Kimberly A. Walker-Thurmond

Bio: Kimberly A. Walker-Thurmond is an academic researcher. The author has contributed to research in topics: Cancer & Body mass index. The author has an hindex of 2, co-authored 3 publications receiving 6702 citations.

Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults.

Abstract: background The influence of excess body weight on the risk of death from cancer has not been fully characterized. methods In a prospectively studied population of more than 900,000 U.S. adults (404,576 men and 495,477 women) who were free of cancer at enrollment in 1982, there were 57,145 deaths from cancer during 16 years of follow-up. We examined the relation in men and women between the body-mass index in 1982 and the risk of death from all cancers and from cancers at individual sites, while controlling for other risk factors in multivariate proportional-hazards models. We calculated the proportion of all deaths from cancer that was attributable to overweight and obesity in the U.S. population on the basis of risk estimates from the current study and national estimates of the prevalence of overweight and obesity in the U.S. adult population. results The heaviest members of this cohort (those with a body-mass index [the weight in kilograms divided by the square of the height in meters] of at least 40) had death rates from all cancers combined that were 52 percent higher (for men) and 62 percent higher (for women) than the rates in men and women of normal weight. For men, the relative risk of death was 1.52 (95 percent confidence interval, 1.13 to 2.05); for women, the relative risk was 1.62 (95 percent confidence interval, 1.40 to 1.87). In both men and women, body-mass index was also significantly associated with higher rates of death due to cancer of the esophagus, colon and rectum, liver, gallbladder, pancreas, and kidney; the same was true for death due to non-Hodgkin’s lymphoma and multiple myeloma. Significant trends of increasing risk with higher body-mass-index values were observed for death from cancers of the stomach and prostate in men and for death from cancers of the breast, uterus, cervix, and ovary in women. On the basis of associations observed in this study, we estimate that current patterns of overweight and obesity in the United States could account for 14 percent of all deaths from cancer in men and 20 percent of those in women. conclusions Increased body weight was associated with increased death rates for all cancers combined and for cancers at multiple specific sites.

Dietary Glycemic Index, Glycemic Load, and Risk of Incident Breast Cancer in Postmenopausal Women

Abstract: Insulin and insulin-like growth factor-I (IGF-I) are associated with increased risk of breast cancer in several studies. Circulating concentrations of insulin increase with dietary consumption of high glycemic index foods, which, in turn, may influence IGF-I levels or activity, but the relevance of such dietary patterns for breast cancer risk is unclear. We investigated whether consumption of carbohydrates with high dietary glycemic index would predict risk of postmenopausal breast cancer among 63,307 United States women in the Cancer Prevention Study II Nutrition Cohort. From baseline in 1992, participants 40-87 years of age and free from cancer and diabetes, were followed for 5 years; 1442 incident breast cancer cases were documented. Diet was assessed at baseline by a validated 68-item food frequency questionnaire from which we calculated dietary glycemic index and glycemic load. Dietary glycemic index and load were not associated with increased risk of postmenopausal breast cancer (rate ratio = 1.03; 95% confidence interval, 0.87-1.22 and rate ratio = 0.90; 95% confidence interval, 0.76-1.08, respectively) after adjustment for multiple breast cancer risk factors. Associations were not modified by body mass index, physical activity, hormone use, or stage of disease. Future evaluations of glycemic index and breast cancer risk may be strengthened by longer follow-up, more complete dietary information, and measurement of plasma insulin and IGF-I levels.

Short Communication Dietary Glycemic Index, Glycemic Load, and Risk of Incident Breast Cancer in Postmenopausal Women

Abstract: Insulin and insulin-like growth factor-I (IGF-I) are associated with increased risk of breast cancer in several studies. Circulating concentrations of insulin increase with dietary consumption of high glycemic index foods, which, in turn, may influence IGF-I levels or activity, but the relevance of such dietary patterns for breast cancer risk is unclear. We investigated whether consumption of carbohydrates with high dietary glycemic index would predict risk of postmenopausal breast cancer among 63,307 United States women in the Cancer Prevention Study II Nutrition Cohort. From baseline in 1992, participants 40 – 87 years of age and free from cancer and diabetes, were followed for 5 years; 1442 incident breast cancer cases were documented. Diet was assessed at baseline by a validated 68-item food frequency questionnaire from which we calculated dietary glycemic index and glycemic load. Dietary glycemic index and load were not associated with increased risk of postmenopausal breast cancer (rate ratio 1.03; 95% confidence interval, 0.87–1.22 and rate ratio 0.90; 95% confidence interval, 0.76 –1.08, respectively) after adjustment for multiple breast cancer risk factors. Associations were not modified by body mass index, physical activity, hormone use, or stage of disease. Future evaluations of glycemic index and breast cancer risk may be strengthened by longer follow-up, more complete dietary information, and measurement of plasma insulin and IGF-I levels.

Obesity is associated with macrophage accumulation in adipose tissue

Abstract: Obesity alters adipose tissue metabolic and endocrine function and leads to an increased release of fatty acids, hormones, and proinflammatory molecules that contribute to obesity associated complications. To further characterize the changes that occur in adipose tissue with increasing adiposity, we profiled transcript expression in perigonadal adipose tissue from groups of mice in which adiposity varied due to sex, diet, and the obesity-related mutations agouti (Ay) and obese (Lepob). We found that the expression of 1,304 transcripts correlated significantly with body mass. Of the 100 most significantly correlated genes, 30% encoded proteins that are characteristic of macrophages and are positively correlated with body mass. Immunohistochemical analysis of perigonadal, perirenal, mesenteric, and subcutaneous adipose tissue revealed that the percentage of cells expressing the macrophage marker F4/80 (F4/80+) was significantly and positively correlated with both adipocyte size and body mass. Similar relationships were found in human subcutaneous adipose tissue stained for the macrophage antigen CD68. Bone marrow transplant studies and quantitation of macrophage number in adipose tissue from macrophage-deficient (Csf1op/op) mice suggest that these F4/80+ cells are CSF-1 dependent, bone marrow-derived adipose tissue macrophages. Expression analysis of macrophage and nonmacrophage cell populations isolated from adipose tissue demonstrates that adipose tissue macrophages are responsible for almost all adipose tissue TNF-alpha expression and significant amounts of iNOS and IL-6 expression. Adipose tissue macrophage numbers increase in obesity and participate in inflammatory pathways that are activated in adipose tissues of obese individuals.

Microenvironmental regulation of tumor progression and metastasis.

Abstract: Cancers develop in complex tissue environments, which they depend on for sustained growth, invasion and metastasis. Unlike tumor cells, stromal cell types within the tumor microenvironment (TME) are genetically stable and thus represent an attractive therapeutic target with reduced risk of resistance and tumor recurrence. However, specifically disrupting the pro-tumorigenic TME is a challenging undertaking, as the TME has diverse capacities to induce both beneficial and adverse consequences for tumorigenesis. Furthermore, many studies have shown that the microenvironment is capable of normalizing tumor cells, suggesting that re-education of stromal cells, rather than targeted ablation per se, may be an effective strategy for treating cancer. Here we discuss the paradoxical roles of the TME during specific stages of cancer progression and metastasis, as well as recent therapeutic attempts to re-educate stromal cells within the TME to have anti-tumorigenic effects.