Orofacial and gastrointestinal hyperplasia and neoplasia in smad4 +/- and elf+/-/smad4+/- mutant mice

Robert S. Redman, Varalakshmi Katuri, Yi Tang, Allan Dillner, Bibhuti Mishra, Lopa Mishra

Research output: Contribution to journalArticlepeer-review


BACKGROUND: 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 a β-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+/-lelf+/- 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+/-lelf+/- mice developed extensive hyperplasia and neoplasia of the gastric mucosa. CONCLUSION: These findings indicate that investi-gating interactions among smad4, 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.

Original languageEnglish (US)
Pages (from-to)23-29
Number of pages7
JournalJournal of Oral Pathology and Medicine
Issue number1
StatePublished - Jan 2005


  • Elf β-spectrin
  • Hyperplasia
  • Mouse
  • Mutant strain
  • Neoplasms
  • Smad4 protein
  • Transforming growth factor-β

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Oral Surgery
  • Otorhinolaryngology
  • Cancer Research
  • Periodontics


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