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Tgfbr1 haploinsufficiency inhibits the development of murine mutant Kras-induced pancreatic precancer
Kevin Adrian; Matthew J. Strouch; Qinghua Zeng; Morgan R. Barron; Eric C. Cheon; Akilesh Honasoge; Yanfei Xu; Sharbani Phukan; Maureen Sadim; et al. (Profiled Authors: David Jason Bentrem; Paul J Grippo)
Cancer Research. 2009;69(24):9169-9174.Abstract
To dissect the role of constitutively altered Tgfbr1 signaling in pancreatic cancer development, we crossed Elastase-KrasG12D (EL-Kras) mice with Tgfbr1 haploinsufficient mice to generate EL-Kras/Tgfbr1 +/- mice. Mice were euthanized at 6 to 9 months to compare the incidence, frequency, and size of precancerous lesions in the pancreas. Only 50% of all EL-Kras/Tgfbr1+/- mice developed preinvasive lesions compared with 100% of EL-Kras (wild-type Tgfbr1) mice. The frequency of precancerous lesions was 4-fold lower in haploinsufficient than in control mice. Paradoxically, the precancerous lesions of EL-Kras/Tgfbr1+/- mice were considerably larger than those in EL-Kras mice. Yet, the mitotic index of precancerous cells and the observable levels of fibrosis, lipoatrophy, and lymphocytic infiltration were reduced in EL-Kras/Tgfbr1+/- mice. We conclude that Tgfbr1 signaling promotes the development of precancerous lesions in mice. These findings suggest that individuals with constitutively decreased TGFBR1 expression may have a decreased risk of pancreatic cancer. ©2009 American Association for Cancer Research.
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