"This is the first risk prediction model to examine the effects of diet and physical activity on the possibility of developing lung cancer," says Michele R. Forman, Ph.D., lead author of the study and a professor in M. D. Anderson's Department of Epidemiology. Forman presented study results at the American Association for Cancer Research "Frontiers in Cancer Prevention Research" meeting Dec. 7 in Philadelphia, Pa. The data are from an ongoing M. D. Anderson case-control lung cancer study involving more than 3,800 participants. Separate epidemiologic risk assessment models were developed for current and former smokers as well as for those who have never smoked ("never smokers").

Forman's study looked at salad consumption and gardening because, "salad is a marker for the consumption of many vegetables and gardening is an activity in which smokers and nonsmokers can participate."

The baseline lung cancer prediction model had moderate risk protection. The study pairs M. D. Anderson lung cancer patients with cancer-free current, former and never smoker counterparts provided through a partnership with Kelsey-Seybold Clinic, a Houston-based HMO. By including diet and physical activity, the discriminatory power of the model was raised to 64 percent, 67 percent and 71 percent respectively for never, former and current smokers.

"This finding is exciting because not only is it applicable to everyone, but it also may have a positive impact on the 15 percent of non-smokers who develop lung cancer," says Forman. The other risk factors include exposure to secondhand smoke and dust, family history of cancer and the patient's history of respiratory disease and smoking.

Lung cancer is the leading cause of cancer death for men and women, with more than 213,000 estimated new cases diagnosed each year according to the American Cancer Society. Smoking tobacco accounts for more than eight of 10 lung cancer cases.

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Metabolic perturbations influence cancer risk, that much is becoming clear to us, and we are learning more about the fundamental issues in biology that guide prostate cancer development, said Gabriel Lai, a doctoral student in the Department of Epidemiology at Johns Hopkins Bloomberg School of Public Health. One interesting possibility is that, over time, diabetics generally have less testosterone in their bloodstream than non-diabetics, which might lower risk of prostate cancer.

Lai and his colleagues used data from a large-scale study known as CLUE II, which had enrolled almost 23,000 adults in Washington County, Maryland in 1989. With funding from the National Cancer Institute, they examined the history of 264 men with confirmed prostate cancer and matched them with a group of 264 men without prostate cancer with a similar distribution of age and race.

For each participant, the researchers measured the amount of C-peptide in the blood they donated when they enrolled in the study. Researchers consider C-peptide to be a surrogate marker for insulin secretion because both molecules derive from the same precursor molecule, with insulin degrading faster than C-peptide. They found that patients that had elevated levels of C-peptide in their bloodstream when they started the study were about one-third less likely to develop prostate cancer later. This was true even among men without diabetes.

The researchers also report a markedly lower risk of non-metastasized prostate cancer. Men with higher C-peptide levels in their blood were half as likely to develop organ-confined prostate cancer, Lai says.

Even though diabetes and obesity are often linked to different types of cancer, our findings illustrate the idea that the link between cancer and metabolic diseases is not the same for every variety of cancer, Lai said. Obviously, having high levels of insulin does not promote health but perhaps such disorders can provide insight into the mechanisms of prostate cancer to help us learn how to eventually prevent prostate cancer.

Post-diagnosis weight change, body mass index, and breast cancer survival. Abstract no. B95:

Gaining weight following a diagnosis of invasive breast cancer could increase a woman's risk of death from the disease by more than half, according to researchers leading the Collaborative Women's Longevity Study. In fact, the researchers associated weight gain with a measurable increase in risk of death due to all causes, not just breast cancer.

Our findings provide additional support for the benefits of maintaining a healthy weight and exercising, said Hazel B. Nichols, a doctoral student in the Department of Epidemiology at Johns Hopkins Bloomberg School of Public Health. According to our results, there is a 14 percent increase in risk for every five kilograms -- about 11 pounds -- of weight gained.

To analyze the effect of weight gain on breast cancer survival, Nichols and her colleagues contacted women who had taken part in one of three previous studies begun in 1988 at sites in Wisconsin, Massachusetts and New Hampshire. Between 1998 and 2001, Nichols' team surveyed the women about post-diagnosis weight, weight gain, physical activity, diet and related items.

Of the original 4,021 breast cancer patients, the researchers identified 121 breast cancer-related deaths and 428 total deaths. For women classified as obese by body mass index “ a measure of weight and height “ the risk of dying from breast cancer was nearly 2.4 times that of women classified with a normal body weight. Obesity was associated with risk of death even after accounting for age, menopausal status or smoking, Nichols said.

Nichols' study was funded by the Susan G. Komen for the Cure Breast Cancer Foundation.

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