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A common tumor suppressor gene was found in the patients with acute leukemia (AL). The finding reveals its synergistic effect between function abnormalities and a variety of different carcinogenic gene, providing an important foundation for research and development of novel leukemia treatment.

Researchers found the transfer functional MLL – NRIP3 carcinogenic gene and SETD2 genetic mutation of catalytic H3K36 trimethylation (h3k36me3) histone methyltransferase through whole genome sequencing for the blood cells of a mixed lineage leukemia (MLL) patients and normal monozygotic twins.

Acute leukemia is a common malignant tumor of blood system, and its incidence is about 2.76/100000. This study indicates that SETD2 is a new tumor suppressor gene in leukemia, and the functional destruction of H3K36me3 – SETD2 pathway is a new epigenetic mechanism in the development of leukemia.

There is a dual meaning of SETD2H3K36me3 function in acute leukemia: clinical significance and scientific significance. In children and adults under the age of 35, the mortality rate of acute leukemia is more than that of any other cancer. And the treatment of some subgroup leukemia effect is very good, while others is very poor. It needs to find new targets associated with cancer pathogenesis, and designs related therapeutic drugs. From a scientific point of view, the traditional tumor is a genetic disease characterized by mutations in DNA. But DNA is wrapped in a complex chromatin, and it has been controversial whether the changes play an important role in tumor biology. Function of h3k36me3 histone modifications disorder in patients with leukemia is confirmed that chromatin mutation plays an important role in the tumorigenesis process, but the chromatin change can play an important biological function in the occurrence of tumor by controlling the understanding of the genetic information in DNA.

One of the major challenges in cancer research currently is whether a variety of oncogenes or the coordination mechanism can lead to malignant cells. The finding will contribute to the understanding of the pathogenesis of leukemia and other cancers, and also contribute to the development of clinical medicine.

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