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Background: East Asians have inherently higher bilirubin levels at birth than whites. The potential for unnecessary treatment makes jaundice a problem of public health and clinical significance. Objectives: To report the occurrence of jaundice diagnoses in East Asian and mixed East Asian/white infants in Washington State in recent years, and to compare the risk of diagnosis with neonatal jaundice among these infants, relatising International Classification of Diseases, Ninth Revision (ICD-9) diagnosis and procedure codes from hospital discharge records. Results: Infants of full East Asian parentage were more likely to be diagnosed with jaundice than were white infants (relative risk [RR], 1.37; 95% confidence interval [CI], 1.16-1.62). For infants with Asian mothers and white fathers, the RR was 1.09 (95% CI, 0.91-1.30). Infants with Asian fathers and white mothers had an RR of 1.26 (95% CI, 1.05-1.52). The risk of severe jaundice requiring phototherapy, blood transfusion, or rehospitalization, however, was significantly elevated only for infants of full East Asian parentage (RR, 1.7; 95% CI, 1.12-2.58). Conclusions: Diagnoses of neonatal jaundice occurred more often among East Asian and mixed Asian/white infants than among white infants. However, the risk of jaundice requiring extended hospital stay, rehospitalization, phototherapy, or blood transfusion was elevated only for infants of full East Asian parentage. [ABSTRACT FROM AUTHOR]

Introduction: There is no current standard of care for patients with high-risk muscle-invasive urothelial carcinoma (MIUC) after neoadjuvant chemotherapy and surgical resection or for those who cannot receive or decline cisplatin-based perioperative chemotherapy. Understanding current, real-world treatment patterns may help inform decisions from clinical, research, and population health management perspectives. We examined real-world treatment patterns, survival outcomes, and prognostic factors among Medicare beneficiaries with high-risk MIUC who did not receive adjuvant treatment after surgical resection.Methods: We identified patients with high-risk MIUC in the linked Surveillance, Epidemiology, and End Results (SEER)-Medicare database who underwent surgical resection (radical cystectomy and/or radical nephroureterectomy). Eligible patients had indicators of high-risk MIUC and surgical resection between 2001 and 2013. Demographic and clinical characteristics, including comorbidities, American Joint Commission on Cancer (AJCC) stage, tumor stage/grade and nodal status, and distribution of neoadjuvant treatment by the year of surgical resection were evaluated. Overall survival (OS) and disease-free survival (DFS) were assessed for the full cohort and by subgroups using Kaplan-Meier survival analysis. Adjusted Cox proportional hazards models were used to evaluate patient demographics and clinical characteristics associated with OS and DFS.Results: A total of 665 patients were included in the analysis, with a mean age of 75.5 years; most were men (61%) and had AJCC stage IIIA disease (69%). Neoadjuvant treatment increased over the entire study period, both overall (from 12% to 46%) and cisplatin based (from 5% to 38%). Median OS for the entire cohort was 23.1 months (95% confidence interval: 18, 27); median DFS was 13.5 months (95% confidence interval: 11.3, 16.8). AJCC stage IIIB/IVA was the most significant predictor of poor prognosis for both OS and DFS, followed by non-white race and comorbidity burden.Conclusion: The prognosis for high-risk patients with MIUC remains poor, with significant risk of mortality within 2 years of radical cystectomy despite increasing use of neoadjuvant treatment. Unmet treatment needs persist for this difficult-to-treat patient population despite the increasing use of cisplatin-based neoadjuvant chemotherapy. [ABSTRACT FROM AUTHOR]

Experimental studies suggest a role for aspirin in the chemoprevention of prostate cancer and epidemiological evidence supports a modest inverse association between regular aspirin use and prostate cancer risk, especially for advanced disease. In a prospective cohort study of 51,529 health professionals aged 40-75 years at baseline, we evaluated long-term aspirin use and the incidence of total, high-grade (Gleason 8-10, n = 488), regionally advanced (T3b-T4 or N1, n = 228) and lethal prostate cancer (M1, bony metastases or prostate cancer death, n = 580) from 1988-2006. We used Cox proportional hazards regression to evaluate risk associated with frequency (days/week), quantity (tablets/week), recency and duration of aspirin use after multivariable adjustment for confounders and other predictors of prostate cancer risk. A total of 4,858 men were diagnosed with prostate cancer during the 18-year study period. Men taking ≥ 2 adult-strength aspirin tablets a week had a 10% lower risk of prostate cancer (p-for-trend = 0.02). For regionally advanced cancer, we observed no significant associations with aspirin use. For high-grade and lethal disease, men taking ≥ 6 adult-strength tablets/week experienced similar reductions in risk hazard ratio [HR = 0.72 (95% confidence intervals [CI]: 0.54, 0.96) and HR = 0.71 (95% CI: 0.50, 1.00)]. Analytical approaches to address bias from more frequent prostate-specific antigen screening among aspirin users did not yield different conclusions. We observed reductions in the risk of high-grade and lethal prostate cancer associated with higher doses of aspirin, but not with greater frequency or duration, in a large, prospective cohort of health professionals. Our data support earlier observations of modest inverse associations with advanced prostate cancer., (Copyright © 2010 UICC.)

Protein expression of p63 is used to differentiate prostate cancer from benign mimickers. Recent studies suggest that it may also distinguish aggressive prostate cancer with down-regulated expression occurring in men with more advanced disease. We conducted a prospective study among 298 men ages 51 to 84 years who were diagnosed with prostate cancer in the Physicians' Health Study in 1983 to 2004 and whose tissue was available for immunohistochemical staining. We used Cox proportional hazards regression to evaluate the association of p63 protein expression with fatal prostate cancer. We correlated p63 expression with tumor cell proliferation (Ki-67) and apoptosis (TUNEL staining). The predominant location of tumor p63 staining occurred in the cytoplasm, an uncommon departure from the strong nuclear staining usually observed in nonneoplastic basal cells. Increasing expression of cytoplasmic p63 (tertiles) was associated with prostate cancer mortality (n = 19 deaths); the hazard ratios (95% confidence intervals) were 1.0 (reference), 4.0 (0.9-18.9), and 5.9 (1.3-27.5; P(trend) = 0.03). The positive trend remained significant (P = 0.047) after multivariable adjustment for age, year of diagnosis, and Gleason score. Higher tertiles of cytoplasmic p63 were also associated with reduced levels of apoptosis (P(trend) = 0.0408) and increased cellular proliferation (P(trend) = 0.0026). We found aberrant expression of p63 in the cytoplasm to be associated with increased prostate cancer-specific mortality up to 20 years after diagnosis. The mislocalized expression was associated with reduced apoptosis and higher proliferative activity and may suggest an oncogenic role in prostate cancer progression and survival.