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Researchers Discover New Therapy for Aggressive Blood Cancer

While AML –Acute Myeloid Leukemia turns out to be one of the most fatal forms of cancers out there, researchers from different parts of the world keep looking for effective therapies for the same.

AML –Acute Myeloid Leukemia turns out to be the most common form of blood cancer. AML is characterized by a significant number of the malignant myeloid progenitor cells. As per the stats, only 25 percent of the AML patients across the world tend to survive past five years after the initial diagnosis. Therefore, there stands an urgent requirement for knowing more about this form of blood cancer and developing new therapeutic systems.

New Therapy for AML

A team of researchers at the Vetmeduni Vienna along with those at the Ludwig Boltzmann Institute for Cancer Research have come up with an innovative therapeutic approach for the treatment of AML –Acute Myeloid Leukemia. The researchers observed that the activity of oncogenic protein “C/EBP-alpha” that is mutated tends to be dependent on some form of epigenetic helper that is functional. The epigenetic helper here is the MLL1 histone methyltransferase complex. When the researchers conducted the laboratory tests, it revealed that the functional perturbation of the MLL1 complex resulted in the death of the AML cells with the mutations of C/EBP-alpha. The given inhibitor treatment resulted in the releasing of the differentiated cancer cell blocks and restoring the normal mutation of the blood cells.

The Results of the Study

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As per the results of the study, the interaction of the protein that was mutated with the epigenetic regulator represented a special vulnerability of the cells with AML with CEBPA mutations. Once the inhibition of the MLL1 complex was successful, the AML cells were observed to have undergone cell death.

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The researchers stated that in combination with genetic, pharmacological, and biochemical approaches, they are now capable of showing that the MLL1 complex proves to be a critical vulnerability in AML cases with CEBPA mutations. The results of the study only tend to broaden the knowledge of AML with CEBPA mutations. It also helps in identifying the MLL1 complex to serve as a therapeutic target for the given type of cancer.

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