COLON AND RECTAL CANCER:

INCIDENCE:
• Is the 4th most frequently diagnosed cancer in US
• UK – 2nd to lung Ca as cause of death
• New Cases in 2015 – 49,700 Colon & 39,610 Rectal
• The incidence is similar in men and women
• Decreasing Incidence 60.5%(1976) to 46.4% in 2005
• Mortality from CRC -  by ~35% (1990) to
47%(2011)
 INCIDENCE:

• Sporadic : 70-80%
• Family h/o CRC : 15-20% HNPCC : 4-7%
• FAP : 1% IBD & others : 1%
Molecular and genetic pathways are involved in the genesis of
colorectal cancer

• Tumor suppressor genes, DNA mismatch repair genes, and

proto-oncogene all
contribute to colorectal neoplasia, both in the sporadic and
inherited forms
• Adenoma-carcinoma sequence, i.e. adenomatous polyp
progresses to cancer
 COLORECTAL TUMORIGENESIS

•
 COLORECTAL POLYPS

• Colorectal polyps can be

– sporadic or hereditary
– neoplastic or non-neoplastic
• Hyperplastic polyp is the most common of all colorectal polyps
• Tubular adenoma : 65--80%
– most common neoplastic polyp
– are most often pedunculated
– generally less atypia in tubular adenomas
• Tubulovillous :: 10--25%
• Villous adenomas :: 5--10%
– are more commonly sessile
– severe atypia or dysplasia (precancerous cellular change) is found more
often in villous adenomas
 COLORECTAL POLYPS

Bigger the polyp, higher the incidence of invasive carcinoma

• More the villous component, higher the incidence of
carcinoma
 RISK FACTORS:

• Aging☞dominant risk factor with incidence rising steadily after age 50

years
☞ More than 90% of cases diagnosed are in people older than age 50 years
• Hereditary Risk Factors☞80% of colorectal cancers occur sporadically,
20% arise in pts with a known family history of colorectal Ca
• Environmental and Dietary Factors☞observation that colorectal
carcinoma occurs more commonly in populations that consume diets
high in animal fat and low in fiber has lead to the hypothesis that
dietary factors contribute to carcinogenesis
 RISK FACTORS:
• Obesity and sedentary lifestyle dramatically  cancer-
related mortality in a number of malignancies
• Cigarette smoking is associated with an risk of colonic
adenomas, especially after > 35 yrs of use
• Pelvic irradiation may  the risk of developing rectal ca,
although it is unclear if this represents a direct effect of
radiation damage or is instead a correlation between the
development of rectal cancer and a history of another pelvic
malignancy
 RISK FACTORS:

• Alcohol intake and incidence of colorectal carcinoma also has

been suggested
• Inflammatory Bowel Disease ☞long-standing colitis from
inflammatory bowel disease are at  risk for the development
of colorectal Ca
• UC > CD
☞chronic inflammation predisposes the mucosa to malignant
changes and there is some evidence that degree of inflammation
influences☞
 CLINICAL PRESENTATION
• S & Sx are nonspecific and generally develop when the
cancer is locally advanced☞Abdominal pain, bloating, and
other signs of obstruction
• Classic 1st Sx are a change in bowel habits and rectal
bleeding.
• Left-sided tumors are more likely to cause obstruction
because of the caliber of the bowel and the consistency of the
stool, n than are right-sided tumors
• Rectal tumors may cause bleeding, tenesmus, and pain
• Patients may be asymptomatic and/or present with
unexplained anemia, weight loss, or poor appetite.
 DIAGNOSIS
• Guaiac-based fecal occult blood test (gFOBT) & fecal
immunochemical test (FIT): Samples of stool (feces) are
checked for blood, which might be a sign of a polyp or
cancer.
• Double contrast barium enema: This is an x-ray test of
the colon and rectum.
• CT colonography (virtual colonoscopy): This is a type of
CT scan of the colon and rectum
• Colonoscopy/Sigmoidoscopy: A longer, flexible tube is
used to look at the entire colon and rectum
• Endorectal Ultrasound
 STAGING OF COLON CANCER

•
Assess the local and distant extent of disease
• • Thorough History & Physical examination
• • Lab tests -- LFT,, CEA
•
• CT scan of abdomen & pelvis
•
– regional tumor extension
• – regional lymphatic disease
•
– distant metastases
•
– tumor-related complications (e.g., obstruction, perforation, fistula
formation)
• • Chest X--ray (or CT chest) to rule out lung metastasis
•
• Endorectal ultrasound for rectal tumors
•
• PET scans
•
– do not add significant information to CT for preoperative staging of
CRC
 PRE OP STAGING OF RECTAL CANCER

• Similar to colon cancer patients, but with two significant differences:

• (1) distance from the anal sphincters:
• - needs precise location of the cancer with respect to the anal sphincters
• (2) extent of local disease: as determined by
• - depth of penetration into the bowel wall and spread to adjacent LN
• Location of the tumor is
• – best determined with a rigid proctosigmoidoscope
• – accurately measure the exact distance from the tumor to the anal sphincter
• Depth of penetration can be evaluated by
• – Digital rectal examination
• -- superficially invasive tumors are mobile and deeper ones are tethered
• – Endorectal ultrasound (EUS) or MRI (with endorectal coil)
• Local lymph node involvement is determined by
• – Endorectal ultrasound (EUS) or MRI with endorectal coil
TNM Staging
Primary Tumor (T)
•
T1 :invades submucosa
•
T2 :invades muscularis propria
• T3 :invades subserosa or
perirectal tissue
•
T4 :invades other organs
Regional lymph nodes (N)
• N1 : metastasis to 1--3 nodes
•
N2 : metasttasis to > 3 nodes
•
Distant metastasis (M)
•
M0 : no distant metastasis
•
M1 : Distant metastasis
Tis : carcinoma in situ
Dukes Staging
• A : confined to bowel wall
• B : penetrates bowel wall into serosa or
• perirectal fat
• C : lymph node metastasis
• D : Distant metastasis
 TNM STAGING OF COLORECTAL
CARCINOMA AND 5-YEAR SURVIVAL
I T1–2, N0, M0 90 <5

IIA T3–4, N0, M0 74 8

IIB T4 N0 M0  65 15

IIIA T1–2 N1 81 6

IIIB T1–2 N2 69 8

IIIB T3 N1 61 11

IIIC T3 N2 48 15

IIIC T4 N1–2 36 19-22

 TREATMENT

Colon cancer
• Stage I, II : Surgery
• Stage IIB*, III : Surgery followed by chemotherapy
• Stage IV : Any modality as indicated
Rectal Cancer
• Stage I : Surgery
• Stage II, III : Pre-op chemoradiation followed by surgery
• Stage IV : Any modality as indicated
 TREATMENT

• The objective of surgery for colorectal adenocarcinoma is

– removal of the primary cancer with adequate margins
– regional lymphadenectomy
– restoration of the continuity of the gastrointestinal tract by
anastomosis, if indicated
• The extent of resection is determined by
–the location of the cancer
– its blood supply and draining lymphatic system
– presence or absence of direct extension into adjacent organ
 OBSTRUCTING COLON CANCER
1. Resect the colon cancer and do primary anastomosis (1 surgery)
2. Two stage procedure
-- Resect the colon cancer, staple off the distal end and bring the proximal
end as an end colostomy (Hartmann’s procedure) (1st surgery).
- After 6-8 weeks, take down the colostomy and do anastomosis (2nd surgery)
3. Three stage procedure
- Do proximal loop colostomy (1st surgery)
- Prep the bowel and do colon resection and do anastomosis (2nd surgery)
- After 6-8 weeks, take down the colostomy (3rd surgery)
4. Resect the cancer and the entire proximal colon and do
anastomosis of ileum to the distal end (1 surgery)
5. Resect the colon cancer,, do an on--table colon lavage and do
•
primary anastomosis (1 surgery)
 PERFORATED COLON CANCER

Present with peritonitis

• Goal of treatment
– remove the diseased segment of colon
– prevent ongoing peritoneal contamination
• Surgical procedure is
– resect the colon cancer, staple off the distal end and bring the
proximal end as an end colostomy (Hartmann’s procedure)
– thorough peritoneal lavage
• Associated with high rate of local recurrence and overal low
survival
 SURVEILLANCE

• History and Physical

– every 3-6 months x 2 years, then
– every 6 months for a total of 5 years
• CEA
– every 3-6 months x 2 years, then
– every 6 months for a total of 5 years
– only for T2 or greater lesions
 SURVEILLANCE

• Colonoscopy
– in 1 year
– repeat in 1 year if abnormal
– every 2-3 years if normal
– if none was done due to an obstructing lesion, do in 3-6 months post-op
• CT of Chest/Abdomen/Pelvis annually for patients with high risk
features
– lymphovascular invasion
– perineural invasion
– poorly differentiated
 PREVENTION:

• Average Risk
Age ≥ 50y/o
No Hx of Adenoma or Sessile Serrated polyp or CRC
No Hx of Inflammatory Bowel Disease
Negative Family Hx for CRC
• Increased Risk
Personal Hx of adenomatous polyps or SSPs,CRC or
Inflammatory Bowel disease
(+) Family Hx of CRC or adenomatous polyps
(+) DM, BRCA + Breast Cancer, Obese
Race & Age ( African-American, ≥50 )
 PREVENTION:

• High Risk
Pxs with family Hx of Lynch Syndrome(HNPCC)
Personal or family Hx of Polyposis Syndrome