A presentation on the basic anatomy and staging of carcinoma colon.

1. Anatomy and Staging of Ca Colon
Dr. Kashish Singh
PGJR-I
Dept. of Radiation Oncology

2. Colon
• Produced by both midgut and
hindgut
• Midgut responsible for
genesis of :-
 cecum
 ascending colon
 proximal ⅔ of the
transverse colon
• Hindgut :-
 distal ⅓ of the trans colon
 descending colon
 the sigmoid colon
 the rectum
 the proximal part of the
anus.

3. Total length of colon -150 cm

4. • The posterior and lateral surfaces of the ascending and
descending colon are in direct contact with the
retroperitoneum, whereas the anterior surface is draped with
peritoneum.
• These posterior attachments can prevent significant mobility,
increasing the difficulty of surgical resection.
• In contrast, the transverse colon is completely surrounded
with peritoneum and supported on a long mesentery.
• As the sigmoid colon evolves distally into the rectum, the
peritoneal coverage recedes.

5. Peritoneal relationships in the colon and rectum

6. • The colonic wall comprises 4 layers, including the :
• – Mucosa
• – submucosa
• – muscularis propria (inner circular layer and outer
longitudinal layer, comprising 3 narrow bands taenia Coli)
• – and serosa

8. Colonic Mucosa
• The function of the colon is to reclaim luminal water and
electrolytes.
• Colonic mucosa has no villi and is flat.
• Mucosa is punctuated by numerous straight tubular crypts
• Crypts contain abundant goblet cells, endocrine cells, and stem
cells.
• Paneth cells are occasionally present at base of crypts in the
cecum& ascending colon
• The regenerative capacity of the intestinal epithelium is
remarkable.
• Cellular proliferation is confined to the crypts
• Turnover of the colonic surface epithelium takes 3 to 8 days

10. Blood supply of large intestine

11. Venous drainage

12. Lymph nodes of the large intestine have been divided into
four groups :-
• epicolic (under the serosa of the wall of the intestine)
• paracolic (on the marginal artery)
• intermediate (along the large arteries [superior and inferior
mesenteric arteries]); and
• principal (at the root of the superior and inferior
mesenteric arteries).
Lymphatic drainage

14. Regional nodes are located :-
1) along the course o f the major vessels supplying the colon and
rectum,
2) along the vascular arcades o f the marginal artery, and
3) adjacent to the colon—that is, along the mesocolic borders o f the
colon.
• Regional lymph nodes are termed pericolic & perirectal/mesorectal
and also found along the ileocolic, right colic, middle colic, left colic,
inferior mesenteric, superior rectal (hemorrhoidal), and internal
iliac arteries.

15. Segment Regional lymph nodes
• Cecum Pericolic, ileocolic, right colic
• Ascending colon Pericolic, ileocolic, right colic, right branch of
the middle colic
• Hepatic flexure Pericolic, ileocolic, right colic, middle colic
• Transverse colon Pericolic, middle colic
• Splenic flexure Pericolic, middle colic, left colic
• Descending colon Pericolic, left colic, sigmoid, inferior mesenteric
• Sigmoid colon Pericolic, sigmoid, superior rectal (hemorrhoidal),
inferior mesenteric
• Rectosigmoid Pericolic, sigmoid, superior rectal(hemorrhoidal),
inferior mesenteric
• Rectum Mesorectal, superior rectal (hemorrhoidal), inferior
mesenteric, internal iliac, inferior rectal
(hemorrhoidal)

16. Frequency and location of colon
and rectal cancers.

18. Resection of the large intestine should include the entire area served by a major artery as well
as the lesion itself. Most of the lymphatic drainage will be included.

21. Risk Factors-Diabetes, Insulin, Insulin-like
growth factor (IGF-1)
• Diabetes, Insulin, and Insulin-like
growth factor:
-Links to  risk of colorectal cancer:
-Elevated circulating IGF-1 (Insulin-
like growth factor)
-Insulin resistance and associated
complications: elevated fasting
plasma insulin, glucose, and free
fatty acids, glucose intolerance, 
BMI, visceral adiposity
-Elevated plasma glucose and
diabetes
-Insulin and IGFs stimulate proliferation
of colorectal cells
-Elevated insulin and glucose
associated with  adenoma risk and
 apoptosis (cell death) in normal
rectal mucosa

23. PATHOLOGY
• Adenoma-carcinoma sequence
• Between 70-90 % of colorectal cancer arise from
adenomatous polyp.
• Adenoma- carcinoma sequence is multi-step process
involving sequential mutations or deletions of genes
• Polyp with tubular histological pattern have the least
malignant potential , whereas villous adenomatuos
polyp have the highest malignant potential
• The larger the polyp ) more than 2cm in diameter) the
greater the risk of cancer

24. Familial Adenomatous Polyposis (FAP)
 FAP:
 Multiple colonic polyps
 Patients with an APC mutation have a
100% lifetime risk of colorectal cancer
if patient fails to undergo total
colectomy
 Adenomas (>100) occur in:
colorectum, small bowel & stomach
 Cancer onset ~39 years
 Screening recommendations:
- DNA testing for APC gene mutation
-Annual colonoscopy starting 10-12
yrs old until 15-20 yrs
-Upper endoscopy (scope through
mouth to examine the
esophagus, stomach and the first
part of the small intestine, the
duodenum). Frequency of 1-3/year
when colonic polyps are detected
-Older than 20 years annual upper
endoscopy and colonoscopy needed

25. Genetic pathways to colorectal carcinoma
A:Chromosomal instability B:euploid but defective in DNA mismatch repair (MMR), resulting in high microsatellite
instability (MSI-hi)

26. Pathology
May appear to the naked eye as:
• - Exophytic cauliflower-type of growth
• - Ulcerating lesion penetrating through the bowel wall
• - Annular constricting growth
• - or as the rare colloid mucus- secreting tumors
Microscopically:
almost all colorectal cancers are adenocarcinoma, but
their histologic appearance is different
• Grade I : well differentiated
• Grade II : moderately differentiated
• Grade III : poorly differentiated

27. Spread of the cancer- generally speaking it is comparatively slow
growing tumor:-
Local spread:
• the growth is limited to the bowel for considerable time,
• it spreads round the intestinal wall & to a certain extent
longitudinally.
• when it invades the bowel wall it affect the near structures like
bladder, uterus, ovaries, etc..
• where it may cause a fistula , or perforate into peritoneal cavity, or
to the pelvic wall
Lymphatic spread:
• to epicolic group of lymph nodes then to
• paracolic group, then
• to main groups of lymph nodes arranged around the main arteries

28. Haematogenous spread :
• through the venous system ( inferior &
superior mesenteric veins) mainly to the liver,
it also goes to lung, bones, etc…
Spread by implantation
Transperitoneal spread

29. INVESTIGATIONS
• Digital Rectal Examination (DRE): is essential & many rectal cancers can
be identified as craggy ulcerated mass
• Fecal occult blood (FOB) for screening
• Blood & electrolytes examination will shows; Anemia of iron deficiency
type especially in right side cancer
• ESR will increase but not specific
• Electrolytes disturbance may be evident as result of, diarrhea obstruction,
vomiting, inadequate flui intake, urea may increase as result of
dehydration
• Carcino-embryonic antigen (CEA) can be detected

30. INVESTIGATIONS- imaging
• plain X-ray will show signs of obstruction &dilated bowel
• CXR for lung metastasis
• Barium enema carcinoma of the colon as a constant, irregular, filling defect ( apple
core deformity) on the other hand negative radiography by no means exclude the
carcinoma
• USG is essential tool of investigations, it can detect the mass, and presence of
metastasis in the liver or pelvic Organs
• Intrarectal USG:-
new tool of investigations with great help of diagnosis and staging of the cancer
especially the rectal cancer.
• CT-scan is needed for evaluation of resectability
• MRI has lower sensitivity and higher specificity than CT scan in T staging.

31. Duke stages
• A - Tumor is confined to bowel mucosa
• B1 - Tumor involved the muscle wall but not
completely
• B2 - Tumor involve the serosa
• C1 - Tumor involve the muscle wall but not
completely, local L.Ns involved
• C2 - Involves the serosa & local LNs
• D - Distant metastasis

32. Dukes’ Staging System

34. TNM Staging System

46. Thank you

47. Risk Factors-Smoking
• Smoking:
-12% colorectal cases are attributed to smoking
-Long term heavy smokers have a 2-3 fold  in
colorectal adenomas
-There is a greater frequency of adenomatous
polyps in former smokers even after 10 years
of smoking cessation
-Incidence of colorectal cancer occurs at a
younger age
-Potential biological mechanisms:
-Carcinogens  cancer growth in colon and
rectum. Could reach colorectal mucosa
through alimentary tract or circulatory system
and then damage or alter expression of
cancer-related genes
- no p53 over expression in heavy cigarette
smokers (p53 is a tumor suppressor gene
that plays a central role in the DNA damage
response)
an adenomatous polyp

49. Risk Factors-Alcohol
• Alcohol:
-regular drinking  2 fold  risk in colorectal
cancer
-Diagnosis at younger age
-Evidence to suggest increase in risk may be
attributed to p53:
-heavy beer consumption associated with p53
over expression in early colorectal neoplasia
-p53 over expression correlated with p53 gene
mutations
-p53 over expression  from adenomatous
polyps  carcinoma in situ  intramucosal
carcinoma
-p53 over expression associated with worse
overall survival after diagnosis, more likely
found in polyps in distal colon and rectum
p53 is a tumor suppressor gene that plays a
central role in the DNA damage response

50. Risk factors – Hereditary Family
Syndromes
• The development of colorectal cancer is a multi-step process involving genetic
mutations in the mucosal cells, activation of tumor promoting genes, and the loss of
genes that suppress tumor formation
Tumor suppressor genes constitute the most important class of genes
responsible for hereditary cancer syndromes
--Familial Adenomatous Polyposis (FAP): A syndrome attributed to a
tumor suppressor gene called Adenomatous Polyposis Coli (APC)
-- Increased risk of colon and intestinal cancers
Tumor suppressor genes are normal genes that slow down cell division, repair
DNA mistakes, and promote apoptosis (programmed cell death). Defects
in tumor suppressor genes cause cells to grow out of control which can
then lead to cancer

51. Juvenile Polyposis Syndrome (JP)
• Juvenile Polyposis:
-occurs in children with sporadic juvenile polyps (benign and isolated, occasionally are multiple
lesions)
-Criteria for JP:
1. >5 hamartomatous (disordered, overgrowth of tissue) polyps in colorectum
2. Any hamartomatous polyps in the colorectum in a patient with a positive family history of JP
3. Any hamartomatous polyps in the stomach or small intestine
-JP occurs in 1:15,000-1:50,000 individuals whereas sporadic juvenile polyps occurs in ~2% of
children

52. Lynch Syndrome (also known as HNPCC)
 Also known as hereditary nonpolyposis
colorectal cancer (HNPCC)
 A rare inherited condition that increases
risk of colon cancer and other cancers
 2-3% colon cancers attributed to Lynch
Syndrome
 Increase risk for malignancy of:
endometrial carcinoma (60%), ovary (15%),
stomach, small bowel, hepatobiliary tract,
pancreas, upper uro-epithelial tract, and
brain
 Caused by autosomal dominant inheritance
pattern (if one parent carries a gene
mutation for Lynch syndrome, then 50%
chance mutation passed to child)
 Cancer occurs at younger age <45 years
 Accelerated carcinogenesis: a small
adenoma may develop into a carcinoma
with in 2-3 yrs as opposed to ~10 yrs in
general population
Autosomal dominant
Affected
father
Unaffected
mother
Affected Unaffected Unaffected Affected
son daughter son daughter

53. Adenoma-carcinoma sequence

54. Summary: Screening
• Screening
– Physical exam
– Fecal occult blood test
– Flexible sigmoidoscopy
– Barium enema
– Virtual colonoscopy
– Colonoscopy
– Guidelines, Advantages, and
Disadvantages
http://www.sdirad.com/images/topic_graphics/VC_combo.jpg

55. Screening Options: Fecal Occult Blood
Test• Stool Blood Test (FOBT or FIT): Used to find small amounts of blood in the stool. If found
further testing should be done.
http://digestive.niddk.nih.gov/ddiseases/pubs/dictionary/pages/images/fobt.gif
http://www.owenmed.com/hemoccult.jpg

56. Screening: Flexible Sigmoidoscopy
• Flexible Sigmoidoscopy: A
sigmoidoscope, a slender,
lighted tube the thickness of a
finger, is placed into lower part
of colon through rectum
• It allows physician to look at
inside of rectum and lower
third of colon for cancer or
polyps
• Is uncomfortable but not
painful. Preparation consists of
an enema to clean out lower
colon
• If small polyp found then will
be removed. If adenoma polyp
or cancer found, then
colonoscopy will be done to
look at the entire colonhttp://www.nlm.nih.gov/medlineplus/ency/images/ency/fullsize/1083.jpg

57. Screening: Barium Enema
• Barium enema with air contrast:
A chalky substance is used to
partially fill and open up the colon
• Air is then pumped in which causes
the colon to expand and allows
clear x-rays to be taken
• If an area looks abnormal then a
colonoscopy will be done
A cancer of the ascending
colon. Tumor appears as oval
shadow at left over right pelvic
bone
http://www.acponline.org/graphics/observer/may2006/special_lg.jpg

58. Screening: Virtual Colonoscopy
• Virtual Colonoscopy: Air is pumped into
the colon in order for it to expand
followed by a CT scan which takes
hundreds of images of the lower
abdomen
• Bowel prep is needed but procedure is
completely non-invasive and no
sedation is needed
• Is not recommended by ACS or other
medical organizations for early
detection. More studies need to be
done to determine its effectiveness in
regard to early detection
• Is not recommended if you have a
history of colorectal cancer, Chron’s
disease, or ulcerative colitis
• If abnormalities found then follow-up
with colonoscopy

59. Screening: Colonoscopy
• Colonoscopy: A colonoscope, a long,
flexible, lighted tube about the thickness of a
finger, is inserted through the rectum up into
the colon
• Allows physician to see the entire colon
• Bowel prep of strong laxatives to clean out
colon, and the day of the procedure an
enema will be given
• Procedure lasts ~15-30 minutes and are
under mild sedation
• Early cancers can be removed by
colonoscope during colonoscopy http://www.cadth.ca/media/healthupdate/Issue6/hta_update_mr-colonograpy2.jpg