The document discusses carcinoma of the colon, including risk factors like diet, hereditary syndromes, and inflammatory bowel diseases. It describes the adenoma-carcinoma sequence and microsatellite instability pathways of pathogenesis. Clinical features, gross findings, microscopy, investigations, staging, spread, and treatment approaches are summarized. Two case studies are presented and diagnosed as probable carcinoma of the cecum and descending colon respectively based on described features.

1. CARCINOMA COLON
DR.N.MANJULA

2. CONTENTS
 RISK FACTORS
 PATHOGENESIS
 CLINICAL FEATURES
 GROSS
 MICROSCOPY
 INVESTIGATION
 STAGING
 SPREAD
 TREATMENT
 SUMMARY

3. CASE HISTORY
 On a routine health checkup and
laboratory evaluation, a 65-year-old
male was found to be having microcytic
hypochromic anemia. His stool sample
was positive for occult blood. A
colonoscopy was performed and
showed a 4 cm bulky, exophytic
(cauliflower-like), polypoid lesion
projecting into the cecum. Biopsy was
performed and microscopic examination
confirmed the clinical suspicion.
 What is the probable diagnosis?
 A 70-year-old man complained of change in
bowel habits for the past one year. He also
complained that the defecation was more
difficult. Physical examination, did not reveal
any significant findings. His stool sample was
examined for occult blood and was found to
be positive. Colonoscopy showed an annular
lesion encircling the descending colon.
Biopsy examination confirmed the diagnosis
and was followed by colonic resection.
 What is the probable diagnosis?

4. RISK FACTORS
 Diet–Animal fat
 Insulin resistance
 Fiber
 Deficiencies of vitamins A, C and E
 Hereditary syndromes
 Polyposis coli
 MYH-associated polyposis
 Nonpolyposis syndrome (Lynch’s syndrome)
 Inflammatory bowel disease
 Ulcerative colitis and
 Crohn disease
Decreased fibre =
decreased stool bulk
 alters the
composition of
intestinal microbiota
and increased
synthesis of toxic by
products  long
contact with intestinal
mucosa  cancer.
Increased fat intake  increased
hepatic synthesis of cholesterol
and bile acids  converted to
carcinogen by intestinal bacteria.

5. RISK FACTORS
 Others
 Streptococcus bovis bacteremia
 Increasing age
 Family history of colonic cancer in first degree relative
 Prior colorectal cancer
 Factors that reduces the risk
 Dietary factors - Diets rich in cruciferous vegetables (e.g., cauliflower,
Brussels sprouts and cabbage) and vitamin A
 Protective effect of aspirin or other NSAIDs Polyp
regression
in FAP

6. PATHOGENESIS
 Two distinct genetic pathways have been described:
1. Classic adenoma carcinoma sequence
2. Microsatellite instability pathway

7. ADENOMA –CARCINOMA SEQUENCE

8. MICROSATELLITE INSTABILITY PATHWAY

10. CLINICAL FEATURES
 LEFT SIDED COLON CANCER
Annular
Napkin ring constriction
Ulcerated in mid region
Distal colon – annular lesions causing ‘napkin-
ring’ constriction.
These produce occult bleeding, altered
bowel habits or pain and discomfort in
the left lower quadrant.
 RIGHT SIDED COLON CANCER
Microsatellite instability
Polypoidal ,exophytic
Proximal colon – polypoid, exophytic masses.
Present with fatigue and weakness due
to iron deficiency anemia.
Iron deficiency anemia in an older man
or postmenopausal woman should be
considered due to GI cancer until
otherwise proved.

11. GROSS
• Exophytic polypoid mass in the right-side of colon
Tumors in the proximal colon usually grow into the
lumen as bulky, exophytic (cauliflower-like), polypoid masses and extend
along one wall of the cecum and ascending colon. They rarely cause
intestinal obstruction.
• Annular and constricting tumors in the left-side of colon
These tumors are annular lesions that produce the
characteristic “napkin-ring” constrictions and luminal narrowing. It may be
associated with intestinal obstruction and dilatation with attenuation and
flattening of the mucosal folds of colon proximal to the tumor. The tumors
are firm due to associated desmoplasia.

12. Diffuse/tubular tumors
These are similar to linitis plastica of the stomach. They
show diffuse flattening and thickening of the colon, initially involving the
mucosa, but later involve the entire wall of intestine.
Infiltrative and ulcerating tumors
These cancers are usually raised, have irregular edges and
a central, excavated ulcerated area that often infiltrate the deep layers of the
bowel wall.

14. MICROSCOPY
 Majority are adenocarcinomas.
 Well-differentiated, Moderately or Poorly differentiated.
 Most of the tumors show glands of variable size separated by moderate
amount of stroma. Mitotic figures are usually abundant.
 The invasive component of these tumors may show stromal desmoplasia
→ causes firm consistency.
 Mucinous adenocarcinomas secrete abundant mucin and accumulate
within the intestinal wall and are associated with poor prognosis.
 Signet-ring carcinoma consists of signet-ring cells similar to those in
gastric cancer.

16. INVESTIGATION
1. Occult blood loss in the stool by Guaiac test.
2. Tumor markers: Carcinoembryonic antigen (CEA) and CA 19-9.
3. Flexible sigmoidoscopy
4. Colonoscopy helps in direct visualization of cancer and may be used to take a biopsy:
Investigation of choice.
5. Radiology:
 Double-contrast barium enema:
It is the radiological investigation of choice, when colonoscopy is
contraindicated. It characteristically shows “apple core” appearance.
 Ultrasonography:
Used as a screening investigation for liver metastases.
 Spiral CT:
In elderly patients when contrast enemas or colonoscopy are not diagnostic
or are contraindicated.

17. PROGNOSIS
 Depth of invasion
 Lymph node metastases.
 Invasion into the muscularis propria reduces the survival rate which
is reduced further in the presence of lymph node metastases.
 Poorly differentiated and mucinous carcinomas are associated with
poor prognosis.
 Dukes and Astler-Coller staging are being used presently replaced
by TNM (tumor-nodes-metastasis) classification and staging system
from the American Joint Committee on Cancer.

18. STAGING
 TNM
 DUKE
 MODIFIED DUKE’S BY ASTLER AND COLLER

21. SPREAD
 Direct spread: The tumor can spread in a transverse, longitudinal, or radial
direction.
 Lymphatic spread: Tumor may spread through lymphatics into the regional
lymph nodes.
 Blood spread: Venous invasion may give rise to blood-borne metastases in
the liver, lungs and bones.
 Transcoelomic spread: Rarely, it can spread by dislodging tumor cells from
the serosa of the bowel or via the subperitoneal lymphatics to other
structures within the peritoneal cavity.

22. TREATMENT
 SURGERY
 CHEMOTHERAPHY
 RADIOTHERAPHY

23. CASE 1
 On a routine health maintenance examination and laboratory evaluation, a
65-year-old male was found to be having microcytic hypochromic anemia.
His stool sample was positive for occult blood. A colonoscopy was
performed and showed a 4 cm bulky, exophytic (cauliflower-like), polypoid
lesion projecting into the cecum. Biopsy was performed and microscopic
examination confirmed the clinical suspicion. It was followed by colonic
resection.
 What is the probable diagnosis?
Ans: Carcinoma of colon /cecum- Exophytic polypoid type.

24. CASE 2
 A 70-year-old man complained of change in bowel habits for the past one
year. He also complained that the defecation was more difficult and the
caliber of stools has decreased. Physical examination, did not reveal any
significant findings. His stool sample was examined for occult blood and
was found to be positive. Colonoscopy showed an annular lesion
encircling the descending colon. Biopsy examination confirmed the
diagnosis and was followed by colonic resection.
 What is the probable diagnosis?
Ans: Carcinoma of descending colon-annular type.

25. SUMMARY
 Clinical features
Right sided colon cancers: symptoms related to iron-deficiency anaemia
Left sided colon cancers: occult bleeding, cramp/pain, altered bowel habits
 Staging
TNM/ Dukes and Astler-Coller modification of Dules system – AJCC staging system
 Prognosis
Depends on depth of invasion and lymph node metastasis.
 Familial cancers
Familial adenomatous polyposis (FAP)
APC mutation
Hereditary non-polyposis colorectal cancer (HNPCC)
DNA mismatch repair gene mutations