Gastric Cancer

self sufficiency from growth signals, resistance to antigrowth signals, metastasis, tissue invasion and sustained angiogenesis (formation of new blood vessels)

Adenocarcinoma (ADC) and squamous cell carcinoma (SCC)

Barret’s Metaplasia (therefore obesity, drugs that relax LOS etc), gender

fruit, vegetables, antioxidants, H.Pylori (reduces risk of ADC if present in corpus due to it causing hypochloridria)

SCC - distal 2/3 to the stomach, ADC proximal third to the LOS

E-Cadherin is a key cadherin in the cadherin zipper component of adherence junctions which holds cells together Suppression of E cadherin can lead to EMT via: inherited E cadherin mutation = hereditary diffuse type gastric carcinoma other epigenetic events e.g. hypermethylation of promoters or expression of SNAIL and SLUG - EMT regulators that supress E cadherin expression

Red meat, aging, obesity and alcohol

Familial Adenomatous Polyposis Coli

Adenomatous Polyposis Coli (APC), is part of a family of proteins which bind to B-catenin in the cytoplasm to direct in to the ubiquitin proteasome pathway if not bound B catenin bind to a TF which migrates into the nucleus and causes transcription of immediate early genes (cyclins) which drive uncontrolled cell proliferation therefore APC binding stops this and is a tumour suppressor gene inherited familial mutations in APC leads to uncontrolled cell proliferation, developing multiple begnin growths along the GI tract which can turn cancerous

removal of parts of the intestine via prophylactic surgery to prevent cancer, however pops can grow in other areas

cetuximab - binds to EGFR a RTK to prevent the activation of K RAS in tumours which causes uncontrolled cell proliferation this treatment only works in tumours related to EGFR mutation / overexpression, in cases such as K RAS switch mutation so that it is always active this treatment is unhelpful