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UC Davis researchers discover genetic switch involved in cells' response to radiation therapy
November 17, 2005Finding could lead to more effective, less toxic radiosensitizing drugs for cancer patients
UC Davis Cancer Center researchers have discovered a genetic switch that causes cancer cells to become more sensitive to a drug administered to enhance radiation therapy effectiveness. The switch does not make the drug more toxic.
The discovery may help scientists design new anti-cancer agents that enhance the effectiveness of radiation therapy with less toxicity than currently available radiosensitizing drugs. The finding is reported in the Priority Reports section of the last issue of the journal Cancer Research (Oct. 17 - Oct. 31).
Allan Chen, assistant professor of radiation oncology at UC Davis Cancer Center, found that Ku86, a gene involved in DNA repair, acts as a switch that, when turned off, makes cells significantly more vulnerable to the radiosensitizing property of the anti-cancer drug camptothecin.
Ku86 had no effect on the radiosensitizing abilities of other anti-cancer agents tested - etoposide, cisplatin and vinblastine. Ku86 also had no effect on camptothecin toxicity.
The team concluded that, like a switch that controls only a certain light bulb, Ku86 uniquely affects radiosensitization, but not cytotoxicity, induced by camptothecin.
The UC Davis researchers started by identifying which enzymes affect radiosensitivity and cytotoxicity, then painstakingly determined a way to control such enzymes.
The investigation focused on an enzyme called DNA topoisomerase I, which is responsible for cutting single DNA strands so that the DNA molecule can rotate and unwind during transcription and replication. Camptothecin stops DNA topoisomerase I during the unwinding process, ultimately killing the cell.
University of California, Davis-Health System
Allan Chen, assistant professor of radiation oncology at UC Davis Cancer Center, found that Ku86, a gene involved in DNA repair, acts as a switch that, when turned off, makes cells significantly more vulnerable to the radiosensitizing property of the anti-cancer drug camptothecin.
Ku86 had no effect on the radiosensitizing abilities of other anti-cancer agents tested - etoposide, cisplatin and vinblastine. Ku86 also had no effect on camptothecin toxicity.
The team concluded that, like a switch that controls only a certain light bulb, Ku86 uniquely affects radiosensitization, but not cytotoxicity, induced by camptothecin.
The UC Davis researchers started by identifying which enzymes affect radiosensitivity and cytotoxicity, then painstakingly determined a way to control such enzymes.
The investigation focused on an enzyme called DNA topoisomerase I, which is responsible for cutting single DNA strands so that the DNA molecule can rotate and unwind during transcription and replication. Camptothecin stops DNA topoisomerase I during the unwinding process, ultimately killing the cell.
University of California, Davis-Health System
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Aiming to avoid damage to neurocognitive areas of the brain during cranial radiation
Radiation oncologists at Rush University Medical Center are intent on finding ways to avoid damage to the critically important hippocampus and limbic circuit of the brain when cranial radiation is required to treat existing or potential metastatic cancers.
Study of concurrent radiotherapy, chemotherapy shows promise in small cell lung cancer
Treating limited stage small cell lung cancer(LSCL) with a combination of accelerated high-dose radiotherapy and chemotherapy has shown encouraging results.
Stereotactic radiotherapy offers noninvasive, effective treatment for frail patients with early-stage lung cancer
Stereotactic body radiation therapy (SBRT) should be considered a new standard of care for early-stage lung cancer treatment in patients with co-existing medical problems, according to results from a national clinical trial led by UT Southwestern Medical Center physicians.
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