Scientists have made a major breakthrough in the development of acute myeloid leukemia therapy!

Recently, scientists from the University of Montreal discovered a key molecular process involved in the action of anti-leukemia drugs. The research was published in the international journal Cancer Cell, and it is expected to help develop a new type of treatment for leukemia in the future. Therapy; in the article, the researchers focused on acute myeloid leukemia (AML), a type of leukemia most common in adults. These diseases originate from hematopoietic stem cells, and about 2,000 people in Canada are diagnosed with AML each year. Even after a patient undergoes chemotherapy and bone marrow transplantation, patients with specific genetic traits have a life expectancy of less than three years.
In this study, the researchers identified genes associated with the pathogenesis of myeloid leukemia, and the researchers sequenced approximately 700 AML patients and tested approximately 5000 drugs for multiple myeloid leukemias. effect. Researcher Sauvageau said that myeloid leukemia and lymphocytic leukemia are a combination of about 20 different hereditary diseases . The leukemia we call is actually a group of symptoms caused by these diseases, so we must detect the above 5000 species. The effect of drugs on multiple AMLs in order to correlate the effects of each drug with a particular gene.
The drugs tested by the researchers were not used to treat leukemia (usually used to treat other human diseases). The researchers analyzed the effects of these drugs on the body cells and human cells of mice carrying the acute myeloid leukemia gene. Molecules may be complementary to multiple AML subtypes by acting in combination with each other. Mubritinib is one of the drugs that is a protein kinase inhibitor that regulates cellular metabolism. Developed to treat breast cancer, the researchers found that the drug mulletinib may have potential therapeutic effects on specific AML subtypes, and that the drug is not toxic to mice and less toxic to humans.
In the article, the researchers analyzed the electrochemical process behind the behavioral model of the drug, mullotinib. In the AML subpopulation, mulletinib can promote cancer cell death by "arresting" oxidative phosphorylation of tumor cells; It is speculated that no matter what type of cancer, tumor cells will not fully utilize oxidative phosphorylation and produce most of the energy in the absence of oxygen. However, the results of the study indicate that oxidative phosphorylation actually exists in specific cells. Moreover, these cells use this process to produce the required energy and proliferate, and if oxidative phosphorylation is blocked, the cell will die.
The study found clarification of the so-called Warburg effect in biochemistry, which is believed to be the basic principle in oncology research, which believes that cancer cells can break through glucose (sugar Instead of using oxygen to produce energy, and the Warburg effect is a key feature of cancer; later researchers will continue to delve into the development of new targeted therapies for the treatment of AML.
Original source: Irène Baccelli, Yves Gareau, Bernhard Lehnertz, et al. Mubritinib Targets the Electron Transport Chain Complex I and Reveals the Landscape of OXPHOS Dependency in Acute Myeloid Leukemia, Cancer Cell (2019). DOI:10.1016/j.ccell.2019.06 .003

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