Inflammation as cause for scar cancers of the lung.

The molecular and cellular basis of inflammation has become a topic of great interest of late because of the association between mechanisms of inflammation and risk for cancer. Inflammatory-mediated events, such as the production of reactive oxygen species (ROS), the activation of growth factors (for wound repair), and the altering of signal-transduction processes to activate cell-proliferation (to replace necrotic/apoptotic tissue cells), events that also can occur independently of inflammation, are all considered to be components of risk for a variety of cancers. Using scar cancer of the lung as an example, mechanisms of inflammation associated with recurring infections with Mycobacterium tuberculosis are discussed in the context that they may, in fact, be the major or sole cause of a cancer.

Exercise, cachexia, and cancer therapy: a molecular rationale.

Evidence from recent publications indicates that repeated exercise may enhance the quality of life of cancer patients. The lack of reported negative effects and the consistency of the observed benefits lead one to conclude that physical exercise may provide a low-risk therapy that can improve patients' capacity to perform activities of daily living and improve their quality of life. Repeated physical activity may attenuate the adverse effects of cancer therapy, prevent or reverse cachexia, and reduce risk for a second cancer through suppression of inflammatory responses or enhancement of insulin sensitivity, rates of protein synthesis, and anti-oxidant and phase II enzyme activities.

Xenoestrogens significantly enhance risk for breast cancer during growth and adolescence.

Breast cancer is one of the most common forms of cancer observed in women, and endogenous estrogen is thought to play a major role in its development. Because of this, any conditions or exposures which enhance estrogenic responses would result in an increased risk for breast cancer. The role of xenoestrogenic compounds, such as DDT, in the etiology of breast cancer is still very controversial.

Running exercise may reduce risk for lung and liver cancer by inducing activity of antioxidant and phase II enzymes.

The effects of exercise, ethanol, and exercise plus ethanol-treatments on activity of superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST) and UDP-glucuronosyl transferase (UDP-GT) in lung and liver were investigated. All treatments induced SOD and CAT activity in the lung while CAT activity was enhanced only by the combined treatments in the liver. Ethanol reduced hepatic SOD activity, while with the combined treatment SOD was normal.

Estrogenic and DNA-damaging activity of Red No. 3 in human breast cancer cells.

Exposure to pesticides, dyes, and pollutants that mimic the growth promoting effects of estrogen may cause breast cancer. The pesticide DDT and the food colorant Red No. 3 were found to increase the growth of HTB 133 but not estrogen receptor (ER) negative human breast cells (HTB 125) or rat liver epithelial cells (RLE).