POLYPS 3

lpeak incidence: 60 to 70 years of age

l< 20% cases before age of 50

ladenomas – presumed precursor lesions for most tumors

lmales affected ≈ 20% more often than females

 lworldwide distribution

lhighest incidence rates in United States, Canada, Australia, New Zealand, Denmark, Sweden, and other developed countries

lgenetic influences:

lpreexisting ulcerative colitis or polyposis syndrome

lhereditary nonpolyposis colorectal cancer syndrome (HNPCC, Lynch syndrome) → germ-line mutations of DNA mismatch repair genes

lenvironmental influences:

ldietary practices

llow content of unabsorbable vegetable fiber

lcorresponding high content of refined carbohydrates

lhigh fat content

ldecreased intake of protective micronutrients (vitamins A, C, and E)

luse of Aspirin® and other NSAIDs: protective effect against colon cancer?

lcyclooxygenase-2 & prostaglandin E2

 l25% of colorectal carcinomas: in cecum or ascending colon

lsimilar proportion: in rectum and distal sigmoid

l25%: in descending colon and proximal sigmoid

lremainder scattered elsewhere

lmultiple carcinomas present → often at widely disparate sites in the colon

lall colorectal carcinomas begin as in situ lesions

ltumors in the proximal colon: polypoid, exophytic masses that extend along one wall of the cecum and ascending colon

lin the distal colon: annular, encircling lesions that produce “napkin-ring” constrictions of the bowel and narrowing of the lumen

lboth forms of neoplasm eventually penetrate the bowel wall and may appear as firm masses on the serosal surface

lall colon carcinomas - microscopically similar

lalmost all - adenocarcinomas

lrange from well-differentiated to undifferentiated, frankly anaplastic masses

lmany tumors produce mucin

lsecretions dissect through the gut wall, facilitate extension of the cancer and worsen the prognosis

lcancers of the anal zone are predominantly squamous cell in origin