Transcript Evaluation of Colonic Polyps 1

Evaluation Of Colonic
Polyps
Kathia E. Rosado Orozco MD
GI and Liver Pathologist
Hato Rey Pathology Associates
► Disclosure:
 I have no financial disclosures to make.
 I will suggest texts and websites for reference
and study, but receive no financial gain from
these.
Colonic Adenomas
► Benign
premalignant proliferation of colonic
epithelium—all have dysplasia (low grade)
and are dysplastic.
► Precursor lesions to colorectal carcinoma.
Classification
► Tubular:
less than 25% villous
► TVA: between 20-80% villous
► Villous Adenoma:
 Less than 5% of adenomas
 More than 30% have high grade dysplasia
 2% have carcinoma
Low grade dysplasia
Colonic Adenomas
►
►
►
►
60-70% of all
endoscopically removed
colonic polyps
Lifetime prevalence: 3050%
50% increase in size with
time
Only some (5-10%)
progress to carcinoma
►
3-5% have invasive
carcinoma at diagnosis
►
Size of adenoma is BEST
predictor of carcinoma risk
►
High grade dysplasia and
villous component more
likely with increase in size
of polyp
Chromosomal Instability Pathway
High Grade Dysplasia
► Also
known as carcinoma in situ
► Present in 5-7 % of adenomas at initial
diagnosis
► More likely if:
 villous
 larger (>1cm)
 older than 60 yrs
Intramucosal Carcinoma
► Neoplastic
cells extend through gland
basement membrane and into lamina
propria BUT NOT through muscularis
mucosae.
► NOT shown to have metastatic risk:
 Paucity of lymphatics in colonic mucosa
 Classified same as high grade in TNM
Pseudoinvasion in Adenomas
► Misplaced
or herniated epithelium in
submucosa.
► Can be mistaken for invasive carcinoma
► Most in left colon, particularly sigmoid—
almost never seen proximal to transverse
colon
► Pedunculated polyps , more than 1 cm with
at least 1 cm stalk.
► Peristalsis related torsion/twisting
Adenoma with Invasive
Adenocarcinoma
Distinguishing Pseudoinvasion vs.
Invasion
1. Compare the epithelium to epithelium you are
confident is adenoma in the same polyp.
2. Compare the stroma to stroma you are
confident is the benign stroma of adenoma in the
same polyp.
3. Look for evidence of definite vascular or
lymphatic space invasion.
4. Cut levels. This will at least buy you a little time,
and you may find more definitive evidence of
submucosal invasion in the deeper sections.
Yerian, L. 2010 USCAP short course
-You can call the clinician to discuss the
endoscopic findings and management plan.
-Benign misplaced epithelium is uncommon in
sessile lesions. If the polyp was not completely
excised and is not endoscopically resectable, then
the patient may need to undergo a resection
irrespective of your assessment of the submucosal
epithelium.
Yerian, L USCAP 2010 Short course
Pseudoinvasion
► Occasionally
a definite distinction between
invasion and pseudoinvasion is not possible and
consensus cannot be reached, even among
experienced GI paths
► Giving a descriptive diagnosis is best and a phone
call to the clinician may be helpful. The pathologist
may choose to describe the finding ("deep
neoplastic glands of uncertain significance"), and
elaborate in a comment as to the diagnostic
problems.
► Yerian, L USCAP 2010 short course
Carcinomas arising in Adenomas
► Surgical
resection if:
 Poorly differentiated
 at or near margin
 lymphovascular invasion
► Endoscopic
polypectomy is adequate if:
 carcinoma is low grade (well or moderately
differentiated)
 margin is free or carcinoma, more than 1 cm away from
margin
 no evidence of lymphovascular invasion
-Up to 30% in asxs
adults over 50 y/o
-Prevalence increases
with age
-Usually less than 5mm
-Smooth, sessile
-Typically do not increase
in size with time (left
sided)
Serrated Adenomas
► Controversial
entity only recently recognized
(1990) as a pathologic lesion distinct from
hyperplastic polyps
► Recognition due to:
 Pts with hyperplastic polyposis have an increased risk
for neoplasia
 Sporadic right-sided hyperplastic polyps more commonly
contain a variety of genetic alterations NOT present in
left-sided counterparts
Serrated adenomas
► Formal
evaluation of their clinical features
and incidence is lacking due to
discrepancies in literature in terms of
nomenclature--called by numerous names
► Are thought to represent 20% of all lesions
with serrated architecture encountered at
endoscopy
Serrated adenomas: Facts
► Epithelial
neoplasm with a distinctive
serrated architecture associated with
abnormal proliferation and associated risk
for colorectal neoplasia
► Slightly more common in left colon
 If Small, endoscopic removal
► In
right side:
 Large (more than 1cm), flat
 Remove entirely
 Can present as an enlarged fold
Serrated polyp neoplasia pathway
► Proposed
to represent an alternative
molecular pathway to colorectal cancer
► Hp--> atypical HP--> serrated adenoma
-->cancer
► Predominant carcinomas of this pathway:
show defective DNA mismatch repair
(MMR)—can be MSI high or low
► 10 to 15% of all colorectal cancers
MSI and Cancer
►
MSI is a key factor in several cancers including colorectal,
endometrial, ovarian and gastric cancers. Colorectal
cancer studies have demonstrated two mechanisms for
MSI occurrence.
► The first is in hereditary nonpolyposis colorectal cancer
(HNPCC) or Lynch Syndrome, where an inherited mutation
in a mismatch-repair gene causes a microsatellite repeat
replication error to go unfixed.
► The second mechanism whereby MSI causes colorectal
cancer is an epigenetic change which silences an essential
mismatch-repair gene.
► In both cases, microsatellite insertions and deletions
within tumor suppressor gene coding regions result in
uncontrolled cell division and tumor growth.
Eosinophilic cytoplasm
Sessisle serrated adenoma, right-sided
Neoplasia in serrated polyp pathway
► Most
if not all sporadic MSI carcinomas have
a serrated histogenesis
► Epidemiological association with smoking
but typical in elderly females
► Can have several histologic patterns:
 Well to poorly differentiated
 Undifferentiated
 Lymphocytic response
-lymphocytic
infiltrate
-solid
-signet ring cells
-mucinous