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Colorectal Carcinoma

Samuel Onedes S.

Alexander B. A.

Denny Setyadi
Intestinal tumors
Non-neoplastic Polyps
Hyperplastic polyps
Hamartomatous polyps
Juvenile polyps
Peutz-Jeghers polyps

Epithelial tumors of the intestines: Inflammatory polyps

major cause of morbidity and Lymphoid polyps
mortality worldwide Neoplastic Epithelial Lesions
Benign polyps
Malignant lesions
Colon, including rectum: Adenocarcinoma
host to more primary neoplasms Squamous cell carcinoma of the anus
than any other organ in the body
Other Tumors
Gastrointestinal stromal tumors
Carcinoid tumor

 98% of all cancers in large intestine

 almost always arise in adenomatous polyps,
generally curable by resection

 peak incidence: 60 to 70 years of age

 < 20% cases before age of 50
 adenomas – presumed precursor lesions for
most tumors
 males affected ≈ 20% more often than females

 worldwide distribution
 highest incidence rates in United States,
Canada, Australia, New Zealand, Denmark,
Sweden, and other developed countries
Risk Factors

 Genetic Predisposition:
◦ Hereditary Polyposis Syndrome:
 Familial Adenomatous Polyposis (FAP)
 Gardner’s syndrome (osteoma, skin tumor, intestine polyposis)
 Turcot’s syndrome (colonic tumors and brain tumors, is also
linked to medulloblastoma)
◦ Hereditary Nonpolyposis Syndrome (HNPCC):
 Lynch I (limited to the colorectum)
 Lynch II (coexist with extracolonic tumors, typically endometrial
Risk Factors

◦ Acquired Somatic Syndrome

◦ Peutz-Touraine-Jeghers Syndrome
◦ Juvenile Polyposis
◦ Family History of Colon Carcinoma or Polyps
Predisposing Medical

 Premalignant conditions:
◦ Inflammatory Bowel Disease
◦ Ulcerative colitis
 Incidence of neoplasia in pancolitis patients is 10% by 20
years’ duration of disease
 More difficult to find in early stage  35% are Dukes C
and D lesions
◦ Granulomatous colitis:
 Crohn’s disease
 Overall incidence is 7% over 20 years’ duration of Crohn’s
Predisposing Medical

 Non-Cancer Surgery:
◦ Some studies suggest that cholecystectomy
increases the incidence of colorectal cancer. The
relationship between cholecystectomy and
colorectal carcinoma is controversial.

 environmental influences:
◦ dietary practices
 low content of unabsorbable vegetable fiber
 corresponding high content of refined carbohydrates
 high fat content
 decreased intake of protective micronutrients (vitamins A, C,
and E)
◦ use of Aspirin® and other NSAIDs: protective effect
against colon cancer?
 cyclooxygenase-2 & prostaglandin E2

 chromosome instability pathway


 mismatch repair (microsatellite instability) pathway


 25% of colorectal carcinomas: in cecum or

ascending colon
 similar proportion: in rectum and distal sigmoid
 25%: in descending colon and proximal sigmoid
 remainder scattered elsewhere
 multiple carcinomas present → often at widely
disparate sites in the colon

 all colorectal carcinomas begin as in situ lesions

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

 in the distal colon: annular, encircling lesions that

produce “napkin-ring” constrictions of the bowel and
narrowing of the lumen
 both forms of neoplasm eventually penetrate the
bowel wall and may appear as firm masses on the
serosal surface

 all colon carcinomas - microscopically similar

 almost all - adenocarcinomas
 range from well-differentiated to undifferentiated,
frankly anaplastic masses
 many tumors produce mucin
 secretions dissect through the gut wall, facilitate
extension of the cancer and worsen the prognosis
 cancers of the anal zone are predominantly
squamous cell in origin

 >90% are adenocarcinomas

 4 morphologic variants:
◦ Ulcerative:
Descending & sigmoid colon
◦ Exophytic (polypoid/ fungating):
Ascending colon (caecum)
◦ Annular (scirrhous):
Descending colon
◦ Other:
 mucoid (colloid); signet-ring cell; adenosquamous;
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
 anemia in females may arise from gynecologic causes, but it is a
clinical maxim that iron deficiency anemia in an older man means
gastrointestinal cancer until proved otherwise
Clinical Features
TNM Staging of Colon Cancer

Tumor (T)
 spread by direct extension into T0 = none evident
Tis = in situ (limited to mucosa)
adjacent structures and by T1 = invasion of lamina propria or submucosa
metastasis through lymphatics T2 = invasion of muscularis propria
T3 = invasion through muscularis propria into
and blood vessels subserosa or nonperitonealized perimuscular
 favored sites for metastasis: T4 = invasion of other organs or structures
 regional lymph nodes
Lymph Nodes (N)
 liver 0 = none evident
1 = 1 to 3 positive pericolic nodes
 lungs 2 = 4 or more positive pericolic nodes
 bones 3 = any positive node along a named blood vessel
 other sites including serosal Distant Metastases (M)
membrane of the peritoneal 0 = none evident
1 = any distant metastasis
 carcinomas of the anal region → 5-Year Survival Rates
T1 = 97%
locally invasive, metastasize to T2 = 90%
regional lymph nodes and T3 = 78%
T4 = 63%
distant sites Any T; N1; M0 = 66%
Any T; N2; M0 = 37%
Any T; N3; M0 = data not available
Any M1 = 4%
Clinical Features

 detection and diagnosis:

 digital rectal examination
 fecal testing for occult blood
 barium enema, sigmoidoscopy
and colonoscopy
 confirmatory biopsy
 computed tomography and
other radiographic studies
 serum markers (elevated blood
levels of carcinoembryonic
 molecular detection of APC
mutations in epithelial cells,
isolated from stools
 tests under development:
detection of abnormal patterns
of methylation in DNA isolated
from stool cells
 Modified Astler-Coller classification of the DUKES
staging system:
Stage Description
A Lesion not penetrating submucosa

B1 Lesion up to, but not through, serosa

B2 Lesion through serosa, with involvement of adjacent organs

C1 Lesion up to, but not through, serosa; regional lymph node

C2 Lesion through serosa, with involvement of adjacent organs;
regional lymph node metastasis
D Distant metastatic disease

Cancer: Principles & Practice of Oncology 6th Ed., 2001


 Futher modified Astler-Coller by Gunderson

and Sosin in DUKES system, subdividing the
patients based on the presence of microscopic
(B2m or C2m) and gross penetration (B2m + g,
and C2m + g) through the bowel wall.

SOURCE: Cancer: Principles & Practice of Oncology 6th Ed., 2001

TNM system:
 Primary tumor (T):
◦ T1 Invades submucosa
◦ T2 Invades muscularis propria
◦ T3 Invades subserosa but not through serosa
◦ T4 Invades through serosa into free peritoneal cavity into
contiguous organ
 Regional lymph nodes (N):
◦ N0 No lymph node metastases
◦ N1 Lymph node metastases in 1-3 nodes
◦ N2 Lymph node metastases in 4 or more nodes
◦ N3 Lymph node metastases in central nodes
 Distant metastases (M):
◦ M0 No distant metastases
◦ M1 Distant metastases present
Tumor, Node,
Metastasis Stage
Stage Tumor (T) Lymph Nodes Metastasis
(N) (M1)
0 Tis N0 M0
I T1 N0 M0
T2 N0 M0
II T3 N0 M0
T4 N0 M0
III Any T N1 M0
Any T N2 M0
IV Any T Any N M1
Cancer: Principles & Practice of Oncology 6th Ed., 2001
Surgical Treatment

 Operative surgery (laparotomy or laparoscopic

resection) is the primary option
 For colon:
◦ Right hemicolectomy
◦ Right radical hemicolectomy 5-YSR:
◦ Transverse colectomy T1-T2 in node-
negative disease:90%
◦ Left hemicolectomy T3: 80%
Node (+): 27-69%
◦ Low anterior resection Unresectable-
◦ Subtotal colectomy metastatic disease:
… 5-YSR:
Node (-): 75-90%
Node (+): 30%
Recurrence rate:
 For rectum: 10-50%
◦ Approaches:
 Abdominoperineal resection
 Low anterior resection
 Coloanal anastomosis
 Transanal approaches
 Transsacral approaches (York-Mason, Kraske)
◦ Procedures:
 Sphincter-Preservation procedure
 Colonic J Pouch

 chemotherapy
 radiotherapy
 radical surgery
 gene therapy
True or false?

98% of all cancers in the large intestine are adenocarcinomas.

Use of Aspirin® and other NSAIDs may cause development of

colon cancer.

Chromosome instability and the mismatch repair are two

carcinogenesis pathways.

Tumors in the proximal colon tend to be annular, encircling

lesions that produce “napkin-ring” constrictions of the bowel and
narrowing of the lumen, while those in the distal colon tend to
grow as polypoid, exophytic masses.

Colorectal carcinoma may remain asymptomatic for years.


 Elsevier. Kumar et al: Robbins Basic Pathology 8e