Most recent advances in cancer treatment tend to target tumors at the primary site of origin.But 9 out of 10 deaths occurs in cancer patients due to the spread of cancer cells from the primary site to other parts of the body and subsequent establishments of secondary tumors, a process otherwise known as metastasis.Metastasis is one of the major constraints in cancer treatment.If cancer cells could be stopped from spreading to other parts,it could greatly enhance the survival chances of millions of cancer patients.
Research in this area has been rather sluggish. But recently scientists from Britain have been able to solve the puzzle of cancer spreading.They have found through their study that a protein called p53 plays a very important role in the detachment of cancer cells from the point of origin.p53 is a tumor suppressor protein that helps protect against cancer in healthy people. It was found that in majority of the cancer patients a mutation occurs in the gene that codes for p53 that leads to an altered p53 that has lost its functions. The research, published in the peer-reviewed journal Cell last week, was carried out by two teams of experts working side by side in the pioneering Cancer Research UK institute. Professor Karen Vousden, co-author and the P53 expert was also involved in the research.
Professor Vousdens team was also joined by integrin experts.The integrins constitute a family of receptor proteins tha function in cell-to-cell and cell-to-extracellular matrix (ECM) adhesive interactions and transduce signals from the ECM to the cell interior and vice versa. Hence, the integrins mediate the ECM influence on cell growth and differentiation. Tumor progression leading to metastasis appears to involve equipping cancer cells with integrin for interaction with the ECM.The study showed that mutation in p53 encourages the movement of integrins along with growth factor receptors into the cell.This is mediated by another protein called rab coupling protein(RCB). Therapies directed at influencing integrin cell expression and function are presently being explored for inhibition of tumor growth, metastasis, and angiogenesis.
Professor Jim Norman, co-author and the integrin and RCP expert, said: “Until now the integrin and P53 fields have sat apart. This research pulls them together. Drugs that simply block the movement of cells won’t work; that’s like blocking the barn door after the horse is bolted. We now know that we must find drugs that can seek out cells which are inappropriately on the move, and then kill them.”