Definition/General
Introduction:
Colorectal tubular adenoma is a benign epithelial neoplasm composed of dysplastic glands with tubular architecture
It represents the most common type of adenomatous polyp (75-85%)
Shows malignant potential through adenoma-carcinoma sequence
Requires complete excision and surveillance.
Origin:
Arises from colonic surface epithelium and crypts
Results from accumulated genetic alterations
Begins with APC gene mutations
Shows monoclonal proliferation
Demonstrates loss of cell cycle control.
Classification:
WHO classification: Tubular adenoma (>75% tubular architecture)
Tubulovillous adenoma (25-75% villous)
Villous adenoma (>75% villous)
Dysplasia grading: Low-grade dysplasia
High-grade dysplasia.
Epidemiology:
Peak incidence in 6th-7th decades
Male predominance (2:1)
More common in Western countries
Increasing incidence in India with lifestyle changes
Left-sided predominance in most populations
Malignant transformation in 5-10% cases.
Clinical Features
Presentation:
Asymptomatic in majority (80-90%)
Rectal bleeding
Change in bowel habits
Mucus discharge
Abdominal pain (uncommon)
Iron deficiency anemia
Detected on screening colonoscopy.
Symptoms:
Occult bleeding (positive FOBT)
Intermittent hematochezia
Mucoid diarrhea (large villous component)
Tenesmus in rectal location
Crampy abdominal pain
Rarely bowel obstruction.
Risk Factors:
Age >40 years
Family history of colorectal cancer
Personal history of adenomas
Inflammatory bowel disease
High-fat, low-fiber diet
Smoking
Alcohol consumption
Obesity
Sedentary lifestyle.
Screening:
Colonoscopy gold standard
Sigmoidoscopy for left-sided lesions
CT colonography
Fecal occult blood test
Stool DNA testing
Surveillance intervals based on findings.
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Gross Description
Appearance:
Polypoid lesion with smooth or lobulated surface
Pink to red coloration
Soft consistency
Pedunculated or sessile morphology
Surface may be granular
No obvious malignant features.
Characteristics:
Well-demarcated from surrounding mucosa
Intact surface usually
Homogeneous cut surface
No necrosis typically
May show surface erosion
Friable consistency.
Size Location:
Size ranges from 0.3-3 cm typically
Sigmoid colon most common (40%)
Rectum (25%)
Descending colon (15%)
Left-sided predominance
Can occur throughout colon.
Multifocality:
Multiple adenomas in 20-30% patients
Synchronous adenomas common
Familial adenomatous polyposis - hundreds of adenomas
Metachronous development frequent
Field effect concept.
Microscopic Description
Histological Features:
Dysplastic epithelium lining tubular glands
Crowded, elongated nuclei
Nuclear stratification
Loss of mucin
Increased mitotic activity
Basement membrane intact.
Cellular Characteristics:
Columnar epithelial cells
Enlarged, hyperchromatic nuclei
Nuclear pseudostratification
Reduced cytoplasmic mucin
Mitoses above basal zone
Prominent nucleoli.
Architectural Patterns:
Tubular architecture predominant (>75%)
Branching glands
Back-to-back arrangement
Surface maturation may be present
Cribriform pattern in high-grade areas
Budding and branching.
Grading Criteria:
Low-grade dysplasia: mild-moderate nuclear atypia, preserved polarity
High-grade dysplasia: severe nuclear atypia, loss of polarity, cribriform architecture
Carcinoma in situ included in high-grade
No invasion of muscularis mucosae.
Immunohistochemistry
Positive Markers:
CK20 positive (apical pattern in normal areas)
CDX2 positive (intestinal marker)
β-catenin nuclear accumulation (Wnt pathway)
Ki-67 increased proliferation
p53 may be positive in high-grade.
Negative Markers:
CK7 negative typically
TTF-1 negative
PSA negative
Chromogranin negative
Synaptophysin negative
Smooth muscle markers negative.
Diagnostic Utility:
β-catenin shows nuclear positivity (APC pathway)
p53 overexpression in progression
Ki-67 shows expanded proliferative zone
CDX2 confirms intestinal differentiation
MLH1, MSH2, MSH6, PMS2 for Lynch syndrome.
Molecular Subtypes:
Microsatellite stable (majority)
Microsatellite instability (Lynch syndrome)
CpG island methylator phenotype
Chromosomal instability pathway
Serrated pathway (different entity).
Molecular/Genetic
Genetic Mutations:
APC mutations (80-90% cases)
KRAS mutations (30-40%)
PIK3CA mutations (15-20%)
TP53 mutations (late event)
SMAD4 mutations
Loss of 18q (DCC region).
Molecular Markers:
Wnt pathway activation (APC loss)
RAS-MAPK pathway (KRAS mutations)
PI3K-AKT pathway
TGF-β pathway alterations
p53 pathway disruption.
Prognostic Significance:
Size >1 cm increases malignancy risk
High-grade dysplasia higher risk
Villous component increases risk
Multiple adenomas indicate field effect
KRAS mutations predict anti-EGFR resistance.
Therapeutic Targets:
Complete polypectomy curative for benign adenomas
Surveillance colonoscopy required
NSAIDs may reduce recurrence
Aspirin chemoprevention
Lifestyle modifications
Genetic counseling if familial.
Differential Diagnosis
Similar Entities:
Hyperplastic polyp - no dysplasia, saw-tooth architecture
Sessile serrated adenoma - serrated architecture, BRAF mutations
Traditional serrated adenoma - eosinophilic cytoplasm, surface serrations
Adenocarcinoma - invasion present
Inflammatory polyp - reactive changes.
Distinguishing Features:
Hyperplastic polyp: no dysplasia, surface maturation, small size
Sessile serrated adenoma: horizontal crypts, dilated bases, BRAF mutations
Traditional serrated adenoma: surface serrations, eosinophilic cells
Adenocarcinoma: stromal invasion, desmoplasia
Inflammatory polyp: ulceration, granulation tissue.
Diagnostic Challenges:
Sampling artifact in small biopsies
Tangential sectioning
Distinguishing high-grade dysplasia from carcinoma
Pseudoinvasion vs true invasion
Differentiating from serrated lesions.
Rare Variants:
Flat adenoma - depressed or flat morphology
Mixed adenoma - multiple architectural patterns
Adenoma with focal high-grade dysplasia
Adenoma arising in IBD
Polyposis syndromes.
Sample Pathology Report
Template Format
Sample Pathology Report
Complete Report: This is an example of how the final pathology report should be structured for this condition.
Specimen Information
Colorectal polyp, [size] cm, [pedunculated/sessile]
Diagnosis
Tubular adenoma with [low-grade/high-grade] dysplasia
Classification
Benign adenomatous polyp, tubular type
Histological Features
Shows tubular architecture (>75%) with dysplastic epithelium. [Low-grade/High-grade] dysplasia present.
Size and Architecture
Size: [X] cm, Architecture: [%] tubular, [%] villous
Margins
Polyp appears completely excised
Special Studies
β-catenin: nuclear positivity (APC pathway)
MSI testing if clinically indicated
Ki-67 shows increased proliferation
Recommendations
Follow-up colonoscopy in [3-5] years based on findings
Final Diagnosis
Tubular adenoma with [low-grade/high-grade] dysplasia, completely excised