Skip Navigation

JNCI Journal of the National Cancer Institute 1999 91(7):578-579; doi:10.1093/jnci/91.7.578
© 1999 by Oxford University Press
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Spitz, M. R.
Right arrow Articles by Di Giovanni, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Spitz, M. R.
Right arrow Articles by Di Giovanni, J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Journal of the National Cancer Institute, Vol. 91, No. 7, 578-579, April 7, 1999
© 1999 Oxford University Press

EDITORIALS

Molecular Dosimeters of Smoking Damage in the Lung

Margaret R. Spitz, Mariza de Andrade, John Di Giovanni

Affiliation of authors: Departments of Epidemiology and Carcinogenesis, The University of Texas M. D. Anderson Cancer Center, Houston.

Correspondence to: Margaret R. Spitz, M.D., Department of Epidemiology, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Box 189, Houston, TX 77030 (e-mail: mspitz@notes.mdacc.tmc.edu).

Traditional epidemiologic research relied on self-reported measures of "external exposure" in defining the association between cigarette smoking and cancer risk. With elucidation of carcinogen-induced genetic and epigenetic events, knowledge of the molecular etiology of smoking-related cancers has expanded rapidly and has facilitated the study of tobacco carcinogenesis.

The dose of tobacco carcinogens to which lung tissue is exposed is modulated by genetic polymorphisms in the enzymes responsible for activation (phase I) and detoxification (phase II) of tobacco carcinogens. For example, the cytochrome(s) P450 multigene superfamily of enzymes is involved in phase I oxidative processes that may create intermediates that are more reactive than the parent compounds and can be carcinogenic or mutagenic. Phase II metabolic processes generally inactivate these . . . [Full Text of this Article]

REFERENCES


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?