Colonic adenomas are benign epithelial tumors that can develop into colorectal cancer over time. They range in size and can be pedunculated or sessile. Microscopically, they are characterized by epithelial dysplasia and nuclear abnormalities. Certain familial polyposis syndromes, like familial adenomatous polyposis and Lynch syndrome, are associated with an increased risk of developing numerous colonic adenomas and colorectal cancer at a young age due to genetic mutations. Surveillance colonoscopy is recommended to screen for and remove adenomas to prevent cancer.

1. Benign Neoplastic Colonic Polyps
Colonic Adenomas
Colorectal Adenomas
Lecture 15
Dr Mohammad Manzoor Mashwani BKMC Mardan

2. Classification- Neoplastic Polyps
• Benign polyps
•
Adenomas
• Malignant lesions (Polyps)
Adenocarcinoma
Squamous cell carcinoma of the anus

3. Adenomas
• A benign epithelial tumor in which the cells form
recognizable glandular structures or in which the
cells are derived from glandular epithelium.

4. Colonic adenoma
The most common and clinically important
neoplastic polyps are colonic adenomas,
benign polyps that give rise to a majority of
colorectal adenocarcinomas. Most
adenomas, however, do not progress to
adenocarcinoma.

5. Adenomatous Polyps
Adenomas
By definition they are dysplastic and have malignant
potential.
Time for development of adenomas to cancer is
about 7 to 10 years.

6. Epidemiology
epithelial dysplasia.
•
Colorectal adenomas are characterized by the presence of
•
These growths range from small, often pedunculated polyps to large sessile lesions.
• There is no gender predilection,
• present in nearly 50% of adults living in the Western world
• beginning age 50.
• surveillance colonoscopy starting at age 50.
•
Because persons with a family history are at risk for developing colon cancer earlier in life, they typically
are screened at least 10 years before the youngest age at which a relative was diagnosed .
•
While adenomas are less common in Asia, their frequency has risen (in parallel with an increasing
incidence of colorectal adenocarcinoma) as Western diets and lifestyles become more common.

7. Types of adenomas
On the basis of epithelial structure
1. Tubular adenomas
2. Villous adenomas
3. Tubulovillous adenomas
4. Sessile Serrated
adenomas
Endoscopic classification:
1. Sessile – base is attached to
colon wall usually large
2. Pedunculated – mucosal stalk
is interposed between the polyp
and the wall
3. Flat – height less than one-half the
diameter of the lesion. Depressed
lesions appear to be particularly likely
to harbor high-grade dysplasia or be
malignant even if small.
Pathologic classification: I. Low grade dysplasia II. High grade dysplasia

8. Gross Morphology
• Size- 0.3 to 10 cm in diameter and
• can be pedunculated or sessile,
• with the surface of both types having a texture resembling velvet or a
raspberry, due to the abnormal epithelial growth pattern.

9. Microscopy
•
Histologically, the cytologic
hallmark of epithelial Dysplasia is
nuclear hyperchromasia, elongation, and stratification.
These changes are most easily appreciated
at the surface of the
adenoma, because the epithelium fails to mature as cells migrate out of the crypt.
Pedunculated adenomas have slender fibromuscular stalks
containing prominent blood vessels derived from the submucosa.
The stalk usually is covered by nonneoplastic epithelium,
but dysplastic epithelium is sometimes present.

10. Morphology
Classification: tubular, tubulovillous, or villous.
• Tubular adenomas- small, pedunculated polyps
composed of small, rounded or tubular glands.
Villous adenomas- larger &sessile, covered by slender villi
• Tubulovillous adenomas- have a mixture of tubular and villous elements.
• Sessile serrated Adenomas- serrated architecture throughout the full length
of the glands, including the crypt base, associated with crypt dilation and lateral growth.
• In hyperplastic polyps serrated architecture is confined to the surface.
Larger size(>4cm) & high grade dysplasia are risk for malignancy in polyps.

12. Colonic adenomas. A, Pedunculated adenoma .B, Adenoma with a velvety surface. C, Lowmagnification photomicrograph of a pedunculated tubular adenoma.

13. Tubular adenoma with a smooth surface and rounded glands. Active
inflammation is occasionally present in adenomas, in this case, crypt
dilation and rupture can be seen at the bottom of the field.

14. Dysplastic epithelial cells (top) with an increased nuclear-to-cytoplasmic ratio,
hyperchromatic and elongated nuclei, and nuclear pseudostratification.

15. Villous adenoma with long, slender projections
that are reminiscent of small intestinal villi .

16. Sessile serrated adenoma lined by goblet cells without typical cytologic features of
dysplasia. This lesion is distinguished from a hyperplastic polyp by extension of the
neoplastic process to the crypts, resulting in lateral growth.

17. Familial syndromes
I. Familial Adenomatous Polyps
• Familial adenomatous polyposis (FAP) is an
autosomal dominant disorder marked by the
appearance of numerous colorectal adenomas by
the teenage years. It is caused by mutations of the
adenomatous polyposis coli gene (APC). A count of
at least 100 polyps is necessary for a diagnosis of
classic FAP, and as many as several thousand may
be present

18. Familial Adenomatous Polyps
•
Except for their remarkable numbers, these
growths are
morphologically indistinguishable from sporadic adenomas.
Colorectal adenocarcinoma develops in 100% of patients
with untreated FAP, often before age 30. As a result,
prophylactic colectomy is standard therapy for
persons carrying APC mutations. However, patients
remain at risk for extra intestinal manifestations,
including neoplasia at other sites.

19. Familial Adenomatous Polyposis
•
Specific APC mutations are also associated with the development of other manifestations
of FAP and explain variants such as Gardner syndrome and Turcot syndrome.
• Clinical features of Gardner syndrome:
• Intestinal polyps, osteomas of mandible, skull, and
long bones; epidermal cysts; desmoid (tendon-like ;
musculoaponeurotic) and thyroid tumors; and
dental abnormalities, including unerupted and
supernumerary teeth.

20. Familial Adenomatous Polyposis
• Turcot syndrome is rarer and is characterized by
intestinal adenomas and tumors of the central nervous
system.
• Two thirds of patients with Turcot syndrome have APC
gene mutations and develop medulloblastomas.
• The remaining one third have mutations in one of several
genes involved in DNA repair and develop glioblastomas.
Some patients who have FAP without APC loss have
mutations of the base excision repair gene MUTYH.

21. II.Hereditary Nonpolyposis Colorectal Cancer
• Hereditary nonpolyposis colorectal cancer (HNPCC), also
known as Lynch syndrome, originally was described as
familial clustering of cancers at several sites
including the colorectum, endometrium, stomach,
ovary, ureters, brain, small bowel, hepatobiliary
tract, and skin.
• Colon cancers inpatients with HNPCC tend to occur
at younger ages than for sporadic colon cancers and
often are located in the right colon.

23. Familial adenomatous polyposis. A, Hundreds of small
colonic polyps are present along with a dominant polyp (right).

24. Familial adenomatous polyposis. B, Three
tubular adenomas are present in this single microscopic field.