Abstract
Much excitement has recently been generated by the discovery of the Smad genes, encoding proteins that transduce signals from the transforming growth factor β family of cytokines. Here, we report the completion of cloning of the six known human Smads, providing novel sequences for Smad5 and Smad6. Previously, Smad4 and Smad2 were shown to be mutated in human cancers. However, analysis of the other four Smad genes revealed no mutations in a total of 167 tumors, including those from colon, breast, lung, and pancreas. These results suggest that the various Smad genes have different functions and demonstrate that mutations in these four genes do not, in general, account for the widespread resistance to transforming growth factor β that is found in human tumors.
Original language | English (US) |
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Pages (from-to) | 2578-2580 |
Number of pages | 3 |
Journal | Cancer Research |
Volume | 57 |
Issue number | 13 |
State | Published - Jul 1 1997 |
ASJC Scopus subject areas
- Oncology
- Cancer Research