There are likely a number of reasons for this, including signalling pathways that only influence a subset of tumours types (e.g. those responsive to hormonal signalling) or different mutations/ amplifications/ deletions that increase cell cycle activity in a similar way but in different tumour types (e.g. cyclin D1 amplifications in Oesophageal carcinoma and cyclin E1 amplifications in Uterine Carcinosarcoma). This evidence concerns the gene CCNE1 and neoplasm.