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Papers of the Month

By Jerry Phelps
March 2006

1) Rao VP, Poutahidis T, Ge Z, Nambiar PR, Horwitz BH, Fox JG, Erdman SE. Proinflammatory CD4+ CD45RB(hi) lymphocytes promote mammary and intestinal carcinogenesis in Apc(Min/+) mice. Cancer Res. 2006 Jan 1;66(1):57-61.

Implications: These studies define a new model for inflammation-driven mammary tumor development, and represent an important new tool to investigate the inflammation/cancer link. The findings also allude to the broader applicability of anti-inflammatory therapies in the treatment of specific types of cancer that are responsive to COX-2 inhibitors and other non-steroidal anti-inflammatory drugs.

2) Metz RP, Qu X, Laffin B, Earnest D, Porter WW. Circadian clock and cell cycle gene expression in mouse mammary epithelial cells and in the developing mouse mammary gland. Dev Dyn. 2006 Jan;235(1):263-71.

Implications: The results of these studies show that circadian clock genes may play a role in mammary gland development and cellular differentiation. The patterns of gene expression also suggest that interactions between these genes and cell cycle control genes may have implications for not only mammary gland development but also the development of breast cancer.

3) Marsit CJ, Karagas MR, Danaee H, Liu M, Andrew A, Schned A, Nelson HH, Kelsey KT. Carcinogen exposure and gene promoter hypermethylation in bladder cancer. Carcinogenesis. 2006 Jan;27(1):112-6.

Implications: The results indicate that in bladder cancer there are specific associations between exposure to arsenic and tobacco smoke and methylation of the promoter region of tumor suppressor genes. This study adds human data to the body of knowledge from laboratory animal studies which have shown that bladder cancer may result from epigenetic alterations instead of mutations or genetic toxicology. It also suggests that exposure to carcinogens in tobacco smoke may silence specific genes in the time period close to the clinical manifestation of tumors, which may have important clinical implications for patients.

4) Rich DQ, Mittleman MA, Link MS, Schwartz J, Luttmann-Gibson H, Catalano PJ, Speizer FE, Gold DR, Dockery DW. Increased risk of paroxysmal atrial fibrillation episodes associated with acute increases in ambient air pollution. Environ Health Perspect. 2006 Jan;114(1):120-3.

Implications: Ozone is known to be an acute lung irritant and has been associated with acute myocardial infarction and exacerbation of asthma and other respiratory conditions. The results from this study identify ozone air pollution as a potential precipitant of ventricular arrhythmia. These findings add to the evidence that poor air quality is a risk factor for atrial fibrillation. They also indicate that persons with pre-existing AF and other heart conditions should reduce activity and remain indoors during periods of high ambient ozone concentration.



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