A team of medical researchers has identified a biomarker that may help in monitoring the response of mutated BRAF gene to BRAF-targeted treatment.
BRAF is a human gene that prepares a protein called B-RAF, involved in sending signals inside growth-promoting cells. However, a faulty gene may cause cancer and congenital anomalies. Melanoma, a serious form of skin cancer, is known to be associated with a defective BRAF gene. This new discovery could help doctors to plan the appropriate kind of treatment for the condition.
The results of the study have been presented at the 2013 AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics on October 19-23 in Boston, Massachusetts. In nearly 50% of cases of melanomas, the BRAF gene undergoes mutation. So far, two medically approved drugs have been used against these faulty genes as a part of treatment in the US. The BRAF-targeted medications may, however, not work in all patients and the disease could relapse after acquiring resistance against them.
Assistant professor, Dr. Ryan Corcoran, at the Massachusetts General Hospital Cancer Center and Harvard Medical School in Boston believes that their study has recognized reduced phosphorylation of the protein S6 post drug treatment. This is possible only through the new functional biomarker that speculates sensitivity of the defective genes to these drugs. Most importantly, Corcoran and colleagues have engineered a less invasive technique to identify any modifications occurring inside the malignant tumors. This is achievable only after knowing the treatment results. Based on the response of the patients to a BRAF-targeted drug, the treatment procedure could be changed or hastened.
Uncontrolled division of cells is the main cause of cancer. In case of melanoma, mutated genes mislead the BRAF proteins and impair the function of various tumor proteins. In this study, the response of the BRAF-mutant cells exposed to a drug called vemurafenib was examined. There was a marked decrease in phosphorylation in the protein S6. The same test was conducted on tumor biopsies of 9 patients with BRAF-mutant melanomas before and after treatment. Out of 9, the S6 phosphorylation of 6 patients lowered drastically.
The last part of the research involved a real-time method coupled with fine-needle aspiration biopsies to monitor changes in S6 phosphorylation in tumor cells. This was, however, done before and during first 2 weeks of BRAF-targeted drug treatment. Findings of the study showed a decrease in phosphorylation post-treatment.
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