The molecular basis of cancer 1

===Lecture Details ===
Caroline Speed; Week 8 MED1011; Biochemistry
===Lecture Content===
DNA damage can be inherited in germ line errors or somatic in acquired mutations. As a person gets older the number of DNA mutations increases causing an increased risk of cancer. Acquired mutations may eventually lead to cancer. They are not passed to offspring. Acquired damage can be induced by radiation, viruses, bacteria, chemical carcinogenesis, age, diet, UV light. High fat, low fiber, obesity and chronic inflammation predispose to cancer. DNA repair enzymes correct these errors, however if there is mutations, loss of repair enzymes, less time for repair mechanisms, accumulation of mutations occurs. Cancer cells have a rapid cell cycle and accumulate more genetic damage. 
Viruses can be causal agents in some cancers, may account for 15% of cancer. Viral infection can be latent and may replicate. Liver cancer associated with hep B, lymphoma/nasopharyngeal with EBV, anogenital with papillomavirus. Viruses can affect DNA- alter critical genes that effect cell growth, can be inserted upstream of an expression protein, can activate replication machinery.
Familial aggregation of mutations occurs: several close or first degree relatives with a common cancer, several close or first degree relatives with related cancer, two members of the same family with the same rare cancer, early onset, bilateral cancers, tumours in two different organs in same person. Cancer has both genetic and environmental influences for expression of phenotype. Some cancers are common, penetrance is variable. BRCA 1 is on 17q, BRCA 2 is on 13q. Lifetime risk of these genes is 83-88% by age 70. Ovarian risk in these groups is 16-60% lifetime.
Gene testing for these is optimally to test youngest affected family member. Not considered appropriate for unaffected family members.
===Readings===