| First Author | Redman RS | Year | 2005 |
| Journal | J Oral Pathol Med | Volume | 34 |
| Issue | 1 | Pages | 23-9 |
| PubMed ID | 15610403 | Mgi Jnum | J:96300 |
| Mgi Id | MGI:3529916 | Doi | 10.1111/j.1600-0714.2004.00246.x |
| Citation | Redman RS, et al. (2005) Orofacial and gastrointestinal hyperplasia and neoplasia in smad4 and elf/smad4 mutant mice. J Oral Pathol Med 34(1):23-9 |
| abstractText | Background: Smad4 is vital to the roles of Smads 2 and 3 in transforming growth factor-beta (TGF)-beta signal transduction, and inactivated Smad4 is common to human gastrointestinal cancers. The embryonic liver fodrin (ELF) is a beta-spectrin that facilitates the nuclear translocation of activated Smad4. Methods: Smad4(+/-) mice, known to develop gastrointestinal cancer, were crossbred with elf(+/-) mice. The smad4(+/-) and smad4(+/-)/elf(+/-) offspring were autopsied as abnormalities developed. Results: In addition to polyps and adenocarcinomas of the stomach and duodenum, the smad4(+/-) mice developed squamous cell carcinomas of the skin, oral mucosa and forestomach, benign neoplasms of connective tissue and lacrimal gland, and a lymphoma. The smad4(+/-)/elf(+/-) mice developed extensive hyperplasia and neoplasia of the gastric mucosa. Conclusion: These findings indicate that investigating interactions among smad4, elf, and other genes involved in TGF-beta 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. |
