Genetic susceptibility to tobacco carcinogenesis.
Lung cancer risk is thus defined by the balance between metabolic activation and detoxification of xenobiotic compounds and by the efficiency of DNA repair. It is most likely that multiple susceptibility factors must be accounted for to represent the true dimensions of gene-environment interactions. The ability to identify smokers with the highest risks of developing cancer has substantial preventive implications. These subgroups could be targeted for the most intensive screening and smoking cessation interventions and could be enrolled into chemoprevention trials. Studying susceptibility to common cancers and widely prevalent exposures may provide further insights into the basic mechanisms of carcinogenesis. Issues that will need to be addressed in the very near future include risk communication to study subjects and the ethical, legal, and social consequences of such testing.
Spitz
M R
MR
Department of Epidemiology, University of Texas M. D. Anderson Cancer Center, Houston, USA.
Wei
Q
Q
Li
G
G
Wu
X
X
D001761:Bleomycin / Q000494:pharmacology; D002471:Cell Transformation, Neoplastic; D004249:DNA Damage; D004260:DNA Repair; D015972:Gene Expression Regulation, Neoplastic; D020022:Genetic Predisposition to Disease; D006801:Humans; D008175:Lung Neoplasms / Q000209:etiology* / Q000235:genetics*; D010947:Plants, Toxic; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects; D014026:Nicotiana / Q000009:adverse effects*
D001761:Bleomycin