• Nicotine addiction genes;
• Gene variants involved in metabolism of chemicals, hormones and folic acid;
• DNA repair genes;
• Agents that push cells to mutate, or change;
• Length of telomeres (protein caps that stabilize chromosomes);
• Genes that control the cell cycle;
• Genes involved in inflammation;
• Methylation (addition of methyl groups that destroy gene function); and
• Genes that control a cell's "microenvironment."

The combined findings eventually will provide a molecular road map to risk of cancer development as well as optimal cancer treatment. If oncologists knew who would be most susceptible to cancer development, it may be possible to use agents or behavior modifications as preventatives. If cancer does develop, oncologists may be able to tailor treatment to an individual's own genetic profile.

The department also has launched the first long-term effort to study health outcomes and risk factors in the Mexican-American population in the Houston metropolitan area, research paid for by philanthropy and tobacco industry settlement funds. Over many years, the study aims to enroll more than 100,000 Mexican-Americans in Texas, and to date more than 10,000 have joined. The study will follow the residents and collect biological samples to relate mortality and disease incidence to genetic, environmental and occupational exposures, diet, other lifestyle factors and health behaviors. A smaller five-year investigation, funded for $2.9 million by the National Cancer Institute, will specifically look at patterns of smoking experimentation and initiation in Mexican-American adolescents - why they begin smoking, how addiction sets in, what may help prevent their smoking and how to help these young smokers quit.

"We may one day be able to answer the 'why me' question - 'why did I get cancer' - or perhaps we might be able to prevent cancer from oc
'"/>

Contact: Nancy Jensen
nwjensen@mdanderson.org
713-794-1584
University of Texas M. D. Anderson Cancer Center
16-Dec-2005