The analyzed molecular alterations have been largely demonstrated to play an important role in: a) deregulating the cell cycle with subsequent induction of abnormal cell proliferation and tumour growth (ERK1-2 phosphorilation and CyclinD1 amplification); b) impairing the apoptotic machinery with subsequent induction of resistance to anticancer agents (p53 downexpression and survivin overexpression); and c) promoting metastasis formation (h-prune amplification). Here, CCND1 is linked to neoplasm.