@article{quist_boorman_cullen_maronpot_remick_swenberg_freshwater_hardisty_2019, title={Reevaluation of Hepatocellular Neoplasms in CD-1 Mice from a 2-year Oral Carcinogenicity Study with Permethrin}, volume={47}, ISSN={["1533-1601"]}, DOI={10.1177/0192623318809304}, abstractNote={ A 24-month oral carcinogenicity study of permethrin was conducted by feeding male and female CD-1 mice diets containing concentrations of 0, 20, 500, and 2,000 ppm of permethrin (males) or 0, 20, 2,500, and 5,000 ppm of permethrin (females). After approximately two years on study, surviving mice were sacrificed for the evaluation of chronic toxicity and/or carcinogenicity. An expert panel of pathologists was convened as a Pathology Working Group (PWG) to review coded liver histology sections from male and female mice and to classify all liver neoplasms according to current nomenclature and diagnostic criteria guidelines. The PWG results indicate that permethrin induced a significant dose-dependent increase in the incidence of hepatocellular neoplasms in treated female mice ( p < .01) as well as a nonstatistically significant increase in the incidence of hepatocellular tumors in treated male mice. Given the continuum of the diagnoses of adenoma and carcinoma, and the difficulty in distinguishing some of the lesions, it is appropriate to consider only the combined incidences of hepatocellular tumors (adenoma and/or carcinoma) for biological significance and risk assessment. }, number={1}, journal={TOXICOLOGIC PATHOLOGY}, author={Quist, Erin M. and Boorman, Gary A. and Cullen, John M. and Maronpot, Robert R. and Remick, Amera K. and Swenberg, James A. and Freshwater, Les and Hardisty, Jerry F.}, year={2019}, month={Jan}, pages={11–17} }
 @inbook{dixon_herbert_sills_boorman_1999, title={Lung, pleura and mediastinum}, booktitle={Pathology of the mouse: reference and atlas (1st ed.)}, publisher={Vienna, IL: Cache River Press}, author={Dixon, D. and Herbert, R. A. and Sills, R. C. and Boorman, G. A.}, year={1999} }
 @article{trukhanova_hong_sills_bowser_gaul_boorman_turusov_devereux_dixon_1998, title={Predominant p53 G -> A transition mutation and enhanced cell proliferation in uterine sarcomas of CBA mice treated with 1,2-dimethylhydrazine}, volume={26}, ISSN={["0192-6233"]}, DOI={10.1177/019262339802600310}, abstractNote={ Mouse uterine tumors were examined for genetic alterations in the ras proto-oncogene and p53 tumor suppressor gene arid for other biologically relevant immunohistochemical markers that may increase our understanding of the events that occur in uterine cancer. Fourteen dimethylhydrazine (DMH)-induced uterine sarcomas, including 3 primary malignant fibrous histiocytomas (MFH), 7 transplanted MFH, 3 stromal sarcomas, and 1 undifferentiated sarcoma, were first screened by immunohistochemistry for p53 missense mutations, followed by single strand conformation polymorphism analysis and DNA sequencing for the identification of point mutations. There was 100% correlation between p53 protein immunopositivity and subsequent detection ofp53 mutations in DMH-induced malignant fibrous histiocytomas. All MFH had a characteristic p53 G:C→A:T transition mutation, consistent with O6-methylguanine mispairing with thymine, the most common DNA lesion caused by alkylating agents. DMH-induced uterine MFH with p53 mutations also had a higher proliferative rate (qualitatively evaluated by immunohistochemical detection of proliferating cell nuclear antigen) when compared with other DMH-induced sarcomas. Uterine sarcomas were further evaluated for biological end points, such as estrogen receptor and desmin. Neoplastic cells from stromal sarcomas (SS), undifferentiated sarcomas (US), and MFH did not stain for desmin. The estrogen receptor was detected in normal uteri and a small portion of MFH, SS, and US. Our data suggest that DMH-induced uterine sarcomas are not consistent with smooth muscle cell origin and that a subset of these tumors, specifically DMH-induced malignant fibrous histiocytomas, have unique p53 G:C→A:T transitions and a high proliferative rate. }, number={3}, journal={TOXICOLOGIC PATHOLOGY}, author={Trukhanova, LS and Hong, HHL and Sills, RC and Bowser, AD and Gaul, B and Boorman, GA and Turusov, VS and Devereux, TR and Dixon, D}, year={1998}, pages={367–374} }