MicroRNA Strongly Linked to Acute Myeloid Leukemia Risk and Recovery

By LabMedica International staff writers
Posted on 29 May 2013
Overexpression of a specific microRNA (miRNA) in patients suffering from cytogenetically normal (CN) acute myeloid leukemia (AML) has been linked to lower complete remission rate as well as to shorter disease-free and overall survival.

MicroRNAs (miRNAs) are snippets of about 20 nucleotides that block gene expression by attaching to molecules of messenger RNA (mRNA) in a fashion that prevents them from transmitting the protein synthesizing instructions they had received from the DNA.

Image: Senior author Dr. Clara D. Bloomfield (Photo courtesy of Ohio State University).

Investigators at Ohio State University (Columbus, USA) measured miRNA levels and expression profiles in the blood and bone marrow of obtained from 363 patients with primary CN-AML. The test population comprised 153 patients under age 60 and 210 aged 60 and over.

Results published in the May 6, 2013, online edition of the Journal of Clinical Oncology strongly linked microRNA-155 (miR-155) to the severity of the disease. Patients with high miR-155 expression were found to be about 50% less likely to achieve complete remission and to have a 60% increase in the risk of death compared to patients with low miR-155 expression.

Although high miR-155 expression was not associated with a distinct miRNA expression profile, it was associated with a gene expression profile enriched for genes involved in cellular mechanisms deregulated in AML. These mechanisms included apoptosis, nuclear factor-kappaB activation, and inflammation.

Senior author Dr. Clara D. Bloomfield, professor of medicine at Ohio State University, said, “Overall, our findings indicate that miR-155 expression is a strong and independent prognostic marker in CN-AML, and they provide clinical validation of data from preclinical models that support a crucial role of miR-155 in leukemia.”

The development of drugs with antagonistic activity toward microRNAs may provide the opportunity for future therapeutic targeting of miR-155 in AML.

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