ABSTRACT:
In the human anatomy, skin is the external cover of the body acting as a mechanical barrier. In a normal cellular process, cell grows, proliferates and dies. However, mutated cells as a substitute of dying, begin to grow and multiply faster than the normal cells. These fast-growing cells accumulate to form tumors. Skin cancer has been reported as the most commonly occurring cancer against the incidence rate of breast, lung, colon and prostate cancer together. Although melanoma is less common but it is a more life-threatening cancer. Melanoma cancer begins in the melanocytes. A gene BRAF produces BRAF protein which is involved in Ras- activated protein kinase cascade regulating cell growth factors, hormones and cytokines through Raf-MEK-ERK signal transduction pathway. BRAF belongs to serine/threonine kinase family. Thus, a continuously activated BRAF protein leads to uncontrolled cell growth. Indicating, that the BRAF protein is highly responsible for melanoma. The tumor cells of melanoma are composed of a higher number of BRAF molecules than normal cells. Mutation in BRAF leads to anan unrestrained proliferation of cells leading toa tumor. A comparative studyof the inhibitors using computational tools helps to design BRAF specific inhibitor for melanoma treatment. A three dimensional model of BRAF and its association on the target site with inhibitor provides an effective complex formation. Thus, results obtained via different computational tools reveal the mechanism of BRAF and propound inhibitors for melanoma with further experimental studies.