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Molecular code can control the genes, thereby destroying leukemia

January 9, 2018 11:04

Researchers cancer have announced that they have developed a way to eliminate one of the most dangerous "bad actors" in leukemia. (Learn aboutthe treatment of leukemia in Israel). Their approach is similar to the molecular key throwing in gear machine that makes the genes to move, allowing the cancer cells to multiply.

In tests on mice, the newly discovered technique has led to the fact that an aggressive form of blood cancer disappeared at the same time, does not adversely affect the function of normal cells.

A new study by Associate Professor Christopher Vakoka and his colleagues at Cold Spring Harbor Laboratory is a part of a lot of work in the laboratory Vakoc to combat fatal acute myeloid leukemia. They cut off part of the functions of the cells - the transcriptional machinery - determines when genes are switched on and off.

The central players in this mechanism are the proteins, called transcription factors, thousands of whom are active in the regulation of genes in our chromosomes. The question raised in the new study was to how to navigate one of the most unpleasant of transcription factors known as MYB. This oncogene, or cancer-causing transcription factor that overcomes all of the locks and the cells begin to grow uncontrollably.

«MYB - this target in cancer research - Vakok says - because he is involved in many types of cancer, especially leukemia, because of previous studies, we know that, focusing on the MYB, you can get AML (acute myeloid leukemia) not just stop growing, but actually regress. The problem of many research laboratories - deactivation of MYB in cancer.

Yali Xu, PhD student in the lab Vakoc leading research discovered how to selectively bring MYB out of the picture for leukemia, throwing the key into the molecular mechanism that normally activates the transcription factor. Firstly, the command is found that MYB activates gene expression by docking with "koaktivatsionnym" protein called TFIID. Then they found a tiny weak spot on a massive protein. This Achilles heel, called TAF12. Then he lied to the team in the MYB binding of short protein fragments, or peptides, which are formed in the same way as a place to TAF12, where MYB binds when it helps leukemia.

Achievement in the study was the creation of a peptide that acts as a decoy. Experiments on mice that model the human acute myeloid leukemia, have shown that the peptide binds and detects the MYB, not allowing him to participate in the coactivator TFIID. This led to the fact that murine leukemia were reduced by about 80% without harming healthy cells.

Although the peptide itself is not a drug, Vakok says that its action may be reproduced in medicine. "This is a concept we are discussing with the pharmaceutical industry, and it will take a lot of work before patients with leukemia can take medication. But we are very excited about this new approach because MYB is an important player in many types of cancer and still eludes the targeted treatment. "

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