Ohio State UniversityLeukemia is said to be cancer of the blood or bone marrow typified by an irregular production of blood cells, generally leukocytes i.e. white blood cells. Researchers from Ohio State University Comprehensive Cancer Center- Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC-James), apparently signify that chronic myeloid leukemia (CML) supposedly advances when immature white blood cells lose a molecule known as miR-328.

Loss of the molecule appears to ambush the cells in a swiftly developing, immature state. The cells apparently soon fill the bone marrow and supposedly spill into the bloodstream, a significant indication that the disease seems to have progressed to the blast crisis stage. The research ought to offer a superior comprehension of the blast-crisis stage of CML, and it could propose a likely new treatment approach for the disease.

“These findings indicate that the loss of miR-328 is probably essential for progression from the chronic phase of the disease to the blast crisis stage,” commented principal investigator Danilo Perrotti, associate professor of molecular virology, immunology and medical genetics and a member of the OSUCCC-James.

Perrotti added, “Our findings also suggest that maintaining the level of this microRNA might represent a new therapeutic strategy for CML blast crisis patients who do not benefit from targeted agents such as imatinib (Gleevec) and dasatinib (Sprycel).”

Moreover, the research seems to divulge a new role for microRNA. Scientists have apparently known long enough that these molecules may aid in controlling the types of proteins that cells generate. But this research appears to exhibit for the first time that microRNA molecules may also fasten directly to protein molecules and modify their function. In this case, miR-328 is said to strap on to a protein that may avert immature blood cells from maturing.

Perotti mentioned, “We believe that it normally acts as a decoy molecule, tying up the protein and enabling the white blood cells to mature as they should.”

During CML progression, nevertheless, the level of miR-328 declines, thereby enabling the protein to be quite active. This is said to prevent the leukemic white blood cells from maturing and apparently adds to the changeover from the chronic-disease phase to blast crisis phase.

The research was published in the journal Cell.