Theme 1 - Part II Flashcards
Women
Breast
Lung
Men
Prostate
Lung
Bowel cancer risk factors [4]
Migration
Food rich in red meat
Food rich in veg, fruit and fibre
Physical activity and lower BMI
Bowel cancer risk factors - conditions [5]
Longstanding ulcerative colitis Crohn’s disease – to a lesser extend than UC Presence of adenoma in the large bowel Previous history of bowel cancer surgery Family history of bowel cancer Old age
High fibre diet [3]
SCFA - induce differentiation, arrest growth of cells and cause apoptosis
Stool bulk: Shorter transit time
Reduce 2ndary BA formation - potentially carcinogenic
Polyp
protrusion into a hollow viscus; can be benign adenoma or malignant
Dysplasia
the cells have morphological features of cancer but without invasion
- low grade
- high grade
Pathological features of polyps [4]
Hyperplastic – more goblet cells than normal mucosa; has a lace - like pattern
Tubular adenoma – has test tube appearance
Villous adenoma – has finger-like appearance
Tubulovillous adenoma – a mixture of the
above
Adenocarcinoma Sequence
Normal mucosa -> adenoma -> cancer
Morphological featyre mirror genetics
Adenocarcinoma Sequence evidence
Peak incidence of polyp predates the cancer e.g. peak age for adenomas is 60, median age for bowel cancer is 71years
Residual adenoma is found in early invasive cancer
Risk of cancer is directly related to the number of polyps e.g. FAP with multiple polyps
Programmes which follow-up patients and remove adenomas reduce the incidence of bowel cancer
Familial Adenomatous Polyposis [5]
Peak incidence 500-2,500 polyps in bowel
Polyps dysplastic = adenoma
100% risk of development of cancer by age of 30
Prophylactic colectomy around 20years
FAP contributes to 1% of bowel cancer
Risk of cancer in the duodenum
Genetics of FAP in Carcinogenesis
Chr 5q21 - AP Coli gene
Germ cell and then somatic
Hereditary non-Polyposis Colorectal Cancer (HNPCC)/Lynch Syndrome
Familial cancer affecting predominantly the caecum and right colon, before the age of 50
Associated with endometrial, ovarian, small bowel and cancer of the urinary tract.
2-3%
Genetics of HNPCC
During replication the DNA base pairs can mismatch e.g. G – T instead G – C
There are mismatch repair genes which act as ‘spell checkers’ and correct these mismatches
MSH2 (2p16) and MLH1 (3p21) genes account for 30% of the HNPCC
PMS1 and PMS2 are the other genes involved in HNPCC
Amsterdam Criteria [4]
3+ relatives - 1 first degree of other 2
2+ successive generations
Cancer in one or more affected relatives should be diagnosed before the age of 50 years;
Familial adenomatous polyposis should be excluded in any cases of colorectal cancer
