L18 colorectal carcinoma


Published on

Published in: Health & Medicine, Technology
  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

L18 colorectal carcinoma

  1. 1. Colorectal CarcinomaLecture 18
  2. 2. ColorectalCarcinomaAdenocarcinoma 98%
  3. 3. Intestinal tumorsNon-neoplastic PolypsHyperplastic polypsHamartomatous polypsJuvenile polypsPeutz-Jeghers polypsInflammatory polypsLymphoid polypsNeoplastic Epithelial LesionsBenign polypsAdenomasMalignant lesionsAdenocarcinomaSquamous cell carcinoma of the anusOther TumorsGastrointestinal stromal tumorsCarcinoid tumorLymphomaEpithelial tumors of the intestines:major cause of morbidity and mortality worldwideColon, including rectum:host to more primary neoplasms than any otherorgan in the body
  4. 4. AdenocarcinomaAdenocarcinoma is a cancer of an epithelium thatoriginates in glandular tissue, adeno means gland.• 98% of all cancers in large intestine almost alwaysarise in adenomatous polyps, generallycurable by resection
  5. 5. EpidEmiology• Old age: peak incidence: 60 to 70 years of age• < 20% cases before age of 50• adenomas – presumed precursor lesionsfor most tumors• males affected ≈ 20% more often thanfemales
  6. 6. Epidemiology cont….•worldwidedistribution• highest incidence rates in United States,Canada, Australia, New Zealand, Denmark,Sweden, and other developed countries
  7. 7. Risk Factors for High grade dysplasia and cancerLarge Size - > 1 cm in diameter are risk factor forcontaining CRCVillous histology – adenomatous polyps with > 25percent villous histology are a risk factor fordeveloping CRCHigh-grade dysplasia – adenomas with high-gradedysplasia often coexist with areas of invasive cancerin the polyp.Number of polyps: three or more is a risk factor
  8. 8. Etiology•I. Genetic influences:– preexisting ulcerative colitis or polyposis syndrome– hereditary nonpolyposis colorectal cancer syndrome(HNPCC, Lynch syndrome) → germ-line mutations ofDNA mismatch repair genes
  9. 9. Etiology cont.II. Environmental influences:– A. dietary practices1. low content of unabsorbable vegetable fiber2. corresponding high content of refined carbohydrates3. high fat content4. decreased intake of protective micronutrients (vitaminsA, C, and E)– B. use of Aspirin®and other NSAIDs: protectiveeffect against colon cancer?• cyclooxygenase-2 & prostaglandin E2
  10. 10. Morphology• 25% : in cecum or ascending colon• 25%: in rectum and distal sigmoid• 25%: in descending colon and proximalsigmoid• 25%: scattered elsewhere• multiple carcinomas present → often atwidely disparate sites in the colon
  11. 11. Morphology cont.• all colorectal carcinomas begin as in situ lesions• tumors in the proximal colon: polypoid, exophyticmasses that extend along one wall of the cecum and ascendingcolon
  12. 12. Morphology cont.• in the distal colon: annular, encircling lesions thatproduce “napkin-ring” constrictions of the bowel andnarrowing of the lumen
  13. 13. Morphology cont.Both forms of neoplasm eventuallypenetrate the bowel wall andmay appear as firm masses on theserosal surface
  14. 14. Morphology cont.• all colon carcinomas - microscopically similar• almost all - adenocarcinomas• range from well-differentiated toundifferentiated, frankly anaplastic masses• many tumors produce mucin• secretions dissect through the gut wall, facilitateextension of the cancer and worsen theprognosis
  15. 15. Squamous CellCarcinomaSquamous Cell Carcinoma of the anus:Cancers of the anal zone arepredominantly squamous cell inorigin.
  16. 16. Clinical Features• may remain asymptomatic for years• symptoms develop insidiously• cecal and right colonic cancers:– fatigue– weakness– iron deficiency anemia• left-sided lesions:– occult bleeding– changes in bowel habit– crampy left lower quadrant discomfort
  17. 17. Clinical features cont.Anemia in females may arise from gynecologiccauses, but it is a clinical maxim thatiron deficiency anemia in an older man meansgastrointestinal cancer until proved otherwise
  18. 18. Clinical Features• spread by direct extension intoadjacent structures and by metastasisthrough lymphatics and blood vessels• favored sites for metastasis:– regional lymph nodes– liver– lungs– bones– other sites including serosalmembrane of the peritoneal cavity• carcinomas of the anal region →locally invasive, metastasize toregional lymph nodes and distantsitesTNM Staging of Colon CancerTumor (T)T0 = none evidentTis = in situ (limited to mucosa)T1 = invasion of lamina propria or submucosaT2 = invasion of muscularis propriaT3 = invasion through muscularis propria intosubserosa or nonperitonealized perimusculartissueT4 = invasion of other organs or structuresLymph Nodes (N)0 = none evident1 = 1 to 3 positive pericolic nodes2 = 4 or more positive pericolic nodes3 = any positive node along a named blood vesselDistant Metastases (M)0 = none evident1 = any distant metastasis5-Year Survival RatesT1 = 97%T2 = 90%T3 = 78%T4 = 63%Any T; N1; M0 = 66%Any T; N2; M0 = 37%Any T; N3; M0 = data not availableAny M1 = 4%
  19. 19. Diagnosis– digital rectal examination– fecal testing for occult blood loss– barium enema, sigmoidoscopy and colonoscopy– confirmatory biopsy– computed tomography and other radiographicstudies
  20. 20. Diagnosis cont.– serum markers (elevated blood levels ofcarcinoembryonic antigen)– molecular detection of APC mutations in epithelialcells, isolated from stools–tests under development: detection of abnormalpatterns of methylation in DNA isolated from stoolcells
  21. 21. Treatment1. Chemotherapy2. Radiotherapy3. Photodynamic therapy4. Radical surgery5. Gene therapy