growth signal are sent to leukemia cells even when FL does not exist, and quezatetini is a special type of FLT3 inhibitor that is currently used to treat AML patients with FLT3 mutations.
researcher Patel said that at first AML patients responded to quezatinine, but usually the disease relapsed quickly after treatment, and we were surprised to see how small molecule inhibitors changed treatment for many leukemia patients;
after using blood and bone marrow samples donated by AML patients, the researchers found that special factors produced by bone marrow-supporting cells could be ingested by leukemia cells, activating survival paths to protect leukemia cells from being killed by the drug quezatine, one of the signaling paths activated in leukemia cells is the STAT5 signal. In addition, the researchers found that these bone marrow factors accelerate the production of energy in leukemia cells, thereby promoting the survival of cancer cells, and in laboratory studies, the use of quezzatini in combination with dasatine to treat leukemia or to overcome the protective effects of bone marrow-supporting cells was more effective in killing leukemia cells than Quezzatini.
Next Researchers plan to build on the results of this paper to further study how chronic granulocytic leukemia develops resistance to TKIs, and in general, the results may be expected to help researchers conduct relevant clinical trials to improve clinical treatment options for leukemia patients.
sources: Patel, A.B., Pomicter, A.D., Yan, D. et al. Dasatinib Overcomes stroma-based resistance to the FLT3 stingor quizartinib using multiple mechanisms. Leukemia (2020). doi:10.1038/s41375-020-0858-1.