colon cancer Flashcards
DIAGRAM colorectal crypts of lieberkuhn
stem cells at the bottom are proliferating, and at top there’s differentiaition eg goblet cells
cell turnover+ significance
very high in colon, so vulnerable to mutations
polyps vs adenomas
projection of mucosal surface vs benign neoplasm of mucosal epithelial cells (type of polyps)
types of polyps
adenomas, hyperplastic, lipomas
hyperplastic polyps
most polyps, no chance of malignancy
DIAGRAM types of adenomas
either tubular (has lots of tubules) or villous- tubular is adenoma of columnar vs mucinous cells- form tubules vs finger-like extensions
adenomatous polyposis coli- what is it, significance, and treatment
thousands of polyps- almost certain to get carcinoma, so must be removed
microsatellite instability and cause
microsatellites are repeat sequences that often mutate, and if there’s mismatch repair genes (problem with repair genes), it leads to microsatellite instability- this occurs due to something called HNPCC/lynch syndrome
adenoma-carcinoma sequence
initially, there is mutation in APC gene (TMS gene)- adenoma then forms due to K-ras mutation (oncogene)- p53 mutation then occurs (TMS), leading to carcinoma
genetic influences to colon cancer
either FAP/APC mutation (adenoma to carcinoma) or HNPCC/lynch syndrome (microsatellite instability)
how APC mutation may cause cancer
beta catenin normally in cytoplasm- if APC mutation occurs, beta catenin moves into nucleus and more proliferation occurs
p53 mutation paradox
cells with more P53 more vulnerable to cancer, as body tries to respond to increased proliferation by producing more P53, but it’s defective
link between fat consumption and colon cancer
theres a positive correlation
dietary deficiency and signficance
lack folates in diet can lead to deficiency in MTHFR gene
link between age and colon cancer
incidence increases with age
