Colorectal cancer begins in the inner lining of the colon or rectum and can spread deeper into the wall of the colon/rectum and to other parts of the body. Risk factors include increasing age, family history, lifestyle factors like smoking, obesity, and lack of physical activity. Symptoms often include changes in bowel habits and bleeding. Screening is recommended regularly beginning at age 50. Treatment depends on the stage and may include surgery, radiation, chemotherapy, and targeted therapies. Prognosis depends on tumor stage and extent at diagnosis.

1. COLORECTAL
CANCER
Dr. Aditya Singla
1

2. Definition
 Malignant growth of tumor that begins from the inner
wall of the colon or rectum.
 Can also involve the anal canal.
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3. 22
ANATOMY

4. Anatomy
 The large intestine consists of the cecum; the ascending,
transverse, descending, and sigmoid colon; and the rectum
 Ascending colon (22% of colorectal carcinomas)
 Transverse colon (11% of colorectal carcinomas)
 Descending colon (6% of colorectal carcinomas)
 Sigmoid colon (55% of colorectal carcinomas)
 4 major tissue layers, from the lumen outward, form the large
intestine:
 The mucosa
 Submucosa
 Muscularis propria
 Serosa
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6. ASCENDING COLON

7. TRANSVERSE COLON

8. DESCENDING COLON

9. SIGMOID COLON

11. EPIDEMIOLOGY
 The 3rd most c ommon malignancy worldwide
 2nd most common cause of mortality in world
 Incidence and death rate stands at 13 th in
India
 The incidence is greatest among males
 Highest incidence rates in economically developed
countries
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12. Age & Colorectal CA
Relationship:
 An individual’s risk of developing cancer of the
colon or rectum increases with advancing age.
 The likelihood of cancer diagnosis ↑ after 40
years of age and rising progressively after age 50.
 The median age at diagnosis is 69 years.
 < 20%of patients are less than 50 years of age at
the time of diagnosis.
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13. Pathophysiology
 The formation of colorectal CA is a multistep process.
 Begins with an abnormal growth of tissue known as a
polyp (precursors to the disease) originating from the
innermost wall of the colon.
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14. ▶ The process of
transformation from polyp
to malignant disease
takes years.
▶ Once transformation
occurs, cancer begins to
spread through the wall
of colon/rectum.
▶ It can eventually invade
blood, L.Ns, or other
organs directly.
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A stalked colon
polyp

15.  95% are adenocarcinoma (glandular tissue).
 The disease can be prevented by removal of precancerous
tissue.
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16. Aetiology
 Aetiology is complex, involving:
 Patient- specific factors
 Environmental factor
 Genetic factors
 Genetic mutations associated with colorectal cancer:
 APC mutation/loss (Tumour suppressor gene).
 P53 mutation
 COX-2 overexpression (growth factor signalling
pathways)
 K-RAS mutation 35%, BRAF mutation 5% (oncogenes)
10

17. Risk Factors
 Increase age: Age >50 (90%of patients)
 Male sex
 Family history.
 Personal history:
(history of colon polyps; multiple adenomas or size
≥10 mm)
 IBD (Ulcerative colitis, Crohn’s disease):
 ↑ 5- to 10-fold
 Risk ↑ with increasing extent of bowel involvement &
disease duration.
11

18. Risk Factors
 Environmental factors/ Lifestyle:
 Physical inactivity & obesity
 Diet:
 fatty food
 Red meats
 processed meats
(hot dogs and some luncheon meats)
 low fibers
 Alcohol (excessive)
 SMOKING:
 Rectal > colon
 Dose relationship (pack/year)
 Duration
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19.  Particularly smoking in early life.
 As compared to never-smokers, the risks of
colorectal cancer and mortality in smokers were
18% and 25% higher, respe ctively.
 Early tobacc o use  influence risk of c ancer
recurrence and mortality among colon cancer
survivors.
13

20. Risk Factors
 Genetic/Hereditary colon C A Syndromes:
 The 2 most common forms of hereditary colon
cancer are:
1. Familial adenomatous polyposis (FAP):
 Risk ↑ 100%
 AD
 Mutations of the adenomatous polyposis coli (APC)
gene
 0.2%to 1%of all colorectal cancers.
 Diagnosed by late teens or early 20s.
 Total colostomy is recommended when detected.
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21. 2. Hereditary non-polyposis colon cancer (HNPCC)/
Lynch Syndrome.
 AD
 2% to 4%
 MMR (mismatch repair) genes mutation in DNA.
 Diagnosed later in life as compared to FAP
 Tend to be located primarily in the right-sided (proximal
colon)
 Other factor can increase risk of colon cancer:
 DM (Type 2)
 in 15 studies (hyperinsulinemia & ↑ levels of free insulin-
like growth factor-1 (IGF-1), promote tumor cell
proliferation
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22.  Factors may ↓ colorectal C A risk:
 Fiber (Fruit & Vegetables)
 Physical activity
 Regular consumption of milk/Calcium & Vitamin D
(May have antiproliferative effects )
 Hormone replacement therapy (HRT). Persist over
10 y
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23. Signs & Symptoms
1. Subtle & nonspecific (generalised symptoms)
2. Asymptomatic (early stage).
3. **Persistent/sudden change in bowel habits:
(*Prolong constipation
*or diarrhea.
*pencil thin stool)
4. Bleeding from rectum or blood
In stool.
5. Vague Cramping or abdominal pain/discomfort,
bloating , N, V  2ndry obstruction, perforation,
bleeding.
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24. Signs and symptoms
6. Weakness and tiredness
(advanced stage).
7. Iron-deficiency anemia.
8. Unintentional weight loss
9. Increased liver enzymes
(sign of liver metastasis) (AST/ALT)
10. Hepatomegaly and jaundice
in advanced disease.
19

25. SYMPTOMS

26. Symptoms 20

27. DIAGNOSIS
 Signs and symptoms
 Entire Large bowel evaluation:
 Colonoscopy
 Double-Contrast Barium Enema
 CT Colonography (detect adenomas at least 6 mm).
 Flexible sigmoidoscopy (FSIG) : examine lower half of
the bowel to the splenic flexure, capable to detect
50%-60% of CA.
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28. DIAGNOSIS 25

29.  Biopsy
(during colonoscopy)
 Ultrasound: Determines
depth of tumor penetration,
assessing L.Ns
 CT scan: same as ultrasound +useful in assessing for
metastasis
 Blood tests: bld count, PT, PTT
, Liver function test.
 CEA (carcinoembryonic antigen)Tumour marker
 Non-sensitive, non specific in early stage
 Usually elevated in metastatic or recurrent colon C A
 Normal 0-3 ng/mL
 Monitor the recurrence.
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30. SCREENING
 Often same as diagnosis
 Colonoscopy: gold standard for colorectal
screening
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31. SCREENING
A. Colonoscopy/ Barium enema/ CT scan
(alternative for individuals who don’t wish to
undergo /not suitable for colonoscopy.)
B. CEA level
C. Fecal screening test:
1. Fecal occult blood testing (FOBT)
 Many early-stage tumors do not bleed.
 High false -ve rate
 Sensitivity 33-75%
 Increased sensitivity & specificity when used in
combination with test 2
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32. 2. Fecal immunochemical test (FIT)
 Can be used to replace FOBT
 Sensitivity 60-85%
 Specific ity > 97%
 No drug or food interactions
 Uses ABs to detect globin protein Hg in stool
D. Digital Rectal Exam (DRE):
Can detect anorectal
palpable mass
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33.  Screening guidelines for early detection of colorectal
CA with the goal of cancer prevention:
Risk Screening recommendation
Average risk
(R.F ≥ 50 ys)
both M/F
 Annual DRE and FOBT/FIT and one of the following:
– Sigmoidoscopy every 5 years
– CT colonography every 5 years
– Colonoscopy every 10 years
– Barium enema every 5 years
Family History Begin screening at age of 35-40 years or 10 years younger from
first-degree relative colorectal cancer diagnosis
IBD Begin screening at 8–15 years after diagnosis
FAP Begin screening at 10-12 years
HNPCC Begin screening at age of 20–25 years or 10 years younger
from 1st-degree relative colorectal CA diagnosis
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34. 32

35. Copyrights apply

37. Treatment
I. Surgery
II. Radiation
III. chemotherapy
IV. Targeted molecular therapies.
 Treat Depend on the location & extent of disease.
 Prognosis depend on extent of tumour
penetration/LNs involvement, Metastases.
 Goals:
 Curative therapy for localized C A
 Palliative therapy for metastatic CA.
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38. Treatment
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 Surgery in CA of the colon or rectum (stage, I, II,III):
 Complete surgical resection of the primary tumor
mass with regional lymphadenectomy
 At least a 5 cm margin of tumor-free bowel &
regional lymphadenectomy
 Selected patients with resectable metastases,
surgical resection may be an option.

39. Treatment
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 If the distal margin clear of tumor is at least 1 cm,
sphincter-preserving surgery may be possible for
patients with CAs in the middle and lower portion of
the rectum (LAR)
 If not C a ndidate for sphincter-preserving surgery 
Abdomino-perineal resection (APR) = remove distal
sigmoid, recto-segmoid, rectum, anus.
 Colostomy (after colectomy) has become an
accepted procedure for colon and rectal cancer.

40. 38

41. 39
 Rectal C A is more difficult to resect with wide margins.
 Local recurrence of rectal C A is more common
compared to colon C A
 If lies closer to the a nal sphincter, so the risk of
localized treatment failure & recurrence at the initial
site of disease is increased
 Radiation (XRT) is usually reserved for rectal cancer
 Adjuvant XRT +chemo. are standard for stage II/III
rectal C A
 Neo- Adjuvant therapy before rectal surgery to:
Shrink the tumour & make it resectable, prevent local
recurrence in rectal CA.

42. Stage Management
Stage I Surgery
Stage II Colon: Surgery (observation +/- chemo.)
Rectal: Surgery + XRT + chemo.
Stage III Colon: Surgery + Chemotherapy
Rectal: Surgery + XRT + chemo.
Stage IV +/- surgery (selected pt.)+ chemo. + MoAB ,
Palliative care
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43. SURVIVAL :
 5-year survival rate:
Disease Stage 5- Year
survival
Early stages (localized/stage I, II) of colon 91 %
Early stages rectal cancer. 88%
Regional disease/Stage III:
Colon & rectal cancer after the tumor has spread
regionally to adjacent LNs or tissues
70%
Metastatic disease ≤ 12%
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