@article{rojas_mcgill_salvador_bautz_threadgill_2021, title={Epithelial-specific ERBB3 deletion results in a genetic background-dependent increase in intestinal and colon polyps that is mediated by EGFR}, volume={17}, ISSN={["1553-7404"]}, DOI={10.1371/journal.pgen.1009931}, abstractNote={ERBB3 has gained attention as a potential therapeutic target to treat colorectal and other types of cancers. To confirm a previous study showing intestinal polyps are dependent upon ERBB3, we generated an intestinal epithelia-specific ERBB3 deletion in C57BL/6-ApcMin/+ mice. Contrary to the previous report showing a significant reduction in intestinal polyps with ablation of ERBB3 on a B6;129 mixed genetic background, we observed a significant increase in polyp number with ablation of ERBB3 on C57BL/6J compared to control littermates. We confirmed the genetic background dependency of ERBB3 by also analyzing polyp development on B6129 hybrid and B6;129 advanced intercross mixed genetic backgrounds, which showed that ERBB3 deficiency only reduced polyp number on the mixed background as previously reported. Increased polyp number with ablation of ERBB3 was also observed in C57BL/6J mice treated with azoxymethane showing the effect is model independent. Polyps forming in absence of ERBB3 were generally smaller than those forming in control mice, albeit the effect was greatest in genetic backgrounds with reduced polyp numbers. The mechanism for differential polyp number in the absence of ERBB3 was through altered proliferation. Backgrounds with increased polyp number with loss of ERBB3 showed an increase in cell proliferation even in non-tumor epithelia, while backgrounds showing reduced polyp number with loss of ERBB3 showed reduced cellular proliferation. Increase polyp number caused by loss of ERBB3 was mediated by increased epidermal growth factor receptor (EGFR) expression, which was confirmed by deletion of Egfr. Taken together, this study raises substantial implications on the use of ERBB3 inhibitors against colorectal cancer. The prediction is that some patients may have increased progression with ERBB3 inhibitor therapy, which is consistent with observations reported for ERBB3 inhibitor clinical trials.}, number={11}, journal={PLOS GENETICS}, author={Rojas, Carolina Mantilla and McGill, Michael P. and Salvador, Anna C. and Bautz, David and Threadgill, David W.}, year={2021}, month={Nov} }
 @article{bautz_sherpa_threadgill_2017, title={Prophylactic vaccination targeting erbb3 decreases polyp burden in a mouse model of human colorectal cancer}, volume={6}, number={1}, journal={Oncoimmunology}, author={Bautz, D. J. and Sherpa, A. T. and Threadgill, D. W.}, year={2017} }
 @article{bautz_broman_threadgill_2013, title={Identification of a Novel Polymorphism in X-Linked Sterol-4-Alpha-Carboxylate 3-Dehydrogenase (Nsdhl) Associated with Reduced High-Density Lipoprotein Cholesterol Levels in I/LnJ Mice}, volume={3}, ISSN={["2160-1836"]}, DOI={10.1534/g3.113.007567}, abstractNote={Loci controlling plasma lipid concentrations were identified by performing a quantitative trait locus analysis on genotypes from 233 mice from a F2 cross between KK/HlJ and I/LnJ, two strains known to differ in their high-density lipoprotein (HDL) cholesterol levels. When fed a standard diet, HDL cholesterol concentration was affected by two significant loci, the Apoa2 locus on Chromosome (Chr) 1 and a novel locus on Chr X, along with one suggestive locus on Chr 6. Non-HDL concentration also was affected by loci on Chr 1 and X along with a suggestive locus on Chr 3. Additional loci that may be sex-specific were identified for HDL cholesterol on Chr 2, 3, and 4 and for non-HDL cholesterol on Chr 5, 7, and 14. Further investigation into the potential causative gene on Chr X for reduced HDL cholesterol levels revealed a novel, I/LnJ-specific nonsynonymous polymorphism in Nsdhl, which codes for sterol-4-alpha-carboxylate 3-dehydrogenase in the cholesterol synthesis pathway. Although many lipid quantitative trait locus have been reported previously, these data suggest there are additional genes left to be identified that control lipid levels and that can provide new pharmaceutical targets.}, number={10}, journal={G3-GENES GENOMES GENETICS}, author={Bautz, David J. and Broman, Karl W. and Threadgill, David W.}, year={2013}, month={Oct}, pages={1819–1825} }