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Researchers find new drug that may benefit blood cancer patients

Researchers at Huntsman Cancer Institute (HCI) at the University of Utah have discovered new science that could provide better therapeutic options for patients.

fitness Updated: Jun 10, 2017 16:30 IST
The drugs broke down the central hub of DNA repair and the HDAC1,2 inhibitor actually reduced different repair protein functions.
The drugs broke down the central hub of DNA repair and the HDAC1,2 inhibitor actually reduced different repair protein functions.

A team of US researchers has found that a drug alone or with combination of chemotherapy may show promising results in treating patients with blood cancer.

The researchers focused on two specific proteins, directly involved in DNA repair, called histone deacetylases (HDAC) 1 and 2. The study, conducted on mice, found that the HDAC1,2 inhibitor or the HDAC1,2/doxorubicin combination, their bone marrow started turning from pale to red, indicating the white blood cells were being replaced with red blood cells.

Researchers at Huntsman Cancer Institute (HCI) at the University of Utah have discovered new science that could provide better therapeutic options for patients. Lead study author Srividya Bhaskara from the University of Utah said that the ALL cancer cells containing the Philadelphia chromosome are addicted to repairing DNA.

Bhaskara noted that when the drug was combined with a low concentration of doxorubicin, it had additional therapeutic benefits and using the combination of drugs, or HDAC1,2 inhibitor alone, is sufficient to decrease the leukemia load. Leukemia is a white blood cell disease where the body produces too many white and not enough red blood cells.

The findings revealed that in mouse models, a 50-70 percent reduction in leukemia was observed with either HDAC1,2 inhibitor alone or when the inhibitor was used with doxorubicin. The team tested the HDAC1,2 inhibitor in patient samples and mice and saw encouraging results, either alone or in combination with a chemotherapy drug called doxorubicin.

The drugs broke down the central hub of DNA repair and the HDAC1,2 inhibitor actually reduced different repair protein functions. The findings could possibly lead to future novel drug treatments.

“Repairing DNA may sound like a good thing when you’re talking about healthy cells,” she explains, “This inhibitor can work at multiple steps and at multiple levels of repair without causing major toxicity,” says Bhaskara. The study is published in the journal Leukemia.

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