This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The CRC Pathology Core has served the entire group by performing comprehensive histo-pathological assessment of most organs and tissues of the APC min- - mouse. This publication, to appear shortly in the International Journal of Experimental Pathology, demonstrates significant differentiation blockade in most proliferating tissues. (You S, Ohmori M, Pena MM, Nassri B, Du-Quiton J, Al-Assad ZA, Liu LL, Wood PA,Berger SH, Liu Z, Wyatt ZA, Price RL, Berger FG, Hrushesky WJM. Histological Evidence of Differentiation Blockade among Proliferative Tissues in Apc Min/+ Mice. In press, International Journal of Experimental Pathology, 2006.) Because of the pro-cancer effects of a mutant mPer2 circadian clock gene, we have mated clock gene mutant mice with ApcMin/+ mice, and have discovered substantial interactive effects of these genotypes on the tumorigenic phenotype. This publication will be submitted for publication shortly. A number of individual COBRE investigators have utilized the Pathology Core. These have included Dr. Lorne Hofseth (quantification of inflammation), James Carson (assessing the effects of circadian disruption by light), Dr. Mike Wyatt and Dr. Sondra Berger (quantification of hematologic, metabolic and carcinogenic effects of the ApcMin mutation), Dr. Philip Buckhaults (collection of colorectal polyps and normal colorectal mucosa from circadian disrupted and normal patients), and James Burch (study of frequency of severe circadian disruption among colorectal polyp patients).
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