HE PREVALENCE OF OBESITY IN the United States has dramatically increased in the past decade. 1 Increased body mass index (BMI) has been linked to death from colon, breast, and many other cancers. 2 Although there are biological bases for increased risk of certain cancers in obese persons, 3 delayed diagnosis may provide an explanation for advanced stage of disease and poor outcome. Obesity presents technical problems for cancer detection, since adiposity may hinder physical examination and interfere with imaging and ancillary tests. 4 Likewise, obesity may negatively affect early diagnosis through assessment of serum concentrations of soluble tumor markers. For example, recent evidence suggests that prostate cancer screening may be adversely affected by increased BMI. 5 In the United States, most prostate cancer cases are diagnosed by needle biopsy of the prostate prompted by a high serum prostate-specific antigen (PSA) concentration. The ability to accurately detect prostate cancer can be compromised by any factor that decreases PSA concentration in the circulation. Multiple studies have found that obese men have lower PSA con-Author Affiliations are listed at the end of this article.

Obesity is associated with higher grade cancer and higher recurrence rates after RP. Black men have higher recurrence rates and greater BMI than white men. These findings support the hypothesis that obesity is associated with progression of latent to clinically significant prostate cancer (PC) and suggest that BMI may account, in part, for the racial variability in PC risk.

A post-treatment PSA-DT of less than 3 months and the specific value of the post-treatment PSA-DT when it is 3 months or more appear to be surrogate end points for prostate cancer-specific mortality after surgery or radiation therapy. We recommend that consideration be given to initiating androgen suppression therapy at the time of a PSA-defined recurrence when the PSA-DT is less than 3 months to delay the imminent onset of metastatic bone disease.

This study provided evidence to support the prediction of time to PCSM after surgery or radiation on the basis of pretreatment risk groups for patients with clinically localized prostate cancer managed during the PSA era.

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Pretreatment total testosterone was an independent predictor of extraprostatic disease in patients with localized prostate cancer. As testosterone decreases patients have an increased likelihood of non-organ confined disease. Low testosterone was not predictive of biochemical recurrence, although trends observed dictate study in larger cohorts with mature followup.

PCGEM1 is a novel, highly prostate tissue-specific, androgen-regulated gene. Here, we demonstrate that PCGEM1 expression is significantly higher in prostate cancer (CaP) cells of African-American men than in Caucasian-American men (P ¼ 0.0002). Further, increased PCGEM1 expression associates with normal prostate epithelial cells of CaP patients with a family history of CaP (P ¼ 0.0400). PCGEM1 overexpression in LNCaP and in NIH3T3 cells promotes cell proliferation and a dramatic increase in colony formation, suggesting a biological role of PCGEM1 in cell growth regulation. Taken together, the cell proliferation/colony formationpromoting functions of PCGEM1 and the association of its increased expression with high-risk CaP patients suggest the potential roles of PCGEM1 in CaP onset/ progression, especially in these high-risk groups.

Recently, the role of various cytokines in the pathogenesis of chronic rhinosinusitis has come under investigation. Various studies have reported increased levels of interleukin-3, interleukin-4, interleukin-5, interleukin-13, and granulocyte macrophage-colony stimulating factor in the sinonasal mucosa of patients with chronic rhinosinusitis. The present study investigated the levels of pro-inflammatory cytokines, including interleukin-1 beta (IL-1 beta), interleukin-5 (IL-5), interleukin-6 (IL-6) interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-alpha), in the sinonasal mucosa of patients with chronic rhinosinusitis, and evaluated the response of these cytokines to oral corticosteroids. Chronic rhinosinusitis subjects (n = 15) and control subjects (n = 9) underwent nasal endoscopy and biopsy of the sinonasal mucosa. Chronic rhinosinusitis subjects were subsequently treated with a 10-day tapering dose of prednisone followed by a second sinonasal endoscopic exam and biopsy. Mucosal biopsy specimens were immunostained for IL-1 beta, IL-5, IL-6, IL-8, and TNF-a. In chronic rhinosinusitis subjects, mucosal levels of IL-1 beta, IL-6, IL-8, and TNF-alpha were significantly elevated when compared with control subjects, and levels of IL-5 demonstrated a strong trend toward elevation. In posttreatment chronic rhinosinusitis subjects, levels of IL-6 were significantly decreased when compared with pretreatment levels, and TNF-alpha levels demonstrated a significant trend toward reduction. These findings support the hypothesis that the inflammatory response in chronic rhinosinusitis is associated with elevated levels of pro-inflammatory cytokines, and suggest that oral corticosteroids may exert a beneficial effect by significantly reducing the levels of IL-6 and TNF-alpha.