Early molecular changes are thought to include p53 mutation, cyclooxygenase-2 (COX2) overexpression, mitochondrial DNA mutations, and hypermethylation of promotors in tumour suppressor genes, with later events including inactivation of the fragile histidine triad (FHIT) and cyclin-dependent kinase inhibitor 2A (CDKN) tumour suppressor genes as well as loss of regions on chromosomes 9, 18, and 22. The gene discussed is PTGS2; the disease is neoplasm.