<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hu Q</submitter><funding>University of Florida</funding><funding>Lung Cancer Research Foundation</funding><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><pagination>170-181</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8947227</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>43(2)</volume><pubmed_abstract>Lung cancer is the leading cause of cancer-related deaths. While tobacco use is the main cause, only 10-20% of smokers eventually develop clinical lung cancer. Thus, the ability of lung cancer risk prediction among smokers could transform lung cancer management with early preventive interventions. Given that DNA damage by tobacco carcinogens is the potential root cause of lung carcinogenesis, we characterized the adductomic totality of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (a potent lung carcinogen in tobacco, commonly known as NNK) in the target lung tissues, the liver tissues and the peripheral serum samples in a single-dose NNK-induced lung carcinogenesis A/J mouse model. We also characterized these adductomic totalities from the two enantiomers of 4-(methylnitrosamino)-1-(3-py</pubmed_abstract><journal>Carcinogenesis</journal><pubmed_title>Characterization of adductomic totality of NNK, (R)-NNAL and (S)-NNAL in A/J mice, and their correlations with distinct lung carcinogenicity.</pubmed_title><pmcid>PMC8947227</pmcid><funding_grant_id>R01 CA193278</funding_grant_id><funding_grant_id>P30 CA077598</funding_grant_id><pubmed_authors>Huo Z</pubmed_authors><pubmed_authors>Aly FZ</pubmed_authors><pubmed_authors>Hecht SS</pubmed_authors><pubmed_authors>Xing C</pubmed_authors><pubmed_authors>Hu Q</pubmed_authors><pubmed_authors>Upadhyaya P</pubmed_authors></additional><is_claimable>false</is_claimable><name>Characterization of adductomic totality of NNK, (R)-NNAL and (S)-NNAL in A/J mice, and their correlations with distinct lung carcinogenicity.</name><description>Lung cancer is the leading cause of cancer-related deaths. While tobacco use is the main cause, only 10-20% of smokers eventually develop clinical lung cancer. Thus, the ability of lung cancer risk prediction among smokers could transform lung cancer management with early preventive interventions. Given that DNA damage by tobacco carcinogens is the potential root cause of lung carcinogenesis, we characterized the adductomic totality of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (a potent lung carcinogen in tobacco, commonly known as NNK) in the target lung tissues, the liver tissues and the peripheral serum samples in a single-dose NNK-induced lung carcinogenesis A/J mouse model. We also characterized these adductomic totalities from the two enantiomers of 4-(methylnitrosamino)-1-(3-py</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Mar</publication><modification>2025-04-29T11:09:26.754Z</modification><creation>2025-04-06T19:49:24.068Z</creation></dates><accession>S-EPMC8947227</accession><cross_references><pubmed>34919675</pubmed><doi>10.1093/carcin/bgab113</doi></cross_references></HashMap>