
Colon-tumor Printer Friendly Version
Last revised 20 December 2006
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See also Colon-nontumor, Anus and perianal area
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Primary references, images needed
Polyps: general, biopsies, aberrant crypt foci, adenoma, carcinoma arising in adenoma, adenoma-carcinoma sequence, atheroemboli, displaced glands, diverticular, fibroblastic, flat adenoma, hyperplastic, hyperplastic polyposis, inflammatory, inflammatory fibroid, inflammatory myoglandular, juvenile, lymphoid, Peutz-Jegher, post-surgical, serrated, transitional, tubular adenoma, tubulovillous adenoma, villous adenoma
Familial polyposis syndromes: APC gene, Cowden’s, Cronkhite-Canada, familial adenomatous polyposis-classic, attenuated, Gardner’s, hereditary mixed polyposis, hyperplastic polyposis, juvenile polyposis, Lynch, Muir-Torre, MUTYH associated, Peutz-Jegher, Turcot’s
Carcinoma: general, molecular pathways, WHO classification, post-treatment changes, intramucosal, adenocarcinoma, adenosquamous, carcinosarcoma, clear cell, glassy cell, hepatoid, lymphoepithelioma-like, medullary, metastases to colon, mucinous, neuroendocrine, papillary, signet ring, small cell, small early flat, squamous cell, villous
Carcinoid tumors: rectum, not rectum
Lymphoma and hematopoietic lesions: general, Burkitt’s, follicular, HHV8, Hodgkin’s, MALT, mantle cell, mast cell sarcoma, T cell
Mesenchymal tumors: general, angiomyolipoma, angiosarcoma, endometrial stromal sarcoma, fibromatosis, ganglioneuromatosis, GANT, GIST, hemangioma, histiocytic sarcoma, idiopathic retractile mesenteritis, idiopathic retroperitoneal fibrosis, inflammatory myofibroblastic tumor, Kaposi’s sarcoma, leiomyoma, leiomyomatosis, leiomyomatosis-like lymphangioleiomyomatosis, leiomyosarcoma, lipoma, lipomatosis, liposarcoma, Mullerian adenosarcoma, perineurioma, perivascular epithelioid cell tumor, pyogenic granuloma, reactive nodular fibrous pseudotumor, schwannoma, solitary fibrous tumor
Other tumors: Langerhans cell histiocytosis, Rosai-Dorfman disease, teratoma
Other: grossing, staging, features to report
Go to Colon-nontumor (normal, congenital anomalies, diverticular disease, inflammatory bowel disease, colitis (non-infectious and infectious), non-neoplastic non-congenital lesions)
AJCC Cancer Staging Manual (6th Ed)
American Journal of Clinical Pathology (AJCP), Jan 1975 to October 2006
American Journal of Surgical Pathology (AJSP), March 1977 to September 2006
Archives of Pathology and Laboratory Medicine (Archives), January 1976 to September 2006
Human Pathology (Hum Path), March 1970 to September 2006
Journal of Clinical Pathology, January 1966 to September 2006
Modern Pathology (Mod Path), January 1988 to September 2006
Biomed Center, to 8 September 2006
Mills: Sternberg's Diagnostic Surgical Pathology (4th ed), 2004
Rosai: Rosai and Ackerman's Surgical Pathology (9th ed), 2004
Websites with images: PathoPic, PEIR digital library
Please refer to these primary references for more detailed discussions and photographs
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Gross, EM and immunohistochemistry images are needed for most disorders
Micro images are particularly needed for these lesions:
Carcinoma - post-treatment changes, intramucosal carcinoma, adenosquamous, glassy cell, hepatoid, metastases to colon, neuroendocrine, squamous cell
Carcinoid - not rectum
Mesenchymal tumors - leiomyomatosis, reactive nodular fibrous pseudotumor, solitary fibrous tumor
Other tumors - hemangioma, Langerhans cell histiocytosis, Rosai-Dorfman disease, teratoma
Polyps of colon
Definition: mass protruding into lumen of gut
Sessile: no stalk
Pedunculated: polyp with stalk, may be due to traction on the mass
Polyps that are due to abnormal mucosal maturation, inflammation or architecture are non-neoplastic
Polyps that are due to proliferation and dysplasia are neoplastic / adenomatous
Polypoid lesions may also be due to mucosal or submucosal tumors
Clinical impression correlates poorly with neoplasia (J Gastroenterol Hepatol 2006;21:563)
Appelman recommends calling “benign mucosal polyp” unless (a) diagnosis is adenoma [the only diagnosis that causes clinicians to do anything different] or (b) you can classify it within 30 seconds
Muciphages, without other abnormalities, have no clinical significance (Histopathology 2000;36:556)
Earliest neoplastic lesion of colon
May predict future adenoma or carcinoma (Am J Gastroenterol 2006;101:1362, Am J Gastroenterol 2005;100:1283)
May be useful to monitor effects of chemoprevention agents (Clin Gastroenterol Hepatol 2005;3:S42)
Micro: crypts are 2-3x larger than normal crypts, are microscopically elevated, have slit-like openings, and have thick epithelial lining that stains darker than normal crypts (particularly with Methylene blue), with large pericryptal zone
References: Cancer Epidemiol Biomarkers Prev 1991;1:57. World J Gastroenterol 2003;9:2642, Anticancer Res 2006;26:107, summary
“Adenoma” is an incorrect term - they are not benign neoplasms, but polypoid areas of epithelial dysplasia
Present in 20% (US) at age 40 years, 50% at age 60; in autopsy studies, almost all have tubular adenomas, <5% have tubulovillous or villous adenomas
Low incidence in developing countries
No gender predilection
Slow growing
Decreased risk of distal colon adenoma associated with dietary fiber intake (Lancet 2003;361:1491), fruit consumption in women (Cancer Res 2006;66:3942); folate intake (J Nutr 2005;135:2468); only weak association between fiber and adenoma recurrence (Am J Gastroenterol 2005;100:2789)
30% develop new polyps after mean 26 month follow up; higher risk if 3 or more adenomas and at least one in proximal colon (Dis Colon Rectum 2004;47:323)
Risk of invasive colorectal adenocarcinoma in the adenoma depends on size: <1% if < 1 cm vs. 10% if > 2 cm; higher risk if villous component
Risk of subsequent carcinoma is related to presence of 3 or more polyps, location at transverse colon or proximal, or [one study] presence of monotonous population of elongated cells (AJSP 2006;30:1120)
Vienna classification (1999) described at J Gastroenterol Hepatol 2006;21:1697.
Treatment: excision of a pedunculated adenoma, even with invasive carcinoma (see below), is considered adequate treatment if margin is negative, there is no vascular or lymphatic invasion and carcinoma is moderate or well differentiated; invasive adenocarcinoma in a sessile polyp requires more than polypectomy
Gross: classified as pedunculated (with stalk), sessile or flat; tubular are red (darker than surrounding mucosa); villous are shaggy with papillary fronds; true margin of resection should be inked when grossing, or can be determined by diathermy artifact
Micro: classify microscopically as tubular, tubulovillous (5%) or villous (1%) adenoma; all contain epithelial proliferative dysplasia; dysplasia can be classified as low grade or high grade, although some GI pathologists recommend not using high grade dysplasia terminology unless clinicians want to know
Low grade: nuclei are elongated and dysplastic, but don’t reach cell surface; apical mucin present
High grade: cytologic and architectural changes of dysplasia; nuclei are enlarged, hyperchromatic or vesicular with prominent nucleoli; nuclei are stratified and reach luminal border; cribriform or irregular budding/branching of crypts is present; prominent mitotic figures; reduced mucin; necrosis may be present; no invasion through muscularis mucosa into submucosa; high grade dysplasia present in 12% of adenomas
Intramucosal carcinoma: invasion of lamina propria only with desmoplastic response; no biologic potential for metastases
References: Am J Gastroenterol 2006;101:255 (prevalence)
Invasive carcinoma arising in a colonic adenoma
Present in 5% of adenomas (G Chir 2001;22:26)
Invasive only if cancer has invaded through muscularis mucosa into submucosa
Recommended to NOT use “carcinoma in situ” terminology in colorectum; use either high grade dysplasia or invasive carcinoma
Report type of carcinoma, grade, presence of angiolymphatic invasion (tumor emboli in true endothelial lined channels away from tumor, not retraction artifact), status of resection margins (close to margin is within one high power field or 1-2 mm from diathermy or at diathermy), presence of dysplasia
Sample report #1: poorly differentiated carcinoma arising within an adenoma, extending to resection margin, no angiolymphatic invasion
Sample report #2: moderately differentiated carcinoma arising with an adenoma; tumor 2.5 cm from resection margin, no angiolymphatic invasion
Case reports: adenoma with carcinoma and mixed carcinoid-adenocarcinoma (Pathol Int 2003;53:457), with sarcoid reaction in regional lymph nodes (J Clin Gastroenterol 1999;28:377), squamous cell carcinoma arising in villous adenoma (Hum Path 1988;19:362), metastatic signet ring carcinoma in adenoma (Archives 2003;127:1509)
Treatment: polypectomy probably adequate unless margin involvement, poorly differentiated or angiolymphatic invasion (J Surg Oncol 1987;36:116)
Recurrent disease, nodal metastases or residual local disease: 20% incidence if cancer is near margin, is poorly differentiated or if angiolymphatic invasion is present
Well characterized series of histopathologic events associated with distinct molecular alterations
There are two general pathways - chromosomal instability (abnormal number of chromosomes, not diploid) and microsatellite instability (diploid but DNA mismatch repair gene alterations)
Chromosomal instability pathway
Carcinomas arise from accumulation of mutations in various genes that initially cause adenomatous polyps (usually), some of which then acquire addition mutations and become malignant (4-10 mutations required to produce malignant phenotype)
Molecular pathway may vary in each particular tumor
Earliest event often involves APC gene (mutated in familial polyposis)
Other early events are DNA methylation changes (Genes Chromosomes Cancer 2006;45:781), which may cause oncogene activation or tumor suppression gene repression
K-ras (10% of adenomas, 50% of adenomas with severe dysplasia, 50% of carcinomas) occurs in larger but not smaller polyps
DPC4 and DCC (18q21, reduced expression in 70% of carcinomas) occur later
p53 mutations (17p, losses in 70% of carcinomas) occur late
Removing adenomas via screening colonoscopy reduces incidence of colorectal cancer (N Engl J Med 1993;329:1977)
Polyposis syndrome patients have increased risk for carcinoma (nearly 100% for familial polyposis and Gardner’s syndrome)
Villous adenomas have higher malignant risk than tubular adenomas
Microsatellite instability pathway
Some carcinomas arise without a polypoid dysplastic stage (AJCP 2006;125:132); associated with DNA mismatch repair or microsatellite instability
BRAF mutations are also associated with the microsatellite instability pathway (Gut 2004;53:1137)
Polyps with no malignant risk: solitary hyperplastic polyps, juvenile polyps and Peutz-Jegher polyps
References: H. Lee Moffitt Cancer Center, eMedicine (#413), National Cancer Centre-Singapore, BMJ 2000;321:886
Atheroemboli associated polyps of colon
May be associated with rectal bleeding (AJSP 1991;15:1078)
Case reports: 68 year old man with diabetes and 2 year history of bloody diarrhea (AJSP 1993;17:1054), polypoid mass without clinical evidence of ischemia (Archives 1994;118:308), cholesterol emboli in polyp (J Clin Gastroenterol 1994;19:231)
Micro: edematous submucosa with superficial ulceration and atheroemboli in arterioles of submucosal polyps
Also called epithelial misplacement
Presence of dysplastic glands from an adenoma beneath the muscularis mucosa due to biopsy related torsion or other trauma
A low power diagnosis
Occurs in 3% of adenomas, usually with well-defined stalks
Resembles intramucosal carcinoma, but cytologic features resemble adenoma
See also below (hyperplastic polyp with misplaced epithelium)
Micro: submucosal glands surrounded by loose inflamed stroma and granulation tissue, but not desmoplastic stroma; glands may have atypia associated with adenoma but not carcinoma
Negative stains: p53, E-cadherin, type IV collagen (AJSP 2002;26:206)
References: AJSP 1993;17:1262, Cancer 1974;33:206
Arises in background of diverticular disease
Usually in sigmoid colon
Part of the “mucosal prolapse” syndrome (Am J Gastroenterol 2002;97:370)
Treatment: high fiber diet is usually effective (Endoscopy 1986;18:84)
Gross: redundant or polypoid mucosal folds
Micro: mucosal hemorrhage and congestion, epithelial hyperplasia with dilated and serrated crypts and bizarre nuclei in stroma, mucosal edema, fibromuscular replacement of lamina propria with thickened and splayed muscularis mucosa; no dysplastic changes
References: AJSP 1991;15:871, Histopathology 1993;23:63
Initially described in 2004 (AJSP 2004;28:374)
May be due to exuberant response to tissue injury (J Clin Gastroenterol 2005;39:778)
May be early stage of inflammatory fibrous polyp (AJSP 2004;28:1397-letter)
Solitary, usually in sigmoid colon
Treatment: excision (benign behavior)
Gross: 2-4 mm
Micro: mucosal polyp composed of bland, plump spindle cells in lamina propria with fibroblastic features; spindle cells are associated with muscularis mucosa, cause separation and disorganization of colonic crypts; often associated with serrated / hyperplastic crypts; no atypia, no mitotic activity, no necrosis
Positive stains: vimentin; occasional weak/focal CD34 or smooth muscle actin
Negative stains: desmin, CD31, CD68, bcl2, c-kit, S100, EMA
EM: sparse cytoplasmic organelles, many intermediate filaments
References: Histopathology 2006;48:431
Also called depressed adenoma
Present in asymptomatic populations (Gut 1998;43:229)
More difficult to detect during endoscopy, but targeted indigo carmine chromoscopy or other methods are useful (article and images)
Diagnosis requires (a) classic endoscopic (gross) appearance of mucosal elevation with flat/rounded surface and height less than half the diameter, (b) not resembling a hyperplastic polyp, and (c) dysplastic changes
Another study defined flat as thickness of 1.3 mm or less or thickness less than twice normal mucosal thickness
Controversial if associated with higher risk for high grade dysplasia (no-Clin Gastroenterol Hepatol 2004;2:905; yes-Dis Colon Rectum 1991;34:981); risk may be higher if central depression, individual history or family history of malignancy (Dis Colon Rectum 2000;43:782), or larger lesion (Dis Colon Rectum 1985;28:847)
Case reports: with deep malignant component (Virchows Arch A Pathol Anat Histopathol 1993;422:415)
Gross: flat or slightly raised plaques, often with a central depression; usually height 2 mm or less; may be multiple
Micro: plaque-like, not polypoid or exophytic; up to twice the thickness of adjacent normal epithelium; usually tubular adenomas that show superficial adenomatous changes at periphery, and centrally may extend throughout the crypt
Also associated with aberrant crypt foci (Am J Gastroenterol 2005;100:1283)
Molecular: some cases have multiple APC mutations (Eur J Hum Genet 1999;7:928)
References: Hum Path 1991;22:70, Am J Gastroenterol 2006;101:172
90% of all polyps
Usually patients age 50+ years, often in rectosigmoid
Present in 30-50% of normal individuals (85% of adults in Western world versus 2% in third world countries)
Due to delayed shedding of surface epithelial cells
Associated with cigarette smoking (Cancer Causes Control 2005;16:1021)
Previously considered to have no/minimal malignant potential (Arch Intern Med 2005;165:382), except for those in hyperplastic polyposis syndrome
Right sided hyperplastic polyps are molecularly more similar to serrated adenomas than to left sided hyperplastic polyps, and are associated with cancers that show microsatellite instability (but see J Clin Pathol 2004;57:1089)
Intermediate (6-9 mm) sized polyps are usually right sided, and are associated with synchronous colorectal carcinoma (J Gastroenterol Hepatol 2005;20:1572)
Case reports: with small invasive carcinoma (Endoscopy 2004;36:825)
Gross: small (< 5 mm), sessile, usually on top of mucosal folds, multiple, same color as surrounding mucosa; lesions up to several cm may occur in right colon but may be serrated adenomas
Micro: well formed, elongated glands and crypts with serrated (saw tooth) or star-shaped appearance resembling secretory endometrium; mixture of goblet cells (with abundant mucin) and absorptive cells; bland cytology with eosinophilic cytoplasm, well defined brush borders, basal nuclei; thickened basement membrane; Paneth cells in 8%; may have multinucleated giant cells (AJSP 2005;29:912); cells at base of crypt may have nuclear elongation, crowding and increased mitotic rate, but this is not adenomatous change; may be splaying of muscularis mucosa fibers into submucosa; large hyperplastic polyps may have adenomatous foci
Molecular: limited changes, no relation to changes in coexisting adenomas (J Clin Pathol 2004;57:1084)
Hyperplastic polyp of colon with misplaced epithelium
Also called “pseudoinvasion”
Some authorities consider it synonymous to inverted hyperplastic polyp, but others consider them different
Simulates adenoma with pseudoinvasion, but benign
Arises in left colon due to local trauma (torsion or twisting of polyp, vigorous peristalsis)
Micro: colonic epithelium in lamina propria with mixed pattern (lobules and irregularly distributed crypts) or lobular pattern; continuous with mucosal portion of polyp in deeper levels; defects are present in muscularis mucosa, and muscle fibers are splayed round misplaced epithelium; often lymphoid aggregates adjacent to misplaced epithelium, fresh hemorrhage, vascular congestion, hemosiderin deposits; usually no significant inflammation, no dysplasia
Positive stains for misplaced epithelium: Ki-67, E-cadherin, collagen IV basement membrane
References: Mod Path 2001;14:869
Inverted hyperplastic polyp of colon
More frequent in right colon
May be more common in women
Case reports: associated with adenoma (Eur J Gastroenterol Hepatol 2004;16:107), inverted hyperplastic polyposis (J Clin Pathol 1993;46:56)
Micro: endophytic growth pattern, penetrates muscularis mucosa (AJSP 1985;9:265)
Uncommon
Also called serrated adenomatous polyposis because polyps appear to be serrated adenomas
WHO definition: (a) at least 5 histologically diagnosed hyperplastic polyps proximal to sigmoid colon, two of which are larger than 1 cm; or (b) any number of hyperplastic polyps proximal to sigmoid colon in patients with a first-degree relative with hyperplastic polyposis; or (c) more than 30 hyperplastic polyps of any size distributed throughout colorectum (Hyperplastic polyposis. Lyon: IARC Press; 2000)
High risk for colorectal carcinoma (Dis Colon Rectum 2004;47:2101, AJSP 2001;25:177); regular surveillance is recommended (Am J Gastroenterol 2004;99:2012), including family members
Case reports: associated with two synchronous carcinomas (Am J Pathol 2000;157:385), inverted hyperplastic polyposis (J Clin Pathol. 1993;46:56)
Gross: polyps are usually sessile
Molecular: extensive methylation in adenomas and in normal mucosa (Gut 2006;55:1467)
Inflamed regenerating mucosa surrounded by ulcerated tissue; also granulation tissue overlying epithelium
Associated with Crohn’s disease or ulcerative colitis; also amebiasis, schistosomiasis, ulcer, anastomotic sites
Usually asymptomatic but may cause obstruction or hemorrhage
Benign; no increased risk of dysplasia compared to surrounding mucosa
Case reports: with ischemia (Am Surg 1993;59:315), with schistosomiasis (J Clin Gastroenterol 1983;5:169), simulating carcinoma due to multiple fused polyps (Am J Gastroenterol 1980;73:441), 5 year old girl (Case Rep Clin Pract Rev 2006;7:212)
Treatment: treat underlying inflammatory condition
Gross: smooth hyperemic or hypervascular appearance; variable surface erosion
Micro: inflamed lamina propria and distorted colonic epithelium (branched, tortuous, elongated or cystic crypts); may have surface erosion, congestion/hemorrhage or crypt abscesses; may have bizarre stromal changes in reactive fibroblasts resembling sarcoma in a fibroblastic or granulation tissue stroma, particularly underneath areas of ulceration; no/few mitotic figures, no atypical mitotic figures, often zonation
Positive stains: vimentin
Negative stains: S100, cytokeratin, CMV
DD: pyogenic granuloma (Ann Diagn Pathol 2005;9:106)
Giant inflammatory polyp / polyposis of colon
Also called filiform polyposis if have long finger-like projections
Uncommon, benign
Usually associated with inflammatory bowel disease
May be diffuse (Archives 2004;128:1286)
May cause obstruction (J Gastroenterol 2005;40:536, Intern Med 1996;35:24) or intussusception (Inflamm Bowel Dis 2004;10:41),
Case reports: no history of colonic disease (Gastroenterol Clin Biol 2006;30:913, Neth J Surg 1987;39:95), with cystic fibrosis and Crohn’s disease (Pediatr Dev Pathol 2006;9:25), with Crohn’s disease (Pathol Int 2002;52:318), remission after topical budesonide (Anticancer Res 2005;25:2961)
Treatment: usually surgery (Z Gastroenterol 2000;38:845) since cannot clinically distinguish dysplastic and inflammatory polyps
EM: fibroblasts, myofibroblasts, mast cells and lymphocytes, collagen fibers, capillaries, venules and hypertrophic autonomous nerve plexuses; also remnants of original epithelium and smooth muscle cells (Dis Colon Rectum 1990;33:773)
References: AJSP 1986;10:420
Inflammatory polyp of colon secondary to mucosal prolapse
Includes inflammatory cap polyposis and diverticular polyp (AJSP 1991;15:871)
Usually rectosigmoid
Associated with chronic straining
Median age 20 years in one study; associated with rectal bleeding and mucous diarrhea (Dis Colon Rectum 2004;47:1208)
Represented 1/3 of inflammatory polyps in children in one study (Arkh Patol 2003;65:29)
Different mucins are expressed than normal colon (Gut 1998;42:135)
Case reports: Japanese woman with polyps throughout colon (Gut 2005;54:1342), associated with protein losing enteropathy (Am J Gastroenterol 2000;95:2095)
Treatment: polypectomy; patients with multiple polyps or other pathology may require resection; infliximab (Gastroenterology 2004;126:1868) and Helicobacter treatment may be useful (Helicobacter 2004;9:651)
Gross: sessile polyp covered by cap of fibrinopurulent exudate
Micro: crypts are elongated, tortuous and distended with goblet cell hypertrophy and serrated tubules; eroded surface with fibrinopurulent inflammatory cap overlying acute and chronically inflamed stroma with fibromuscular obliteration of lamina propria and proliferation of muscularis mucosa
References: Am J Gastroenterol 2002;97:370, Histopathology 1993;23:63
Uncommon in colon
Any age, no clinical associations
Benign
Treatment: endoscopic excision if small (Intern Med 2000;39:25), resection if large
Case reports: 40 year old man with positive fecal occult blood test (Dig Liver Dis 2005;37:968), causing intussusception (Dis Colon Rectum 1979;22:575), with neurofibromatosis (Ann Acad Med Singapore 2004;33:797)
Gross: mean 3-4 cm, polypoid with broad base; tan-gray-yellow; overlying mucosa may be ulcerated
Micro: usually limited to submucosa; spindle cell lesion in fibrovascular stroma with chronic inflammatory infiltrate including eosinophils; may be sparsely cellular with myxoid stroma; cellular areas may have up to 2 mitotic figures/HPF; may have rarefaction (zone of loose connective tissue) around muscular-walled blood vessels
Positive
stains: vimentin, muscle
specific actin, smooth muscle actin, CD34; variable S100
Negative stains: desmin, CD117
DD: fibromatosis (invades bowel secondarily), arteriovenous malformation (J Gastroenter 2004;39:575)
Inflammatory myoglandular polyp of colon
Mean age 53 years
Distal colon; rarely in ileum where it may cause intussusception
Associated with mucous diarrhea, tenesmus and hematochezia
Case reports: 80 year old man (Turk J Gastroenterol 2004;15:117), with rectal bleeding (Pathol Res Pract 2003;199:837)
Gross: solitary, pedunculated, red with smooth surface (Endoscopy 2003;35:363)
Micro: inflammatory granulation tissue in lamina propria, branching and dilated glands arising within proliferating smooth muscle (resembling Peutz-Jegher polyp)
DD: inflammatory polyp (no abundant smooth muscle), Peutz-Jegher polyp (no prominent inflammation)
References: AJSP 1992;16:772
Most common childhood polyp
Usually children < 5 years, may occur in adults
80% in rectum
Commonly presents with rectal bleeding (Gastroenterol Jpn 1979;14:425); polyps may autoamputate (10%) due to torsion
Usually sporadic; rarely associated with juvenile polyposis syndrome (see below)
Not neoplastic by themselves, but may be associated with dysplasia (Archives 1996;120:1032)
Case reports: in esophageal colon interposition (J Pediatr Surg 1998;33:1418), with intramucosal carcinoma (Archives 1987;111:200), causing intussusception (Postgrad Med 1978;64:188)
Gross: hamartomatous, large (1-3 cm) lesions with long (1-2 cm) stalks, red granular or glistening surface; may see cystic cavities
Micro: granulation tissue and ulcer covering abundant cystically dilated glands filled with mucus in an edematous and inflamed stroma; 20% have hyperplastic changes; minimal epithelium or smooth muscle; no atypia; rarely osseous metaplasia, foreign-body giant cell reaction to ruptured glands
DD: inflammatory polyp
Lymphoid polyp of colon
Also called lymphoid hyperplasia
All ages; may be associated with bleeding or prolapse
Usually solitary, sessile, in rectum
Case reports: 51 year old woman (J Clin Pathol 1997;50:1034), 8 year old boy with lymphoid hyperplasia throughout bowel (Z Gastroenterol 1997;35:271), causing massive bleeding in a transplant patient (Indian J Gastroenterol 1996;15:20)
Treatment: excision
Gross: soft, superficial polyp covered by intact, smooth, gray mucosa; single or multiple
Micro: mucosal or submucosal lymphoid follicles with germinal centers that may distort muscularis mucosa or involve muscularis propria
DD: lymphoma
Develops up to 40 years after uterosigmoidostomy
Features of retention and adenomatous polyp
Case reports: Prog Urol 1996;6:590, Dis Colon Rectum 1988;31:961, Eur Urol 1986;12:360, Am J Gastroenterol 1984;79:453, Cancer 1984;53:1006
First described in 1990 (AJSP 1990;14:524)
The definition and significance of this entity is not well established
Neoplastic, 1-2% of all polyps
Combination of hyperplastic and adenomatous polyp
Usually in sigmoid colon and rectum (Anticancer Res 2000;20:1141)
Often have microsatellite-instability mutations and DNA methylation; right sided lesions may be precursor of sporadic microsatellite-unstable colorectal carcinoma, particularly if large, multiple and part of giant hyperplastic polyposis (J Natl Cancer Inst 2001;93:1282)
May be associated with attenuated (<100 polyps) familial adenomatous polyposis (Gut 2002;50:402)
Risk of subsequent carcinoma is 5-6% (AJCP 2005;123:349, World J Gastroenterol 2006;12:2770)
6% of colorectal carcinomas are associated with coexisting serrated adenomas (Pathol Int 2001;51:215)
Inhibition of apoptosis in upper and middle crypts of hyperplastic polyps and serrated adenomas may be due to reduced Fas expression and may cause serrated appearance (AJSP 2002;26:249)
Case report: developing into carcinoma within 2 years (J Gastroenterol 2002;37:467), polyp with intraepithelial carcinoma (Pathol Int 2001;51:215), associated with multiple “serrated adenocarcinomas” (J Pathol 2000;190:444)
Gross: mean 6-9 mm
Micro: variable, ranging from clearly adenomatous to resembling a hyperplastic polyp
Proposed definition: surface epithelial nuclear dysplasia (elongation, increased N/C ratio, nucleoli, atypia) and serration of 20%+ of lesional crypts (Mod Path 2003;16:417)
Left sided: have “normal proliferation” - less pronounced adenomatous features; may be vesicular cell type with prominent serration, irregular thickening of muscularis mucosa, decreased or dystrophic goblet cells, mucin in vesicular cells similar to hyperplastic polyp; also goblet cell type with less prominent serration but thick mucosa and thick basal membrane; also mucin poor type (rare) with prominent serration, no mucin
Right sided: usually large, with abundant mucin (intra/extracellular), abnormal proliferation (i.e. adenomatous changes), dilated and distorted crypts, often secondary papillae
Positive stains: CK7 and CK20 (Dig Dis Sci 2005;50:1741); similar mucin profiles as hyperplastic polyp and gastric antral mucosa (Pathol Int 2004;54:401), KI-67 (19%, intermediate between hyperplastic polyp and adenoma, proliferation in basal or intermediate [but not superficial] crypts, Pathol Int 2003;53:277); also p53 (29-50%) and hTERT (46-53%) (Scand J Gastroenterol 2002;37:1194), COX2 (Dis Colon Rectum 2001;44:1319)
Molecular: MLH1 and PMS2 is often lost in zones of dysplasia or early carcinoma (AJCP 2006;126:1); K-ras mutations in 40%, particularly in nodular and rectal lesions (Dis Colon Rectum 2003;46:327); more highly methylated than tubular adenomas (Am J Pathol 2003;162:815), often BRAF mutations (Virchows Arch 2005;447:597, Cancer Res 2003;63:4878)
DD: adenoma, hyperplastic polyp, colchicine effect (Archives 2002;126:615)
References: AJSP 2003;27:65, Batts: USCAP 2004
Serrated polyp of colon with abnormal proliferation
Also called sessile serrated adenoma
Precedes microsatellite-unstable adenocarcinoma (AJCP 2003;119:778)
MIB staining not helpful in differentiating (AJCP 2006;125:407)
Cases with focal invasive adenocarcinoma or high grade dysplasia: most of polyp is nonmalignant, with abrupt transition to malignancy; hMLH1 negative (AJCP 2006;125:132)
Micro: expanded crypt proliferative zone, exaggerated serrated architectural outline in basilar crypt region, basilar crypt dilation, inverted crypts, and predominance of dysmaturational crypts (crypts with minimal cell maturation); also horizontal extension of the crypt base along the muscularis mucosa J Clin Pathol 2004;57:682)
Positive stains: Ki-67, Kras, BRAF and methylation present, but this does not distinguish these polyps from traditional hyperplastic polyps (AJCP 2006;125:407) or serrated adenomas (AJSP 2004;28:1452)
Negative stains: p53 (usually); reduced expression of hMHL1 and hMSH2 (AJSP 2003;27:65)
References: Cesk Patol 2006;42:133
Only rarely described
Resemble transitional mucosa surrounding carcinoma and adenoma in the colon (Pathol Res Pract 1987;182:690)
Gross: small polypoid lesion
Micro: elongated and widened crypts, enlarged goblet cells, increased mucin
Positive stains: sialomucins
References: Endoscopy 1982;14:174
90% of GI tubular adenomas occur in colon; also stomach and small intestine
50% are single
Prevalence of 30% in adults at autopsy, increasing with age
Risk of subsequent adenomas or colorectal carcinoma is related to size; higher risk if 6-10 mm or larger, multiple adenomas or family history (Ann Intern Med 1998;129:273, Gut 2002;51:424)
May bleed due to twisting; large polyps may cause change in bowel habits or intussusception
Associated with hypertriglyceridemia (World J Gastroenterol 2006;12:1261)
Case reports: osseous metaplasia (J Clin Pathol 2005;58:220), metastatic signet ring cell carcinoma in adenoma (Pathol Res Pract 2004;200:707, Archives 2003;127:1509), metastatic melanoma in adenoma (Dis Colon Rectum 2002;45:1681)
Gross: usually < 1 cm and pedunculated, but may be sessile; darker color than surrounding mucosa; multiple polyps tend to cluster