Toni K Choueiri

Harvard Medical School, Boston, Massachusetts, United States

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Publications (244)1599.26 Total impact

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    ABSTRACT: The past several years have witnessed a resurgence of interest in cancer immunotherapy. The development of blocking antibodies against the inhibitory programmed death-1 (PD-1) pathway represents a clinical breakthrough in the treatment of solid tumors such as melanoma, and these agents show great promise in renal cell carcinoma (RCC). The early data have been surprising in that they demonstrate that blockade of a single immune checkpoint can elicit objective responses in patients with RCC, despite the recognized complexity of the immunosuppressive tumor microenvironment. Reinvigorating the patient's own immune cells to reactivate and to target the tumor has the potential advantages of more selective killing and thus decreased toxicity. In addition, checkpoint blockade immunotherapy has the advantage of inducing a memory response that is unattainable with our current cytotoxic and targeted therapies. This Crossroads overview will highlight the emerging investigation of PD-1 blockade in RCC and how this T cell-targeted strategy may thwart the tumor's escape mechanisms and shift the immune system/tumor balance back to a state of equilibrium and even to tumor elimination. Cancer Immunol Res; 2(12); 1132-41. ©2014 AACR. ©2014 American Association for Cancer Research.
    Cancer immunology research. 12/2014; 2(12):1132-1141.
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    ABSTRACT: Death within 1 month of surgery is considered treatment related and serves as an important healthcare quality metric. We sought to identify the incidence of and factors associated with 1-month mortality after cancer-directed surgery. We used the Surveillance, Epidemiology and End Results Program to study a cohort of 1,110,236 patients diagnosed from 2004-2011 with cancers that are among the 10 most common or most fatal who received cancer-directed surgery. Multivariable logistic regression analyses were used to identify factors associated with 1-month mortality after cancer-directed surgery. 53,498 patients (4.8%) died within 1 month of cancer-directed surgery. Patients who were married, insured, or who had a top 50th percentile income or educational status had lower odds of 1-month mortality from cancer-directed surgery ([adjusted odds ratio (AOR) 0.80; 95% CI 0.79 - 0.82; P<0.001], [AOR 0.88; (0.82 - 0.94); P<0.001], [AOR 0.95; (0.93 - 0.97); P<0.001], and [AOR 0.98; (0.96 - 0.99); P=0.043], respectively). Patients who were non-white minority, male, or older (per year increase), or who had advanced tumor stage 4 disease all had a higher risk of 1-month mortality after cancer-directed surgery, with AORs of 1.13 (1.11 - 1.15), P<0.001; 1.11 (1.08 - 1.13), P<0.001; 1.02 (1.02 - 1.03), P<0.001; and 1.89 (1.82 - 1.95), P<0.001 respectively. Unmarried, uninsured, non-white, male, older, less educated, and poorer patients were all at a significantly higher risk for death within 1 month of cancer-directed surgery. Efforts to reduce 1-month surgical mortality and eliminate sociodemographic disparities in this adverse outcome could significantly improve survival among patients with cancer. © The Author 2014. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oup.com.
    Annals of oncology : official journal of the European Society for Medical Oncology / ESMO. 11/2014;
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    ABSTRACT: A trial-level meta-analysis of randomized phase II/III controlled trials (RCT) was conducted to determine the relative risk (RR) of hepatotoxicity associated with vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKI) approved by the U.S. FDA. Citations from PubMed/Medline, abstracts from major conferences, clinicaltrials.gov and manufacturer's package inserts were reviewed to include RCTs comparing arms with or without a VEGFR TKI. The RR of all-grade ALT, AST, ALP and bilirubin elevation in 18,282 patients from 52 trials was 1.57 (95% CI 1.38-1.79, p < 0.001), 1.57 (95% CI 1.36-1.81, p < 0.001), 1.20 (95% CI 1.09-1.83, p < 0.001) and 1.55 (95% CI 1.21-1.97, p < 0.001) respectively, and high-grade elevation was 1.66 (95% CI 1.25-2.20, p = 0.001), 1.61 (95% CI 1.21-2.14, p = 0.001), 1.02 (95% CI 0.70-1.47, p = 0.932) and 1.34 (95% CI 1.0-1.81, p = 0.054) respectively compared to those in the non-TKI group. However, the incidence of hepatic failure with VEGFR TKI was only 0.8%. Better post-marketing reporting may modify this calculated risk.
    Critical Reviews in Oncology/Hematology. 11/2014;
  • Journal of clinical oncology : official journal of the American Society of Clinical Oncology. 11/2014;
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    ABSTRACT: Taxanes such as paclitaxel and docetaxel are commonly employed for second or third-line salvage systemic therapy for metastatic urothelial carcinoma (UC). Although trials have generally excluded previous exposure to taxanes when employing a taxane in a salvage therapy trial, taxanes may not be completely cross-resistant. Hence, we aimed to study outcomes with docetaxel following prior paclitaxel and the reverse sequence to identify the level of cross-resistance between these taxanes.Patients and methodsData from a randomized phase II trial that compared salvage therapy with docetaxel combined with either placebo or vandetanib for advanced UC were analyzed. Both arms were combined for analysis since no differences in any outcomes were observed. Data were also requested from institutions for patients that received paclitaxel following prior docetaxel. Descriptive statistics were used to summarize patient and treatment characteristics as well as outcomes. The primary clinical endpoint of interest was OS.ResultsOf 148 patients that received docetaxel plus either vandetanib or placebo, 21 had received prior paclitaxel. No difference in OS, progression-free survival (PFS) and response rate was observed with docetaxel based on prior paclitaxel after adjusting for known prognostic factors. Among the 8 patients who received paclitaxel following prior docetaxel, partial response was observed in 1 patient (12.5%) and stable disease in 2 patients (25%).Conclusions Docetaxel after prior paclitaxel and the reverse sequence demonstrates activity in advanced UC. There is no strong evidence to disallow patients with prior exposure to a taxane to enroll into a clinical trial involving another taxane.
    Clinical Genitourinary Cancer 11/2014; · 1.43 Impact Factor
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    ABSTRACT: To assess contemporary characteristics, hospital admissions, charges, and mortality in patients with prostate cancer (CaP) who have bone metastases and skeletal-related events in an observational study.
    Urologic Oncology: Seminars and Original Investigations. 10/2014;
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    ABSTRACT: Primary androgen deprivation therapy (pADT) is commonly used to treat elderly men diagnosed with localized prostate cancer (CaP), despite the lack of evidence supporting its use. To examine the effect of pADT on mortality and to assess contemporary trends of pADT use in elderly men with CaP. Men older than 65 yr residing in Surveillance, Epidemiology, and End Results (SEER) registry areas diagnosed with localized or locally advanced CaP between 1992 and 2009 and not receiving definitive therapy. Propensity score (PS)-weighted Cox proportional hazards models were used to estimate the effect of pADT use on overall survival among patients receiving pADT. The interaction between comorbidity-adjusted life expectancy (LE) and pADT use was assessed within the Cox and PS-weighted models. Contemporary (2004-2009) trends for pADT use were analyzed by linear regression. The primary cohort included 46 376 men, of whom 17 873 received pADT (39%). Patients with >10 yr LE had lower pADT utilization rates than patients with short LE. Between 2004 and 2009, the use of pADT in men with localized CaP decreased by 14% (from 36% to 22%). Relative to observation, pADT was associated with a survival disadvantage, with a hazard ratio for all-cause mortality of 1.37 (95% confidence interval 1.20-1.56). Limitations included biases not accounted for by the PS-weighted model, changes in CaP staging over the study period, the absence of prostate-specific antigen (PSA) data prior to 2004, and the limits of retrospective analysis to demonstrate causality. The use of pADT in elderly men with localized CaP has decreased over time. For men forgoing primary definitive therapy, the use of pADT is not associated with a survival benefit compared to observation, and denies men an opportunity for cure with definitive therapy. The deleterious effect of pADT is most pronounced in men with prolonged LE. In this report, we assessed the effect of primary androgen deprivation (pADT) on prostate cancer mortality and determined current trends in the use of pADT. We showed that use of pADT in men aged >65 yr with localized prostate cancer has decreased over time. We also found that pADT is detrimental to men with localized prostate cancer, and particularly men with longer life expectancy. Therefore, we conclude that ADT should not be used as a primary treatment for men with prostate cancer that has not spread beyond the prostate. Copyright © 2014 European Association of Urology. Published by Elsevier B.V. All rights reserved.
    European urology. 10/2014;
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    ABSTRACT: Definitive treatment of high-risk prostate cancer with radical prostatectomy or radiation improves survival. We assessed whether racial disparities in the receipt of definitive therapy for prostate cancer vary by regional income.
    Urologic oncology. 10/2014;
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    ABSTRACT: Background The complete remission (CR) rate with salvage systemic therapy for urothelial carcinoma (UC) is unclear and its value as an intermediate endpoint and association with survival are unknown. Materials and methods Data from Phase II trials of salvage chemotherapy and/or biologic agents were pooled. Data regarding response, overall survival (OS), progression-free survival (PFS), time from prior chemotherapy (TFPC), hemoglobin (Hb), performance status (PS) and liver metastasis (LM) status were collected. Cox proportional hazards regression was used to evaluate the association of CR and other prognostic factors with outcomes. Results 789 of 818 patients enrolled in 12 phase II trials were evaluable. CR and partial response (PR) were seen in 14 (1.8%) and 109 (13.8%) patients. Median (95% CI) OS for those with a CR was 21.5 (14.2-34.3) months, compared with 6.7 (6.0-7.0) months in those without a CR (p<0.001). Median (95% CI) PFS for those with a CR was 15.7 (8.2-27.1) months, compared with 2.6 (2.4-2.8) months for those without a CR (p<0.001). Prior cisplatin and TFPC ≥3 months were associated with CR (p<0.05). The presence of poor prognostic factors and suboptimal response to prior therapy did not preclude CR. Conclusions CR occurs in 1.8% of patients receiving salvage therapy for advanced UC, and is strongly associated with durable OS and PFS. CR warrants validation as an intermediate endpoint and may help select agents for further investigation and tumors for molecular interrogation.
    Clinical Genitourinary Cancer 10/2014; · 1.43 Impact Factor
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    ABSTRACT: Background Targeted therapies improve survival in metastatic renal cell carcinoma (mRCC). However, survival patterns can be divergent and patients at the two extremes of the survival spectrum need to be characterized. Patients and Methods Data from 2161 patients included in the International mRCC Database Consortium (IMDC) were analyzed. We identified patients based on their duration of survival. Long-term survivors (LTS) were defined as overall survival (OS) ≥ 4 years and short-term survivors (STS) were patients with OS ≤ 6 months from the start of targeted therapy. Baseline characteristics including demographic, clinico-pathologic, and laboratory data were compared between LTS and STS. Treatment response by the RECIST criteria was summarized for the two survival groups. Results 152 patients were LTS and 218 were STS. Adverse clinical and laboratory prognostic factors previously described in the IMDC prognostic model were significantly more frequent in the STS group (p<0.0001). In the LTS group, 138 patients (91%) had non-progressive disease (non-PD) as best response to first-line targeted therapy, and 56 of 94 patients (60%) who received second-line therapy had non-PD. In the STS group, only 51 patients (23%) had non-PD on first-line therapy. None of 21 the patients who received second-line therapy had non-PD as best response. In LTS, the median duration of therapy was 23.6 months (range: 0.4, 81.8+) for first-line and 11.5 months (range: 0.6-45.7) for second-line compared to 2.0 and 0.8 months for the STS respectively. Conclusion Baseline prognostic criteria and absence of PD after first and second-line targeted therapy may characterize long-term survivors.
    Clinical Genitourinary Cancer 10/2014; · 1.43 Impact Factor
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    ABSTRACT: Outcomes and prognosis of metastatic sarcomatoid renal cell carcinoma (sRCC) in the targeted-therapy era are not well described. This retrospective series of 230 patients with metastatic sRCC examined the role anti-VEGF agents as a treatment option. The validity of the IMDC prognostic model in patients with metastatic sRCC was confirmed. Sarcomatoid histology was found to be an independent factor for adverse prognosis. Background Sarcomatoid RCC (sRCC) is associated with poor prognosis. Data regarding outcome in the targeted therapy era is lacking. Methods Clinical, prognostic, and treatment parameters in mRCC patients with and without sarcomatoid histology treated with targeted therapy were retrospectively analyzed. Results 2,286 patients were identified (sRCC (n=230); non-sRCC (n=2,056)). sRCC patients had significantly worse IMDC prognostic criteria compared to non-sRCC (11% vs. 19% favorable risk, 49% vs. 57% intermediate risk, and 40% vs. 24% poor risk; p<0.0001). Time from original diagnosis to relapse (excluding synchronous metastatic disease) was shorter in the sRCC group (18.8 vs. 42.9 months; p<0.0001). There was no significant difference in the incidence of CNS metastases (6-8%) or underlying clear cell histology (87-88%). Greater than 93% of patients received VEGF inhibitors as first line therapy; objective response was less common in sRCC whereas primary refractory disease was more common (21% vs. 26% and 43% vs. 21%; p<0.0001, for both). sRCC patients had significantly less use of second- (p=0.018) and third-line (p<0.0001) systemic therapy. The median PFS / OS was 4.5 / 10.4 months in sRCC patients and 7.8 / 22.5 months in non-sRCC patients (p<0.0001 for both). Sarcomatoid histology was associated with a significantly worse PFS and OS after adjusting for individual IMDC risk factors in multivariable analysis (HR 1.5, p<0.0001 for both). Conclusions Patients with sRCC have a shorter time to relapse, worse baseline prognostic criteria, and worse clinical outcome to targeted therapy. Additional insight into the biology of sRCC is needed to develop alternative therapeutics.
    Clinical Genitourinary Cancer 09/2014; · 1.43 Impact Factor
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    ABSTRACT: Program Death Ligand-1 (PD-L1) expression in non-clear cell RCC (non-ccRCC) and its association with clinical outcomes are unknown.
    Annals of oncology : official journal of the European Society for Medical Oncology / ESMO. 09/2014;
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    ABSTRACT: Sarcomatoid metastatic renal cell carcinoma (mRCC) is associated with a poor prognosis and the biology of the disease has been inadequately characterized. RNA sequencing (RNA-seq) was performed on adjacent benign, clear cell, and sarcomatoid components from clinical specimens with sarcomatoid mRCC. M phase and cell cycle pathways were enriched in sarcomatoid versus adjacent clear cell components, suggesting greater cell proliferation. The expression of aurora kinase A (AURKA) was increased as part of these pathways, and its increased expression was validated by quantitative PCR (qPCR). Immunohistochemical (IHC) analysis revealed that AURKA levels were increased in sarcomatoid tissue compared to their benign or clear cell parts. The increase in AURKA correlated with increased mTOR pathway activity, as evidenced by increased expression of phosphorylated mTOR (S2448) and ribosomal protein S6K (T389). When AURKA was stably expressed in a RCC cell line (Renca), it resulted in increased expression and activity of mTOR, suggesting that over-expression of AURKA can activate the mTOR pathway. These results warrant the analysis of a larger clinical cohort and suggest that targeting AURKA and/or mTOR in patients with sarcomatoid mRCC should be explored. Implications: Comparative RNA-seq of adjacent sarcomatoid and clear cell histology renal cell carcinoma indicates a proliferative phenotype and increased AURKA-dependent activation of mTOR signaling in sarcomatoid RCC, which could be targeted by available agents.
    Molecular cancer research : MCR. 09/2014;
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    ABSTRACT: Therapeutic inhibition of the vascular endothelial growth factor (VEGF) signaling pathway (VSP) is increasingly employed in the contemporary treatment of many cancer types. VSP inhibitors include the anti-VEGF monoclonal antibody (bevacizumab), soluble VEGF receptors (VEGF Trap), and small molecule tyrosine kinase inhibitors (TKIs) targeting the intracellular kinase domain of VEGF receptors. These agents are associated with cardiovascular toxicities such as hypertension, thrombosis, myocardial ischemia, and left ventricular (LV) dysfunction. Data on VSP inhibitor-associated LV dysfunction are largely limited to retrospective studies. Prospective studies are needed to establish the clinical significance of VSP inhibitor-associated LV dysfunction in the general population. Pre-clinical models of VSP inhibitor-associated LV dysfunction have identified mechanisms of cardiotoxicity and may improve our understanding of the pathophysiology underlying other cardiomyopathies. This review provides an overview of LV dysfunction that can occur in patients treated with VSP inhibitors. Potential strategies for clinical detection and management of this cardiotoxicity are explored, while acknowledging that currently available data specific to VSP-inhibitor LV dysfunction are limited. Avenues for future research are suggested.
    Current Treatment Options in Cardiovascular Medicine 09/2014; 16(9):335.
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    ABSTRACT: BACKGROUNDVEGF signaling pathway inhibitor (anti-VEGF) therapy is associated with hypertension, but little is known about predisposing clinical characteristics. This study describes the real-world association between baseline clinical characteristics, blood pressure (BP) response, and survival in patients prescribed anti-VEGF therapies.METHODS Clinical data from Partners HealthCare in Massachusetts was obtained from adults treated with anti-VEGF therapies (2002-2013). Treatment-induced hypertensive response was defined as worsening of preexisting hypertension or new diagnosis of hypertension (if no prior hypertension history).RESULTSData from 1120 patients with renal cell carcinoma (32.2%), hepatocellular carcinoma (11.6%), gastrointestinal stromal tumors (12.5%), and other sarcomas (15.3%) were analyzed. Most patients received sunitinib (52%), sorafenib (25.9%), or pazopanib (18%). A treatment-induced hypertensive response was identified in 49.7% of treated patients. Preexisting hypertension, present in 65.4%, was an independent risk factor for BP elevation (odds ratio [OR], 1.56; 95% confidence interval [CI], 1.27-1.92); other risk factors included age ≥60 years (OR, 1.26; 95% CI, 1.06-1.52), and body mass index (BMI) ≥25 kg/m2 (OR, 1.26; 95% CI, 1.04-1.53). Race, sex, anti-VEGF therapy prescribed, and baseline antihypertensive class were not significant risk factors. The absolute observed mean increase in BP was 21 mm Hg (systolic)/15 mm Hg (diastolic), both in patients with and without preexisting hypertension. The development of hypertension predicted improved survival (hazard ratio, 0.76; 95% CI, 0.65-0.89).CONCLUSIONS Preexisting hypertension, age, and BMI identify patients at risk for significant anti-VEGF therapy-induced BP elevation. Hypertension appears to be a clinical biomarker of efficacy of anti-VEGF therapies in a broad range of malignancies. Cancer 2014. © 2014 American Cancer Society.
    Cancer 09/2014; · 5.20 Impact Factor
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    ABSTRACT: To examine the burden of mental health issues (MHI), namely anxiety, depressive disorders, and suicide, in a population-based cohort of older men with localized prostate cancer and to evaluate associations with primary treatment modality.
    Urologic oncology. 08/2014;
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    ABSTRACT: Cisplatin-based chemotherapy is the standard of care for patients with muscle invasive urothelial carcinoma. Pathologic downstaging to pT0/pTis after neoadjuvant cisplatin-based chemotherapy is associated with improved survival, although molecular determinants of cisplatin response are incompletely understood. We performed whole exome sequencing on pre-treatment tumor and germline DNA from 50 patients with muscle invasive urothelial carcinoma who received neoadjuvant cisplatin-based chemotherapy followed by cystectomy (25 pT0/pTis "responders", 25 pT2+ "non-responders") to identify somatic mutations that occurred preferentially in responders. ERCC2, a nucleotide excision repair gene, was the only significantly mutated gene enriched in the cisplatin responders compared with non-responders (q < 0.01). Expression of representative ERCC2 mutations in an ERCC2-deficient cell line failed to rescue cisplatin and UV sensitivity compared to wild-type ERCC2. Lack of normal ERCC2 function may contribute to cisplatin sensitivity in urothelial cancer and somatic ERCC2 mutation status may inform cisplatin-containing regimen usage in muscle invasive urothelial carcinoma.
    Cancer Discovery 08/2014; · 15.93 Impact Factor
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    ABSTRACT: Objectives To determine if androgen deprivation therapy (ADT) is associated with excess cardiac-specific mortality (CSM) in men with prostate cancer and no cardiovascular comorbidity, coronary artery disease risk factors, or congestive heart failure (CHF) or past myocardial infarction (MI).Subjects/patients and methodsFive thousand seventy-seven men (median age, 69.5 years) with cT1c-T3N0M0 prostate cancer were treated with brachytherapy with or without neoadjuvant ADT (median duration, four months) between 1997 and 2006. Fine and Gray's competing risks analysis evaluated the association of ADT with CSM, adjusting for age, year of brachytherapy, and ADT treatment propensity score among men in groups defined by cardiac comorbidity.ResultsAfter a median follow-up of 4.8 years, no association was detected between ADT and CSM in men with no cardiac risk factors (1.08% at 5 years for ADT vs 1.27% at five years for no ADT, adjusted hazard ratio (AHR) 0.83; 95% confidence interval (CI), 0.39-1.78; P=0.64; n=2653) or in men with diabetes mellitus, hypertension, or hypercholesterolemia (2.09% vs 1.97%, AHR, 1.33; 95% CI, 0.70-2.53; P=0.39; n=2168). However, ADT was associated with significantly increased CSM in men with CHF or MI (AHR 3.28; 95% CI 1.01-10.64; P=0.048; n=256). In this subgroup, the five-year cumulative incidence of CSM was 7.01% (95% CI 2.82-13.82%) for ADT vs 2.01% (95% CI 0.38-6.45%) for no ADT.ConclusionADT was associated with a five percent absolute excess risk of CSM at five years in men with CHF or prior MI, suggesting that administering ADT to 20 men in this potentially vulnerable subgroup could result in one cardiac death.
    BJU International 08/2014; · 3.05 Impact Factor
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    ABSTRACT: Objectives To investigate whether mortality is increased for patients with metastatic prostate cancer (mCaP) admitted over the weekend.Patients and methodsUsing the Nationwide Inpatient Sample (NIS) between 1998-2009, admitted patients with a diagnosis of prostate cancer and concomitant metastases were identified. Rates of in-hospital mortality, complications, utilization of imaging and procedures were assessed. Adjusted logistic regression models examined associations of mortality and complications.ResultsA weighted sample of 534,011 patients with mCaP was identified, including 81.7% weekday and 18.3% weekend admissions. Of these, 8.6% died following a weekday vs. 10.9% after a weekend admission (p<0.001). Patients admitted over the weekend were more likely treated at rural (17.8 vs. 15.7%), non-teaching (57.6 vs. 53.7%) and low volume hospitals (53.4 vs. 49.4%) (all p<0.001) compared to weekday admissions. They presented higher rates of organ failure (25.2 vs. 21.3%), and were less likely to undergo an interventional procedure (10.6 vs. 11.4%) (all p<0.001). More patients admitted over the weekend had pneumonia (12.2 vs. 8.8%), pyelonephritis (18.3 vs. 14.1%) and sepsis (4.5 vs. 3.5%) (all p<0.001). In multivariate analysis, weekend admission was associated with an increased likelihood of complications (Odds ratio [OR]: 1.15, 95% Confidence Interval [CI]: 1.11-1.19) and mortality (OR: 1.20, 95% CI: 1.14- 1.27).Conclusion In patients with mCaP, weekend admissions are associated with a significant increase in mortality and morbidity. Our findings suggest that weekend patients may present with more acute medical issues; alternatively, the quality of care over the weekend may be inferior.
    BJU International 08/2014; · 3.05 Impact Factor
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    ABSTRACT: Background:The Affordable Care Act (ACA) aims to expand health insurance coverage to over 30 million previously uninsured Americans. To help evaluate the potential impact of the ACA on prostate cancer care, we examined the associations between insurance coverage and prostate cancer outcomes among men <65 years old who are not yet eligible for Medicare.Methods:The Surveillance, Epidemiology and End Results Program was used to identify 85 203 men aged <65 years diagnosed with prostate cancer from 2007 to 2010. Multivariable logistic regression modeled the association between insurance status and stage at presentation. Among men with high-risk disease, the associations between insurance status and receipt of definitive therapy, prostate cancer-specific mortality (PCSM) and all-cause mortality were determined using multivariable logistic, Fine and Gray competing-risks and Cox regression models, respectively.Results:Uninsured patients were more likely to be non-white and come from regions of rural residence, lower median household income and lower education level (P<0.001 for all cases). Insured men were less likely to present with metastatic disease (adjusted odds ratio (AOR) 0.23; 95% confidence interval (CI) 0.20-0.27; P<0.001). Among men with high-risk disease, insured men were more likely to receive definitive treatment (AOR 2.29; 95% CI 1.81-2.89; P<0.001), and had decreased PCSM (adjusted hazard ratio 0.56; 95% CI 0.31-0.98; P=0.04) and all-cause mortality (adjusted hazard ratio 0.60; 0.39-0.91; P=0.01).Conclusions:Insured men with prostate cancer are less likely to present with metastatic disease, more likely to be treated if they develop high-risk disease and are more likely to survive their cancer, suggesting that expanding health coverage under the ACA may significantly improve outcomes for men with prostate cancer who are not yet eligible for Medicare.Prostate Cancer and Prostatic Disease advance online publication, 1 July 2014; doi:10.1038/pcan.2014.23.
    Prostate cancer and prostatic diseases. 07/2014;

Publication Stats

3k Citations
1,599.26 Total Impact Points

Institutions

  • 2008–2014
    • Harvard Medical School
      • Department of Radiation Oncology
      Boston, Massachusetts, United States
    • Dana-Farber Cancer Institute
      • • Department of Radiation Oncology
      • • Department of Medical Oncology
      • • Lank Center for Genitourinary Oncology
      Boston, Massachusetts, United States
    • The Bracton Centre, Oxleas NHS Trust
      Дартфорде, England, United Kingdom
  • 2013
    • Lancaster General Hospital
      Lancaster, Pennsylvania, United States
    • Comprehensive Cancer Centers of Nevada
      Las Vegas, Nevada, United States
    • Georgetown University
      • Department of Urology
      Washington, D. C., DC, United States
    • Albert Einstein College of Medicine
      • Department of Medical Oncology
      New York City, NY, United States
    • Memorial Sloan-Kettering Cancer Center
      • Genitourinary Oncology Service
      New York City, New York, United States
  • 2012–2013
    • University of Alabama at Birmingham
      • Department of Medicine
      Birmingham, AL, United States
    • Stanford University
      • Stanford Cancer Institute
      Stanford, CA, United States
    • Seoul National University Hospital
      Sŏul, Seoul, South Korea
  • 2009–2013
    • Harvard University
      • Department of Nutrition
      Cambridge, Massachusetts, United States
    • Tom Baker Cancer Centre
      Calgary, Alberta, Canada
    • Beth Israel Deaconess Medical Center
      • Division of Hematology/Oncology
      Boston, MA, United States
    • Analysis Group
      Boston, Massachusetts, United States
  • 2011–2012
    • Brigham and Women's Hospital
      • • Department of Medicine
      • • Center for Brain Mind Medicine
      Boston, MA, United States
    • The University of Calgary
      Calgary, Alberta, Canada
    • Vancouver Prostate Centre
      Vancouver, British Columbia, Canada
    • Boston Medical Center
      Boston, Massachusetts, United States
  • 2010–2011
    • University of Texas MD Anderson Cancer Center
      • • Department of Urology
      • • Division of Radiation Oncology
      Houston, TX, United States
    • Tulane University
      New Orleans, Louisiana, United States
    • Parc de Salut Mar
      Barcino, Catalonia, Spain
  • 2006–2010
    • Cleveland Clinic
      • Department of Solid Tumor Oncology
      Cleveland, OH, United States
  • 2007
    • Institut de Cancérologie Gustave Roussy
      Île-de-France, France