Abstract |
Patients with inflammatory bowel disease may develop dysplasia in the cryptal epithelium, polypoid neoplasias, and nonpolypoid (flat) adenomas, lesions at risk to proceed to colorectal carcinoma. The onset of invasion in nonpolypoid adenomas may occur without changes in the shape or the size of the lesion. In experimental animals, some colonotropic carcinogens induce polypoid and nonpolypoid neoplasias and others induce polypoid neoplasias exclusively. Some of the biologic attributes of nonpolypoid adenomas in humans can be demonstrated in laboratory animals.
|
Authors | Carlos A Rubio, Premysl Slezak |
Journal | Gastrointestinal endoscopy clinics of North America
(Gastrointest Endosc Clin N Am)
Vol. 24
Issue 3
Pg. 455-68
(Jul 2014)
ISSN: 1558-1950 [Electronic] United States |
PMID | 24975536
(Publication Type: Journal Article, Review)
|
Copyright | Copyright © 2014 Elsevier Inc. All rights reserved. |
Chemical References |
- KRAS protein, human
- Mucins
- Proto-Oncogene Proteins
- Tumor Suppressor Protein p53
- Proto-Oncogene Proteins p21(ras)
- ras Proteins
|
Topics |
- Adenoma
(etiology, metabolism, pathology)
- Animals
- Apoptosis
- Carcinoma
(etiology, pathology)
- Cell Proliferation
- Colonic Polyps
(etiology, pathology)
- Colonoscopy
- Colorectal Neoplasms
(etiology, metabolism, pathology)
- Humans
- Inflammatory Bowel Diseases
(complications, pathology)
- Mucins
(metabolism)
- Precancerous Conditions
(etiology, pathology)
- Proto-Oncogene Proteins
(metabolism)
- Proto-Oncogene Proteins p21(ras)
- Rats
- Tumor Suppressor Protein p53
(metabolism)
- ras Proteins
(metabolism)
|