Experimental drug to stop radiation damage
Andrei V. Gudkov, a chairperson of Cell Stress Biology within the Roswell Park Cancer Institute (Buffalo, New York, U.S.A.), is the lead researcher in the study of a drug that protect against lethal damage from radiation.
Radiation has and is used to kill cancerous cells, but does have adverse effect on healthy tissues, bone marrow, GI tract, and other cells in the body.
The drug of interest has been named CBLB502, a polypeptide drug derived from Salmonella flagellin.
Gudkov and his team found that when defective cells are stopped from spreading through apoptosis.
Apoptosis is prevented from occurring in cancer; that is, bad cells are killed but good cells are also adversely affected. Thus, it causes cancerous tumors to occur.
Gudkov and his team found that when apoptosis is prevented from occurring, a pathway called NFKB is also blocked.
The NFKB pathway is activated by flagellin, a protein in gut bacteria, and is normally used by apoptosis to destroy bad cells while leaving good cells alone.
Once the Gudkov team learned of the connection among apoptosis, NFKB, and flagellin, they decided to try to simulate the same pathway.
They injected the drug CBLB502 into mice and rhesus monkeys, waited from fifteen to sixty minutes, and then exposed the laboratory animals to lethal doses of radiation.
The investigators found that the drug improved survival rates, helping to protect bone marrow and the GI tract. The animals had more protection when the wait time was 60 minutes versus shorter times.
Especially important for radiation treatments for cancer patients, the drug CBLB502 did not prevent radiation from treating tumors in the mice as it protected healthy tissues.
This drug has now become the interest of the U.S. Department of Defense (DOD), since it could help citizens in case of a nuclear attack.
Radiation has and is used to kill cancerous cells, but does have adverse effect on healthy tissues, bone marrow, GI tract, and other cells in the body.
The drug of interest has been named CBLB502, a polypeptide drug derived from Salmonella flagellin.
Gudkov and his team found that when defective cells are stopped from spreading through apoptosis.
Apoptosis is prevented from occurring in cancer; that is, bad cells are killed but good cells are also adversely affected. Thus, it causes cancerous tumors to occur.
Gudkov and his team found that when apoptosis is prevented from occurring, a pathway called NFKB is also blocked.
The NFKB pathway is activated by flagellin, a protein in gut bacteria, and is normally used by apoptosis to destroy bad cells while leaving good cells alone.
Once the Gudkov team learned of the connection among apoptosis, NFKB, and flagellin, they decided to try to simulate the same pathway.
They injected the drug CBLB502 into mice and rhesus monkeys, waited from fifteen to sixty minutes, and then exposed the laboratory animals to lethal doses of radiation.
The investigators found that the drug improved survival rates, helping to protect bone marrow and the GI tract. The animals had more protection when the wait time was 60 minutes versus shorter times.
Especially important for radiation treatments for cancer patients, the drug CBLB502 did not prevent radiation from treating tumors in the mice as it protected healthy tissues.
This drug has now become the interest of the U.S. Department of Defense (DOD), since it could help citizens in case of a nuclear attack.
posted by Antonio at 9:29 PM
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