The gene that produces the precursor RNA transcript to the three largest structural rRNA molecules (rDNA) is present in multiple copies and organized into gene clusters. The 10 human rDNA clusters represent <0.5% of the diploid human genome but are critically important for cellular viability. Individual genes within rDNA clusters possess very high levels of sequence identity with respect to each other and are present in high local concentration, making them ideal substrates for genomic rearrangement driven by dysregulated homologous recombination. We recently developed a sensitive physical assay capable of detecting recombination-mediated genomic restructuring in the rDNA by monitoring changes in lengths of the individual clusters. To prove that this dysregulated recombination is a potential driving force of genomic instability in human cancer, we assayed the rDNA for structural rearrangements in prospectively recruited adult patients with either lung or colorectal cancer, and pediatric patients with leukemia. We find that over half of the adult solid tumors show detectable rDNA rearrangements relative to either surrounding nontumor tissue or normal peripheral blood. In contrast, we find a greatly reduced frequency of rDNA alterations in pediatric leukemia. This finding makes rDNA restructuring one of the most common chromosomal alterations in adult solid tumors, illustrates the dynamic plasticity of the human genome, and may prove to have either prognostic or predictive value in disease progression. [Cancer Res 2009;69(23):9096-104]
Obesity affects over 30% of the United States population. Over the past 10 years, there has been increased recognition of the prevalence of obesity and its contribution to worse outcomes among medical and surgical patients. In particular, obesity has been validated as a risk factor for surgical site infection (SSI) among patients undergoing major abdominal surgery with some reports demonstrating an increased risk of SSI as high as sixty percent (60%) among obese patients. For patients undergoing elective colon and rectal surgery, a higher incidence of SSI (up to 45%) has been reported in comparison to outcomes of other surgical procedures. Obesity, as well as numerous other variables, have been implicated as a potential source for this increased incidence. Although the pathophysiology of obesity-related SSI has been suggested (decreased wound oxygen tension, impaired tissue antibiotic penetration, altered immune function, etc.), the true effect of obesity has not been clearly described. The purpose of this review is to examine the growing epidemic of obesity and its specific impact on SSI for both general and colorectal surgical patients. The proposed mechanisms for why obesity increases the risk of SSI will be briefly discussed, as well.
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