<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Christensen ND</submitter><funding>American Cancer Society</funding><funding>NIDCR NIH HHS</funding><funding>Penn State Hershey Cancer Institute</funding><funding>NCI NIH HHS</funding><pagination>109321</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9340668</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>333</volume><pubmed_abstract>HPV infections in the oral cavity that progress to cancer are on the increase in the USA. Model systems to study co-factors for progression of these infections are lacking as HPVs are species-restricted and cannot grow in preclinical animal models. We have recently developed a mouse papillomavirus (MmuPV1) oral mucosal infection model that provides opportunities to test, for the first time, the hypothesis that tobacco carcinogens are co-factors that can impact the progression of oral papillomas to squamous cell carcinoma (SCC). Four cohorts of mice per sex were included: (1) infected with MmuPV1 and treated orally with DMSO-saline; (2) infected with MmuPV1 and treated orally with the tobacco carcinogen, dibenzo[def,p]chrysene (DBP); (3) uninfected and treated orally with DMSO-saline, and (</pubmed_abstract><journal>Chemico-biological interactions</journal><pubmed_title>The environmental pollutant and tobacco smoke constituent dibenzo[def,p]chrysene is a co-factor for malignant progression of mouse oral papillomavirus infections.</pubmed_title><pmcid>PMC9340668</pmcid><funding_grant_id>R21 DE028650</funding_grant_id><funding_grant_id>R01 CA173465</funding_grant_id><pubmed_authors>Aliaga C</pubmed_authors><pubmed_authors>Balogh KK</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Stairs DB</pubmed_authors><pubmed_authors>Shearer D</pubmed_authors><pubmed_authors>El-Bayoumy K</pubmed_authors><pubmed_authors>Chen KM</pubmed_authors><pubmed_authors>Atkins H</pubmed_authors><pubmed_authors>Christensen ND</pubmed_authors><pubmed_authors>Hu J</pubmed_authors><pubmed_authors>Walter V</pubmed_authors><pubmed_authors>Viscidi R</pubmed_authors><pubmed_authors>Sun YW</pubmed_authors><pubmed_authors>Gowda K</pubmed_authors><pubmed_authors>Amin S</pubmed_authors><pubmed_authors>Brendle SA</pubmed_authors></additional><is_claimable>false</is_claimable><name>The environmental pollutant and tobacco smoke constituent dibenzo[def,p]chrysene is a co-factor for malignant progression of mouse oral papillomavirus infections.</name><description>HPV infections in the oral cavity that progress to cancer are on the increase in the USA. Model systems to study co-factors for progression of these infections are lacking as HPVs are species-restricted and cannot grow in preclinical animal models. We have recently developed a mouse papillomavirus (MmuPV1) oral mucosal infection model that provides opportunities to test, for the first time, the hypothesis that tobacco carcinogens are co-factors that can impact the progression of oral papillomas to squamous cell carcinoma (SCC). Four cohorts of mice per sex were included: (1) infected with MmuPV1 and treated orally with DMSO-saline; (2) infected with MmuPV1 and treated orally with the tobacco carcinogen, dibenzo[def,p]chrysene (DBP); (3) uninfected and treated orally with DMSO-saline, and (</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Jan</publication><modification>2025-04-19T06:02:20.091Z</modification><creation>2025-04-19T06:02:20.091Z</creation></dates><accession>S-EPMC9340668</accession><cross_references><pubmed>33186600</pubmed><doi>10.1016/j.cbi.2020.109321</doi></cross_references></HashMap>