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- Title
Orofacial and gastrointestinal hyperplasia and neoplasia insmad4<sup>+/−</sup> andelf<sup>+/−</sup>/smad4<sup>+/−</sup> mutant mice.
- Authors
Redman, Robert S.; Katuri, Varalakshmi; Tang, Yi; Dillner, Allan; Mishra, Bibhuti; Mishra, Lopa
- Abstract
Smad4 is vital to the roles of Smads 2 and 3 in transforming growth factor-beta (TGF)-β signal transduction, and inactivated Smad4 is common to human gastrointestinal cancers. The embryonic liver fodrin (ELF) is aβ-spectrin that facilitates the nuclear translocation of activated Smad4.Smad4+/− mice, known to develop gastrointestinal cancer, were crossbred withelf+/− mice. Thesmad4+/− andsmad4+/−/elf+/− offspring were autopsied as abnormalities developed.In addition to polyps and adenocarcinomas of the stomach and duodenum, thesmad4+/− mice developed squamous cell carcinomas of the skin, oral mucosa and forestomach, benign neoplasms of connective tissue and lacrimal gland, and a lymphoma. Thesmad4+/−/elf+/− mice developed extensive hyperplasia and neoplasia of the gastric mucosa.These findings indicate that investigating interactions amongsmad4,elf, and other genes involved in TGF-β signaling should be useful in further delineating the processes of neoplasia in a wide variety of tissues.J Oral Pathol Med(2005)34: 23–9
- Subjects
INTESTINAL cancer; GROWTH factors; PEPTIDES; MUCOUS membranes; BLOOD proteins; SQUAMOUS cell carcinoma
- Publication
Journal of Oral Pathology & Medicine, 2005, Vol 34, Issue 1, p23
- ISSN
0904-2512
- Publication type
Article
- DOI
10.1111/j.1600-0714.2004.00246.x