Scientists in Singapore have uncovered an interaction between two molecules that could soon lead to a new treatment for acute myeloid leukemia (AML), one of the most aggressive types of blood cancer..

In addition, one of these molecules could become an AML biomarker that could be used in personalized therapy..

A joint team of researchers from the Cancer Institute of Singapore (CSI Singapore) and the National University of Singapore (NUS) published their findings in the January issue of Experimental Hematology..

Acute myeloid leukemia, or acute non-lymphoblastic leukemia, is a type of blood cancer that has a poor prognosis.. Develops very rapidly, sometimes resulting in death within weeks or months.

As AML progresses, more and more non-functional white blood cells accumulate in the blood. At the same time, the growth of normal blood cells, including red blood cells and platelets, is suppressed.. The disease mainly affects people under 45 years of age..

There were 18,860 new cases of AML and 10,460 related deaths in the US in 2014, according to the American Cancer Society..

PRL-3 and STAT3 are regulators of AML development.

Two molecules that the authors of the latest study found were previously suspected of being involved in the development of leukemia.. These are the STAT3 transcription factor and the PRL-3 gene. A transcription factor is a protein that turns a specific gene on and off by binding DNA to other proteins..

Singapore team discovers for the first time increased expression of the PRL-3 gene in 47% of patients with acute myeloid leukemia. The authors report that the STAT3 protein level was above normal in about 50% of these patients.. But the most important thing is that scientists have proven for the first time that PRL-3 and STAT3 molecules regulate the development of acute myeloid leukemia..

Lead study author Chang Wee Joo, a lecturer at the NUS School of Medicine and co-director of the Cancer Institute of Singapore, said: “Researchers have previously studied the role of PRL-3 in other types of cancer, but only recently have they begun to look at the role of this gene in blood cancer.. The mechanism of action of PRL-3 in AML has never been considered at all..

On the threshold of promising discoveries.

All available scientific literature on the STAT3 protein was reviewed, including the latest findings. Scientists have concluded that half of patients with acute myeloid leukemia have elevated levels of this protein, and they also have higher than normal expression of the PRL-3 gene..

Using human and mouse cells, scientists have found that artificially reducing STAT3 levels leads to a decrease in the number of cancer cells in the blood..

Therefore, regulation of the STAT3–PRL-3 loop can be used to treat AML.. And the PRL-3 gene itself can serve as a cancer biomarker, with which it is easy to track the activity of the disease..

Recall that in April 2014, a report appeared on the pages of the journal Science Signaling that scientists from the United States had found a small “hidden” gene that is responsible for poor prognosis and the rapid development of the disease in acute myeloid leukemia in some patients..

medbe. en.