Abstract
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. Smad4+/- mice, known to develop gastrointestinal cancer, were crossbred with elf+/- mice. The smad4+/- and smad4+/-/elf+/- offspring were autopsied as abnormalities developed. 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. 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.
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