Leo1 Gene Increases Risk for Developing Acute Myelogenous Leukemia (AML)
the Cancer Therapy Advisor take:
According to a new study published in the journal Cancer Research, researchers from the Cancer Science Institute of Singapore at the National University of Singapore in Singapore, Singapore, have discovered that an overexpression of a gene called Leo1 leads to an increased risk for developing acute myelogenous leukemia (AML).
Furthermore, the researchers found that by inhibiting Leo1 and Leo1 downstream signaling pathways may be a potential target of treatment to fight AML.
In addition, researchers found that overexpression of the protein PRL-3 alters the regulation of ribonucleic acid (RNA)-related processes, leading to the progression and spread of a variety of cancers, including breast, cervical, gastric, liver, lung, and ovarian cancer. They found that PRL-3 was overexpressed in approximately 47% of patients with AML, making PRL-3 a potential target for AML treatment as well.
The researchers discovered that PRL-3 phosphatase targets the Leo1 gene leading to overexpression of the gene. By targeting PRL-3 in patients with AML, the findings suggest that Leo1 and Leo1 downstream signaling pathways can be inhibited.
A gene called Leo1 leads to an increased risk for developing AML.
A novel study by the Cancer Science Institute of Singapore (CSI Singapore) at the National University of Singapore (NUS) found that an increase in a gene known as Leo1 affects other genes that are directly implicated in acute myelogenous leukaemia (AML), increasing the incidence of cancer.
Led by Associate Professor Chng Wee Joo, Deputy Director and Senior Principal Investigator at CSI Singapore and Director of the National University Cancer Institute, Singapore, the scientists discovered that inhibition of Leo1 and Leo1 downstream signalling pathways provide an avenue for targeted treatment of AML. The findings were recently published in Cancer Research, the official journal of the American Association of Cancer Research.
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