Colon tumor
Tubular adenoma

Author: Andrew L.J. Dunn, M.D.
Senior Author: Raul S. Gonzalez, M.D.
Editor-in-Chief Review: Debra Zynger, M.D.

Revised: 5 November 2018, last major update September 2018

Copyright: (c) 2003-2018,, Inc.

PubMed Search: Tubular [title] adenoma colon

Cite this page: Dunn, ALJ, Gonzalez, RS. Tubular adenoma. website. Accessed December 12th, 2018.
Definition / general
  • Neoplastic colon polyp with at least low grade dysplasia
  • Precursor to invasive adenocarcinoma
Essential features
  • Dysplastic nuclei (elongated and hyperchromatic pseudostratification)
  • < 25% villous component
ICD coding
  • Found more commonly in the left colon and rectum compared with other polyps
  • Has a well documented "adenoma to carcinoma” sequence that involves mutations in KRAS, TP53, APC and beta-catenin (Cell 1990;61:759)
  • Activation of KRAS leads to downstream signaling that influences survival, anti-apoptosis and proliferation (J Gastroenterol Hepatol 2012;27:1423)
  • Wnt pathway: activation of Wnt pathway leads to beta-catenin accumulation in the nucleus and subsequent transcription and cell proliferation
  • Mutations include loss of function of APC or beta-catenin mutations that resist degradation by APC (J Gastroenterol Hepatol 2012;27:1423)
Diagrams / tables

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Wnt/β-catenin pathway

Clinical features
  • <1 cm: usually asymptomatic and detected by screening colonoscopy
  • >1 cm: may bleed, lead to iron deficiency anemia, obstruction; increased risk of progressing to carcinoma
  • Mostly left sided in spontaneous polyps and in familial adenomatous polyposis; right sided in Lynch syndrome (Gut 2002;50:382)
  • Diagnosis is made by histologic confirmation
Case reports
  • Colonoscopy is diagnostic and potentially curative (via polypectomy)
  • High grade dysplasia and large polyps may warrant endoscopic mucosal resection or partial colectomy
Clinical images

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Large sigmoid polyp

Gross description
  • May be sessile or pedunculated
  • Typically dark red compared with mucosa
  • Features concerning for high grade dysplasia or malignancy include size >1 cm, villous architecture and ulceration / friability
Gross images

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Contributed by Laleh Montaser, M.D. (Beth Israel Deaconess Medical Center)

Colonic tubular adenoma

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Tubular adenoma

Hemorrhagic surface

Multiple cecal polyps

Microscopic (histologic) description
  • Polypoid colonic mucosa covered with dysplastic epithelium comprised of hyperchromatic, elongated nuclei arranged in a pseudostratified manner
  • Dysplasia is typically low grade but may also be high grade, with architectural (cribriforming, luminal necrosis) and cytologic changes (vesicular chromatin, nucleoli, loss of basal polarity)
  • Abrupt transition from normal to dysplastic mucosa is commonly present
  • Variable amounts of mucin loss
  • Metaplasia may be present: osseous (J Clin Pathol 2005;58:220), squamous (J Surg Oncol 1984;26:130) or Paneth cells
  • Pseudoinvasion can mimic progression to adenocarcinoma but displaced glands are benign and surrounded by lamina propria and often hemosiderin (Mod Pathol 2015;28:S88)
Microscopic (histologic) images

Images hosted on PathOut server:

Contributed by Andrew L.J. Dunn, M.D.

Nuclear crowding

Transition to dysplasia

Dark nuclei with pseudostratification

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Attached on a stalk

Compared to normal mucosa

Pseudocarcinomatous invasion

Positive stains
  • BCL2 (almost all cases), increased CEA (in atypical areas)
Negative stains
  • p53 (usually)
Molecular / cytogenetics description
  • One-third are aneuploid
  • Depending on the villous component, two types of tubular adenomas can be identified (Am J Surg Pathol 2011;35:212):
    • TA1: less than 1% villous component, lower rate of p53 overexpression, KRAS mutation and MGMT loss
    • TA2: 1 - 20% villous component, higher rate of TP53 and KRAS mutation and MGMT loss
  • KRAS mutations may account for up to 60% of mutations in tubular adenomas (J Gastroenterol Hepatol 2012;27:1423)
Differential diagnosis
Board review question #1
    Which of the following gene mutations is implicated in a majority of tubular adenomas?

  1. ALK
  2. BAP1
  3. KRAS
  4. MDM2
Board review answer #1
C. KRAS mutations are implicated in up to 60% of adenomas and adenocarcinomas. BAP1 mutations are present in a subset of melanocytic tumors and mesotheliomas. MDM2 is amplified in liposarcoma and some of its variants. ALK mutations can be seen in inflammatory myofibroblastic tumor, anaplastic large cell lymphoma and a subset of lung adenocarcinomas.

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