 Normally , a cell divides only in response to signals called growth factors and stops growing once in contact with surrounding cells and in response to growth @-@ inhibitory signals . It usually then divides a limited number of times and dies , staying within the epithelium where it is unable to migrate to other organs . To become a cancer cell , a cell has to accumulate mutations in a number of genes ( 3 – 7 ) that allow it to bypass this regulation : it no longer needs growth factors to divide , it continues growing when making contact to neighbor cells , and ignores inhibitory signals , it will keep growing indefinitely and is immortal , it will escape from the epithelium and ultimately may be able to escape from the primary tumor , cross the endothelium of a blood vessel , be transported by the bloodstream and will colonize a new organ , forming deadly metastasis . Although there are some genetic predispositions in a small fraction of cancers , the major fraction is due to a set of new genetic mutations that originally appear and accumulate in one or a small number of cells that will divide to form the tumor and are not transmitted to the progeny ( somatic mutations ) . The most frequent mutations are a loss of function of p53 protein , a tumor suppressor , or in the p53 pathway , and gain of function mutations in the ras proteins , or in other oncogenes . 
