<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.urologiconcology.org/?rss=yes"><title>Urologic Oncology: Seminars and Original Investigations</title><description>Urologic Oncology: Seminars and Original Investigations RSS feed: Current Issue.    
 
 
 
 Urologic Oncology: Seminars and Original Investigations  is the official journal of the Society 
of Urologic Oncology. This new journal combines the original research from  Urologic Oncology  with the comprehensive single topic 
overviews from  Seminars in Urologic Oncology . The combined publication delivers timely clinical research and up-to-date comprehensive 
reviews of critical scientific relevance. Each issue comprises original articles and reviews including an in depth Seminar examining 
a specific clinical dilemma. All articles are of significant interest to all clinicians involved in the practice of urologic oncology 
including urologists, oncologist and radiologists. 
 
 Urologic Oncology' s Impact Factor is 3.172, ranking it among the top 
urology journals in the Urology-Nephrology category* 
 
   </description><link>http://www.urologiconcology.org/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2012 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:issn>1078-1439</prism:issn><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:publicationDate>January 2012</prism:publicationDate><prism:copyright> © 2012 Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS107814391100442X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143911004388/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS107814391100439X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143910003285/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS107814390900283X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909002956/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909003548/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909003767/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909003652/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909003597/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909003421/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909003639/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909003500/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909004062/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909003020/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909003627/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143911003115/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143911002808/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143911002584/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143911003140/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS107814391100305X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143911004534/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143911004078/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS107814391100408X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143911004091/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143911004108/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS107814391100411X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143911004121/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143911004133/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143911004145/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143911004157/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143911004169/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143911004704/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143911004819/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.urologiconcology.org/article/PIIS107814391100442X/abstract?rss=yes"><title>Masthead</title><link>http://www.urologiconcology.org/article/PIIS107814391100442X/abstract?rss=yes</link><description></description><dc:title>Masthead</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1078-1439(11)00442-X</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>iv</prism:startingPage><prism:endingPage>iv</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143911004388/abstract?rss=yes"><title>Editorial Board</title><link>http://www.urologiconcology.org/article/PIIS1078143911004388/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1078-1439(11)00438-8</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>v</prism:startingPage><prism:endingPage>v</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS107814391100439X/abstract?rss=yes"><title>Contents</title><link>http://www.urologiconcology.org/article/PIIS107814391100439X/abstract?rss=yes</link><description></description><dc:title>Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1078-1439(11)00439-X</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>vi</prism:startingPage><prism:endingPage>vii</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143910003285/abstract?rss=yes"><title>Prostate-specific antigen (PSA) should drive doing prostate biopsies</title><link>http://www.urologiconcology.org/article/PIIS1078143910003285/abstract?rss=yes</link><description>In some respects, prostate-specific antigen (PSA) screening has fallen victim to its own success. From 1990–1991 to 2006, death rates from cancer in general have decreased by 21.0% among U.S. men . Nearly 80% of this decrease in the cancer death rates can be explained by declining mortality rates from lung, prostate, and colorectal cancers. Overall, there has been approximately a 40% reduction in the age-specific prostate cancer mortality rates during the PSA era. In 2010, 32,050 deaths from prostate cancer are projected, compared with approximately 27,360 in 2009 . Although this increase likely reflects an aging population and variability in the model projections, these figures nevertheless demonstrate that prostate cancer continues to represent a major public health threat.</description><dc:title>Prostate-specific antigen (PSA) should drive doing prostate biopsies</dc:title><dc:creator>Stacy Loeb, William J. Catalona</dc:creator><dc:identifier>10.1016/j.urolonc.2010.10.007</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2011-04-04</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2011-04-04</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>News and Topics</prism:section><prism:startingPage>1</prism:startingPage><prism:endingPage>2</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS107814390900283X/abstract?rss=yes"><title>The multi-disciplinary management of high-risk prostate cancer</title><link>http://www.urologiconcology.org/article/PIIS107814390900283X/abstract?rss=yes</link><description>Abstract: 
Prostate cancer is the most frequently diagnosed cancer and the second most common cause of cancer death in men in the United States. Such men can experience a continuum of disease presentations from indolent to highly aggressive. For physicians who care for these men, a significant challenge has been and continues to be identifying and treating those men with localized cancer who are at a higher risk of dying from their disease. We discuss the risk stratification of patients in order to better identify those patients at higher risk of progression. A comprehensive review of the literature was then performed reviewing the roles of surgery, radiotherapy, hormone therapy, and chemotherapy, as well as combinations of these modalities, in treating these challenging patients. An integrated approach combining local and systemic therapies can be beneficial in the management of high-risk localized prostate cancer. The choice of therapy or combination of therapies is dependant upon many considerations, including patient preference and quality of life aspects. It is becoming clearer that the addition of hormonal therapies or chemotherapies to established therapies, such as radiotherapy or surgery, will have significant benefits. As evidence accumulates regarding the efficacy of these new regimens, our hope is that the challenge of optimizing the management of high-risk prostate cancer will be delivered. However, many important questions remain unresolved regarding the optimal type, combination, timing of therapy, and duration of therapy. Such questions will only be answered with large, well-designed prospective clinical trials.
</description><dc:title>The multi-disciplinary management of high-risk prostate cancer</dc:title><dc:creator>Jonathan C. Picard, Ali-Reza Golshayan, David T. Marshall, Krisha J. Opfermann, Thomas E. Keane</dc:creator><dc:identifier>10.1016/j.urolonc.2009.09.002</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2009-11-30</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2009-11-30</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Review Article</prism:section><prism:startingPage>3</prism:startingPage><prism:endingPage>15</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909002956/abstract?rss=yes"><title>GREB1 tissue expression is associated with organ-confined prostate cancer</title><link>http://www.urologiconcology.org/article/PIIS1078143909002956/abstract?rss=yes</link><description>Abstract: 
Objective: 
By reason of its heterogeneous behavior, it is difficult to determine the prognosis of many prostate cancer cases. Patients with the same clinicopathologic conditions may present varying clinical findings and rates of progression. We determined the role of new genes as potential molecular markers for prostate cancer prognosis.

Materials and methods: 
We performed a microarray analysis of two pools of patients with prostate cancer divided according to their clinicopathologic characteristics. After that, we validated these results by testing the genes with most different expressions between the two pools using the quantitative real time polymerase chain reaction method. We analyzed gene expression in 33 patients with localized prostate cancer according to prostate specific antigen (PSA), pathologic stage, Gleason score, and biochemical recurrence. For statistical analysis we used the Mann-Whitney Test.

Results: 
The microarray analysis revealed that 4,147 genes presented a different expression between the two pools. Among them, 3 genes, TMEFF2, GREB1, and TH1L, were at least 13-times overexpressed, and 1 gene, IGH3, which was at least 5times under-expressed in pool 1 (good prognosis) compared with pool 2 (bad prognosis), were selected for analysis. After the validation tests, GREB1 was significantly more overexpressed among patients with stage T2 compared with T3 (P = 0.020). The expressions of other 3 genes did not present significant differences according to the clinicopathological variables.

Conclusions: 
Tissue expression of GREB1 is associated with organ-confined prostate cancer and may constitute a gene associated with a favorable prognosis.
</description><dc:title>GREB1 tissue expression is associated with organ-confined prostate cancer</dc:title><dc:creator>Alberto A. Antunes, Kátia R. Leite, Sabrina T. Reis, Juliana M. Sousa-Canavez, Luiz H. Camara-Lopes, Marcos F. Dall'Oglio, Miguel Srougi</dc:creator><dc:identifier>10.1016/j.urolonc.2009.09.014</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2009-11-30</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2009-11-30</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Clinical - Prostate</prism:section><prism:startingPage>16</prism:startingPage><prism:endingPage>20</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909003548/abstract?rss=yes"><title>Biopsy accuracy in identifying unilateral prostate cancer depends on prostate weight</title><link>http://www.urologiconcology.org/article/PIIS1078143909003548/abstract?rss=yes</link><description>Abstract: 
Objective: 
To evaluate the association between prostate weight and the diagnostic performance of routine biopsy schemes in detecting unilateral prostate cancer (PCa) that may be amenable to focal therapy.

Methods and Materials: 
Retrospective analysis of patients undergoing radical prostatectomy at Duke University Medical Center from 1990 to 2007. The cohort was dichotomized according to prostate weight (≤40 and &gt;40 g) and further divided by biopsy scheme: 6–9 (sextant) and 10–20 cores (extended). Diagnostic accuracy, sensitivity, specificity, and positive and negative predictive values were calculated within each prostate weight group and compared between biopsy schemes.

Results: 
A total of 859 patients were included in the study. Patients with prostates &gt;40 g were generally older and had higher PSA levels (P &lt; 0.0001 and P = 0.036, respectively). Unilateral disease was more common in prostates &gt;40 g both on biopsy (69% vs. 60%, P = 0.009) and on final pathology (21% vs. 14%, P = 0.017) despite larger total tumor volume (6.1 vs. 4.8 cc, P &lt; 0.001). Low grade PCa was also more common in larger glands (P = 0.003). Overall, extended biopsy schemes performed better than sextant but the benefit was statistically significant only in prostates &gt;40 g.

Conclusions: 
Despite having higher tumor volumes, men with prostate weight &gt;40 g were more likely to have unilateral PCa than those with smaller prostates. In prostates &gt;40 g, increasing the number of cores harvested at biopsy increased the diagnostic performance for detecting cancer laterality. Therefore, our results suggest that the benefit of more extensive tissue sampling may be higher in larger prostates compared with smaller ones when selecting candidates for prostate hemiablation.
</description><dc:title>Biopsy accuracy in identifying unilateral prostate cancer depends on prostate weight</dc:title><dc:creator>Matvey Tsivian, Daniel M. Moreira, Leon Sun, Vladimir Mouraviev, Masaki Kimura, Judd W. Moul, Thomas J. Polascik</dc:creator><dc:identifier>10.1016/j.urolonc.2009.11.001</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2010-01-07</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-01-07</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Clinical - Prostate</prism:section><prism:startingPage>21</prism:startingPage><prism:endingPage>25</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909003767/abstract?rss=yes"><title>Nerve-sparing robotic prostatectomy in preoperatively high-risk patients is safe and efficacious</title><link>http://www.urologiconcology.org/article/PIIS1078143909003767/abstract?rss=yes</link><description>Abstract: 
Objective: 
Given the higher likelihood of extraprostatic extension in high-risk patients, many urologists will sacrifice the neurovascular bundles in such patients in an attempt to decrease the risk of positive surgical margins. In contrast, we frequently perform nerve-sparing in high-risk patients. We analyzed our outcomes in patients with preoperatively high-risk prostate cancer according to the D'Amico risk group classification, and stratified by nerve-sparing status.

Materials and methods: 
An institutional database of 1,503 robotic-assisted laparoscopic prostatectomies (RALP) was queried for patients presenting with PSA &gt; 20 ng/ml, Gleason 8 or higher on biopsy, or clinical stage T2c or higher. Interfascial nerve-sparing was performed whenever oncologically feasible. Validated questionnaires were used to assess baseline and postoperative functional outcomes.

Results: 
Adequate follow-up was available in 123 high-risk patients. Mean serum PSA was 10.8. Bilateral, unilateral, and non-nerve-sparing was performed on 58%, 15%, and 27%, respectively. On final histopathology, 42% were organ confined; 55 patients had extraprostatic extension, and 35 had seminal vesicle invasion. Positive surgical margins occurred in 31%: 15% focal and 16% extensive. Favorable pathologic outcomes (organ-confined and negative surgical margins) were observed in 40%. Biochemical recurrence occurred in 20%. Nerve-sparing was associated with more favorable pathologic features, possibly due to selection bias. When controlling for adverse pathologic features, nerve-sparing was not associated with higher rates of positive surgical margins or biochemical recurrence. At a median follow-up of 13 months, 78% were continent and 56% were potent. The “trifecta” of continence, potency, and freedom from recurrence was achieved in 28 patients (23%).

Conclusions: 
Nerve-sparing robotic-assisted laparoscopic prostatectomy can be safely performed in patients with preoperatively high risk prostate cancer. Histopathologic and short-term oncologic outcomes at 13-month median follow-up are comparable to those in open surgical series from similar cohorts.
</description><dc:title>Nerve-sparing robotic prostatectomy in preoperatively high-risk patients is safe and efficacious</dc:title><dc:creator>Hugh J. Lavery, Fatima Nabizada-Pace, John R. Carlucci, Jonathan S. Brajtbord, David B. Samadi</dc:creator><dc:identifier>10.1016/j.urolonc.2009.11.023</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2010-03-02</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-03-02</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Clinical - Prostate</prism:section><prism:startingPage>26</prism:startingPage><prism:endingPage>32</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909003652/abstract?rss=yes"><title>C-reactive protein as an adverse prognostic marker for men with castration-resistant prostate cancer (CRPC): Confirmatory results</title><link>http://www.urologiconcology.org/article/PIIS1078143909003652/abstract?rss=yes</link><description>Abstract: 
We previously reported that higher serum concentrations of C-reactive protein (CRP) are associated with shorter survival in men with castration-resistant prostate cancer (CRPC). To confirm this finding in an independent data set, we used 119 CRPC patients enrolled in 6 phase II clinical trials and examined the relationship of CRP, alkaline phosphatase, hemoglobin, age, ECOG PS, and prostate specific antigen (PSA) with survival. Median follow-up was 19.7 months (0.9–98.5 months), and 89% have died. After analyzing the form of the risk function using the generalized additive model method, univariate and multivariate Cox proportional hazard models were used to assess associations between baseline individual categorical and continuous variables. Quartiles of CRP were: 0–1.0, 1.1–4.9, 5.0–17.0, and 17.1–311 mg/L. In a Cox multivariate model, log2 (CRP) (HR 1.106, P = 0.013) as well as hemoglobin and alkaline phosphatase were independently associated with survival, confirming that higher CRP is associated with shorter survival in CRPC. Since CRP is a marker of inflammation, this finding suggests that inflammation may play an important role in the natural history of advanced prostate cancer. CRP is a readily measurable biomarker that has the potential to improve prognostic models and should be validated in a prospective clinical trial.
</description><dc:title>C-reactive protein as an adverse prognostic marker for men with castration-resistant prostate cancer (CRPC): Confirmatory results</dc:title><dc:creator>Renee C. Prins, Brooks L. Rademacher, Solange Mongoue-Tchokote, Joshi J. Alumkal, Julie N. Graff, Kristine M. Eilers, Tomasz M. Beer</dc:creator><dc:identifier>10.1016/j.urolonc.2009.11.012</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2010-03-08</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-03-08</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Clinical - Prostate</prism:section><prism:startingPage>33</prism:startingPage><prism:endingPage>37</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909003597/abstract?rss=yes"><title>Orthotopic bladder substitution following radical cystectomy in women: Comparative study between sigmoid and ileal neobladders</title><link>http://www.urologiconcology.org/article/PIIS1078143909003597/abstract?rss=yes</link><description>Abstract: 
The objective of this study was to retrospectively compare the clinical outcomes of sigmoid and ileal neobladders (NBs) created in women. This study included 18 and 14 women who underwent orthotopic NB reconstruction using sigmoid and ileal segment, respectively, after radical cystectomy, and postoperative clinical outcomes between the sigmoid and ileal NB groups (SNBG and INBG) were compared. Eighteen early and 7 late complications occurred in 12 and 6 women, respectively; however, there was no significant difference in the incidence of complications between SNBG and INBG. The proportion of patients who could void spontaneously in SNBG (94.4%) was significantly greater than that in INBG (64.3%), while there was no significant difference in continent status between these 2 groups. Despite the lack of significant differences in maximal flow rate and voided volume, post-void residual in SNBG (15.7 ml) was significantly smaller than that in INBG (62.0 ml). SF-36 survey for postoperative quality of life (QOL) did not show any significant differences in 7 of the 8 scores between the 32 women with NB and an age-matched control population; however, 3 of the 8 scores in SNBG were significantly superior to those in INBG. During the observation period of this study, urethral recurrence did not occur in any woman, and there was no significant difference in cancer-specific survival between the 2 groups. These findings suggest that it might be preferable to create sigmoid rather than ileal NB in women following radical cystectomy considering the favorable voiding function and QOL in SNBG.
</description><dc:title>Orthotopic bladder substitution following radical cystectomy in women: Comparative study between sigmoid and ileal neobladders</dc:title><dc:creator>Hideaki Miyake, Junya Furukawa, Mototsugu Muramaki, Atsushi Takenaka, Masato Fujisawa</dc:creator><dc:identifier>10.1016/j.urolonc.2009.11.006</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2010-01-07</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-01-07</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Clinical - Bladder</prism:section><prism:startingPage>38</prism:startingPage><prism:endingPage>43</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909003421/abstract?rss=yes"><title>The presence of circulating tumor cells does not predict extravesical disease in bladder cancer patients prior to radical cystectomy</title><link>http://www.urologiconcology.org/article/PIIS1078143909003421/abstract?rss=yes</link><description>Abstract: 
Objective: 
Due to imprecise clinical staging, the finding of extravesical and node-positive disease at the time of radical cystectomy (RC) for patients with clinically localized bladder cancer is not uncommon. Circulating tumor cells (CTCs) have been shown to be present in the peripheral blood of patients with metastatic urothelial carcinoma. The object of this study was to evaluate the ability of CTCs to predict extravesical disease in bladder cancer patients prior to RC.

Materials and methods: 
Peripheral blood samples from 43 patients with bladder cancer were evaluated using the CellSearch (Veridex, LLC, Raritan, NJ) CTC assay prior to RC. The sensitivity, specificity, and positive predictive value (PPV) of CTC status in predicting extravesical disease was calculated. Receiver operating characteristic (ROC) curves were generated to quantify the ability of CTCs to predict extravesical and node-positive disease.

Results: 
CTCs were detected in 9 (21%) patients prior to RC. The sensitivity, specificity, and PPV of CTC status in predicting extravesical disease were 27%, 88% and 78%, respectively. The accuracy of CTC status in predicting extravesical (≥pT3 or node-positive) disease for the entire cohort was 0.576. In a model incorporating preoperative hydronephrosis, CTC status did not improve the predictive accuracy for extravesical disease (0.576 vs. 0.585, P = 0.915).

Conclusion: 
CTCs were detected in low numbers in a small percentage (21%) of patients prior to undergoing RC at our institution. CTC status was not a robust predictor of extravesical or node-positive disease in this cohort. CTC status is not likely to be a clinically useful parameter for directing therapeutic decisions in patients with ≤cT2 bladder cancer.
</description><dc:title>The presence of circulating tumor cells does not predict extravesical disease in bladder cancer patients prior to radical cystectomy</dc:title><dc:creator>Thomas J. Guzzo, Brian K. McNeil, Trinity J. Bivalacqua, Debra J. Elliott, Lori J. Sokoll, Mark P. Schoenberg</dc:creator><dc:identifier>10.1016/j.urolonc.2009.10.008</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2009-12-14</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2009-12-14</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Clinical - Bladder</prism:section><prism:startingPage>44</prism:startingPage><prism:endingPage>48</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909003639/abstract?rss=yes"><title>Subepithelial growth patterns in urothelial carcinoma—frequency and prognostic significance</title><link>http://www.urologiconcology.org/article/PIIS1078143909003639/abstract?rss=yes</link><description>Abstract: 
Purpose: 
Most urothelial carcinomas are exophytic, but some tumors exhibit subepithelial components, either in the form of endophytic growth pattern (EGP) or as von Brunn's nests involvement (VBNI). The purpose of this study was to investigate the frequency, inter-relations and clinical significance of these forms of subepithelial neoplasia in urothelial carcinoma.

Patients and methods: 
Between June 1995 and December 2007, 760 patients (mean age of 67.5 years) underwent transurethral resection of bladder tumors in our institution, including 478, 157, and 112 patients with stage Ta, T1, and ≥T2 disease, respectively. Isolated or concomitant Tis were present in 137 (18%) patients. Median postoperative follow-up period was 53 months.

Results: 
EGP was found in 86 cases (11.3%) and VBNI in 30 (3.9%) patients. Both forms of subepithelial growth were significantly more common in higher stage and grade tumors and were associated with each other. Multivariate analysis showed that EGP is an independent prognostic factor of stage progression (HR 4.6, P &lt; 0.0001) and disease specific mortality (HR 2.6, P = 0.001) but not of tumor recurrence (HR 1.2, P = 0.51). VBNI was found an independent prognostic factor of tumor progression (HR 5.1, P &lt; 0.0001), but neither of tumor recurrence nor disease specific mortality.

Conclusions: 
Subepithelial growth is not an uncommon in bladder cancer. It is more frequent in high-grade and high-stage tumors. The findings of this study suggest that subepithelial growth carries a higher risk for stage progression (EGP and VBNI) and mortality (EGP), but not tumor recurrence.
</description><dc:title>Subepithelial growth patterns in urothelial carcinoma—frequency and prognostic significance</dc:title><dc:creator>Ofer N. Gofrit, Amos Shapiro, Dov Pode, Ran Katz, Vladimir Yutkin, Kevin C. Zorn, Galina Pizov</dc:creator><dc:identifier>10.1016/j.urolonc.2009.11.010</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2010-03-08</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-03-08</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Clinical - Bladder</prism:section><prism:startingPage>49</prism:startingPage><prism:endingPage>54</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909003500/abstract?rss=yes"><title>Detection of inguinal lymph node involvement in penile squamous cell carcinoma by 18F-fluorodeoxyglucose PET/CT: A prospective single-center study</title><link>http://www.urologiconcology.org/article/PIIS1078143909003500/abstract?rss=yes</link><description>Abstract: 
Background: 
The extent of lymph node involvement is the most relevant prognostic factor in patients with penile cancer.

Objective: 
To prospectively analyze the diagnostic accuracy of 18F-FDG-PET/CT-scan in the assessment of inguinal lymph node involvement in patients with invasive penile carcinoma.

Patients and methods: 
Thirty-five patients with invasive penile carcinoma were staged prospectively by 18F-FDG-PET/CT-scan, and blindly evaluated by 2 nuclear medicine physicians. In total, lymph node involvement was assessed in 70 inguinal groins. Reference standard was either histology or clinical follow-up with a minimum of 31 months (mean: 48.4 months; range: 31–68 months).

Results: 
18-FDG-PET/CT showed a sensitivity of 88.2% and a specificity of 98.1%. Positive predictive value (PPV) was 93.8%, while negative predictive value (NPV) was 96.3%. In two groins, metastasis of 5 and 7 mm were missed by PET/CT scan.

Conclusion: 
18F-FDG-PET/CT is a promising staging tool in assessing the inguinal lymph node involvement of patients with penile carcinoma. Integration of PET/CT scanning into preoperative staging algorithms may avoid surgical staging in selected patients.
</description><dc:title>Detection of inguinal lymph node involvement in penile squamous cell carcinoma by 18F-fluorodeoxyglucose PET/CT: A prospective single-center study</dc:title><dc:creator>Boris Schlenker, Bernhard Scher, Reinhold Tiling, Sabine Siegert, Edwin Hungerhuber, Christian Gratzke, Derya Tilki, Oliver Reich, Peter Schneede, Peter Bartenstein, Christian G. Stief, Michael Seitz</dc:creator><dc:identifier>10.1016/j.urolonc.2009.10.012</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2009-12-21</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2009-12-21</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Clinical - Testis</prism:section><prism:startingPage>55</prism:startingPage><prism:endingPage>59</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909004062/abstract?rss=yes"><title>Primary vs. post-chemotherapy retroperitoneal lymph node dissection (RPLND) in patients with presence of teratoma at orchiectomy</title><link>http://www.urologiconcology.org/article/PIIS1078143909004062/abstract?rss=yes</link><description>Abstract: 
Objective: 
The presence of teratoma in the primary orchiectomy specimen creates controversies for subsequent management. Although predominant teratoma is less likely to metastasize, teratoma in the retroperitoneum may be less amenable to chemotherapy. In order to elucidate the issues about teratoma in the primary tumor, we reviewed differences between primary retroperitoneal lymph node dissection (P-RPLND) vs. post-chemotherapy RPLND (PC-RPLND) in patients with teratoma at orchiectomy.

Materials and methods: 
Patients who had undergone RPLND at our institution from 2001 to 2008 were identified, and clinical charts reviewed. Eighty-three patients with teratoma at orchiectomy were identified and perioperative data were obtained.

Results: 
Of the 83 patients with teratoma at orchiectomy who underwent RPLND, 44 (53%) and 39 (47%) underwent primary and PC-RPLND, respectively. Median follow-up was 1.4 years. Of the 83 patients with primary teratoma at orchiectomy, there were 7 (8%) patients with pure teratoma and 76 (92%) patients with mixed histology. Of the patients with mixed histology, 72 (87%) patients had embryonal carcinoma and 36 (43%) had LVI. There were 19 (43%) positive lymph nodes for P-RPLND, of which 13 (30%) contained teratoma. For the PC-RPLND group, 30 (77%) of lymph nodes were positive, of which 28 (72%) contained teratoma. There were 3 (4%) recurrences overall, all of which recurred in the PC-RPLND group. There were 11 (13%) perioperative complications total. There were no deaths in either group.

Conclusions: 
Patients with teratoma at orchiectomy were associated with other high risk features and are at significant risk for metastatic disease. Patients with post-chemotherapy retroperitoneal findings are at significant risk for viable GCT and/or teratoma and should undergo PC-RPLND.
</description><dc:title>Primary vs. post-chemotherapy retroperitoneal lymph node dissection (RPLND) in patients with presence of teratoma at orchiectomy</dc:title><dc:creator>Stephen B. Williams, Ravi Kacker, Graeme S. Steele, Jerome P. Richie</dc:creator><dc:identifier>10.1016/j.urolonc.2009.12.006</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2010-03-02</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-03-02</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Clinical - Testis</prism:section><prism:startingPage>60</prism:startingPage><prism:endingPage>63</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909003020/abstract?rss=yes"><title>The orthotopic Fischer/AY-27 rat bladder urothelial cell carcinoma model to test the efficacy of different apaziquone formulations</title><link>http://www.urologiconcology.org/article/PIIS1078143909003020/abstract?rss=yes</link><description>Abstract: 
Objectives: 
Apaziquone used intravesically showed significant activity in phase I and II marker lesion studies in non-muscle-invasive bladder cancer. The objective of this study was to assess antitumor activity and safety of 3 different formulations of intravesical apaziquone in an orthotopic rat bladder cancer model.

Materials and methods: 
Female Fischer F344 rats were instilled with 1.5 × 106 AY-27 urothelial cell carcinoma cells and divided in 3 treatment groups (n = 10) and 1 placebo group (n = 6). Intravesical treatment was administered for 1 hour on days 2 and 5. Rats were treated with apaziquone in the formulation used in phase I/II clinical trials (group 1); apaziquone with an altered buffering capacity being used in phase III clinical trials (group 2), and apaziquone as in group 2, but without propylene glycol in the diluent (group 3). On days 5 and 14, the bladder wall was inspected by cystoscopy and evaluated for macroscopic tumor growth. After sacrificing the rats (day 14), cystectomy was performed and the bladders were investigated.

Results: 
There were no signs of any toxicity due to the study drug. On histopathologic examination of the bladders 0, 1, and 2 tumors per group were found in group 1, 2, and 3, respectively. In the placebo-treated group, 60% of animals developed tumor, which is comparable to untreated animals.

Conclusions: 
Apaziquone showed an excellent antitumor activity. The effectiveness of apaziquone in this orthotopic rat bladder tumor model corroborates the clinical observations and implies the validity of this model.
</description><dc:title>The orthotopic Fischer/AY-27 rat bladder urothelial cell carcinoma model to test the efficacy of different apaziquone formulations</dc:title><dc:creator>Harm C. Arentsen, Kees Hendricksen, Christina A. Hulsbergen-van de Kaa, Guru Reddy, Egbert Oosterwijk, J. Alfred Witjes</dc:creator><dc:identifier>10.1016/j.urolonc.2009.10.002</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2009-11-30</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2009-11-30</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Laboratory</prism:section><prism:startingPage>64</prism:startingPage><prism:endingPage>68</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909003627/abstract?rss=yes"><title>Rictor-dependent AKT activation and inhibition of urothelial carcinoma by rapamycin</title><link>http://www.urologiconcology.org/article/PIIS1078143909003627/abstract?rss=yes</link><description>Abstract: 
Objective: 
We previously reported a very high cumulative incidence of urothelial carcinoma in Taiwanese kidney transplant recipients. Rapamycin, the inhibitor of mTOR Complex 1, provides alternative immunosuppressive therapy after kidney transplantation with less neoplastic potential. We examined the in vivo and in vitro effects of rapamycin on urothelial carcinoma.

Materials and methods: 
The rat model of urothelial carcinoma was induced by 0.05% N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) in Fischer F344 rats. The anti-tumor effect of rapamycin was assessed grossly, microscopically, and by Western blot analysis. The mechanism of rapamycin's attenuation of urothelial carcinoma was also evaluated by T24 cells.

Results: 
Rapamycin significantly reduced urinary bladder tumor growth in the rat model of 0.05% BBN-induced urothelial carcinoma (P &lt; 0.001). The blood trough levels of rapamycin were correlated with the occurrence of urothelial carcinoma. In vitro, rapamycin also inhibited the cell proliferation, migration, and invasion, as well as the protein expression of vascular endothelial growth factor-A of T24 urothelial carcinoma cells, whereas rapamycin did not induce significant apoptosis in T24 cells. Rapamycin decreased the expression of phospho-mTOR, phospho-S6K, cyclin D1, and VEGF-A. Rapamycin also activated AKT in T24 cells in the rat model of urothelial carcinoma. The rapamycin-associated activation of AKT was inhibited by rictor siRNA, but not raptor siRNA.

Conclusions: 
This study provides in vitro and in vivo evidence that rapamycin may inhibit the development of urothelial carcinoma. The present findings also suggest rictor-dependent AKT activation as a consequence of mTORC1 inhibition.
</description><dc:title>Rictor-dependent AKT activation and inhibition of urothelial carcinoma by rapamycin</dc:title><dc:creator>Ming-Ju Wu, Chi-Hao Chang, Yung-Tsung Chiu, Mei-Chin Wen, Kuo-Hsiung Shu, Jian-Ri Li, Kun-Yuan Chiu, Yen-Ta Chen</dc:creator><dc:identifier>10.1016/j.urolonc.2009.11.009</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2010-03-08</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-03-08</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Laboratory</prism:section><prism:startingPage>69</prism:startingPage><prism:endingPage>77</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143911003115/abstract?rss=yes"><title>Impact of poverty and race/ethnicity on treatment and management of urologic cancers</title><link>http://www.urologiconcology.org/article/PIIS1078143911003115/abstract?rss=yes</link><description>Poverty and race/ethnicity have long been factors associated with disparities in access to care, severity of disease at diagnosis, receipt of treatment, and outcomes of care. It is important to understand the history of efforts to address these disparities as well as to recognize the significant progress that has already been made, even though disparities persist. Since 1959, poverty has been measured by the U.S. Census Bureau as a set of money income thresholds based on family size . In the early 1960s, poverty rates were 22.2% overall and varied greatly by race, with a poverty rate of 18.1% among Whites, and an astounding 55.1% among Blacks . On January 8, 1964, Lyndon Johnson took action, declaring a War on Poverty by instituting major health care, education, and jobs programs to address high poverty rates . These programs included Medicare and Medicaid, Food Stamps, Job Corps, Upward Bound, Head Start, and College Work Study, all of which still exist today.</description><dc:title>Impact of poverty and race/ethnicity on treatment and management of urologic cancers</dc:title><dc:creator>Katherine S. Virgo, Stacey A. Fedewa</dc:creator><dc:identifier>10.1016/j.urolonc.2011.09.007</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2011-11-29</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2011-11-29</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Seminar Section Introduction</prism:section><prism:startingPage>78</prism:startingPage><prism:endingPage>80</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143911002808/abstract?rss=yes"><title>Disparities in bladder cancer</title><link>http://www.urologiconcology.org/article/PIIS1078143911002808/abstract?rss=yes</link><description>Abstract: 
Among men, bladder cancer is the fourth most common malignancy and ninth leading cause of death from cancer in the United States. In contrast, it is the 11th most common malignancy and 12th leading cause of death from cancer among women. The successful management of bladder cancer largely depends on its timely diagnosis and treatment. Unfortunately, barriers disproportionately delay detection and treatment for individuals with social, economic, and community disadvantages. This imbalance creates health disparities (i.e., differences in health outcomes that are closely linked to these disadvantages), which negatively affect vulnerable populations, such as racial and ethnic minority groups, those from lower socioeconomic classes, and the uninsured. To obtain a better understanding of this issue, we review the current state of bladder cancer disparities research.
</description><dc:title>Disparities in bladder cancer</dc:title><dc:creator>Bruce L. Jacobs, Jeffrey S. Montgomery, Yun Zhang, Ted A. Skolarus, Alon Z. Weizer, Brent K. Hollenbeck</dc:creator><dc:identifier>10.1016/j.urolonc.2011.08.011</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2011-11-29</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2011-11-29</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Seminar Articles</prism:section><prism:startingPage>81</prism:startingPage><prism:endingPage>88</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143911002584/abstract?rss=yes"><title>The role of socioeconomic status in renal cell carcinoma</title><link>http://www.urologiconcology.org/article/PIIS1078143911002584/abstract?rss=yes</link><description>Abstract: 
Gender, race, income level, and socioeconomic status (SES) are factors in the decision to diagnose and treat patients with localized and advanced renal cell carcinoma (RCC). These variables affect both health care delivery at the provider level as well as health care receipt and decision-making at the patient level. The purpose of this article is to review current literature regarding the role of socioeconomic status and patient demographics on the risk of developing, diagnosing, and treating RCC. The article will also address RCC-related treatment costs and reimbursements.
</description><dc:title>The role of socioeconomic status in renal cell carcinoma</dc:title><dc:creator>Nicholas J. Hellenthal, Carlos E. Bermejo</dc:creator><dc:identifier>10.1016/j.urolonc.2011.08.003</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2011-09-12</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2011-09-12</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Seminar Articles</prism:section><prism:startingPage>89</prism:startingPage><prism:endingPage>94</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143911003140/abstract?rss=yes"><title>Testicular cancer: A narrative review of the role of socioeconomic position from risk to survivorship</title><link>http://www.urologiconcology.org/article/PIIS1078143911003140/abstract?rss=yes</link><description>Abstract: 
Background: 
Testicular cancer (TC) is one of the most curable cancers. Given survival rates of close to 100% with appropriate therapy, ensuring proper treatment is essential. We reviewed and summarized the literature on the association of socioeconomic position (SEP) along the cancer control spectrum from risk factors to survivorship.

Methods: 
We searched PubMed from 1966 to 2011 using the following terms: testicular cancer, testicular neoplasm, poverty, and socioeconomic factors, retrieving 119 papers. After excluding papers for the non-English (10) language and non-relevance (46), we reviewed 63 papers. We abstracted information on socioeconomic position (SEP), including occupation, education, income, and combinations of the 3. Five areas were examined: risk factors, diagnosis, treatment, survival, and survivorship.

Results: 
Most studies examined area-based measures, not individual measures of SEP. The majority of studies found an increased risk of developing TC with high SEP though recent papers have indicated increased risk in low-income populations. Regarding diagnosis, recent papers have indicated that lower levels of education and SEP are risk factors for later-stage TC diagnosis and hence higher TC mortality. For treatment, 1 study that examined the use of radiation therapy (RT) in stage I seminoma reported that living in a county with lower educational attainment led to lower use of RT. For survival (mortality), several studies found that men living in lower SEP geographic areas experience lower survival and higher mortality.

Conclusion: 
The strongest evidence for SEP impact on testicular germ cell tumor (TGCT) was found for the risk of developing cancer as well as survival. The association of SEP with TGCT risk appears to have changed over the last decade. Given the highly curable nature of TGCT, more research is needed to understand how SEP impacts diagnosis and treatment for TGCT and to design interventions to address disparities in TGCT outcomes and SEP.
</description><dc:title>Testicular cancer: A narrative review of the role of socioeconomic position from risk to survivorship</dc:title><dc:creator>Lisa C. Richardson, Antonio J. Neri, Eric Tai, Jeffrey D. Glenn</dc:creator><dc:identifier>10.1016/j.urolonc.2011.09.010</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2011-11-29</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2011-11-29</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Seminar Articles</prism:section><prism:startingPage>95</prism:startingPage><prism:endingPage>101</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS107814391100305X/abstract?rss=yes"><title>Prostate cancer survivorship: Lessons from caring for the uninsured</title><link>http://www.urologiconcology.org/article/PIIS107814391100305X/abstract?rss=yes</link><description>Abstract: 
Since 2001, UCLA has operated IMPACT: Improving Access, Counseling, and Treatment for Californians with Prostate Cancer (CaP). Funded by the California Department of Public Health, with a cumulative budget of over $80 million, the program provides comprehensive care for low-income, uninsured Californian men with biopsy-proven CaP. Health services research conducted with program enrollees, through the UCLA Men's Health Study, yields an opportunity to perform qualitative and quantitative assessments of patient-reported outcomes in these men, all members of historically underserved, primarily minority populations. This review summarizes data from several studies in which validated instruments were administered longitudinally in 727 participants, prospectively measuring health-related quality of life (HRQOL), self-efficacy in interactions with physician interactions, social and emotional health, symptom distress, satisfaction with care, and other patient-reported outcomes.
</description><dc:title>Prostate cancer survivorship: Lessons from caring for the uninsured</dc:title><dc:creator>Karim Chamie, Sarah E. Connor, Sally L. Maliski, Arlene Fink, Lorna Kwan, Mark S. Litwin</dc:creator><dc:identifier>10.1016/j.urolonc.2011.09.001</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2011-11-29</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2011-11-29</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Seminar Articles</prism:section><prism:startingPage>102</prism:startingPage><prism:endingPage>108</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143911004534/abstract?rss=yes"><title>Survey Section Editorial Board</title><link>http://www.urologiconcology.org/article/PIIS1078143911004534/abstract?rss=yes</link><description></description><dc:title>Survey Section Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1078-1439(11)00453-4</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>109</prism:startingPage><prism:endingPage>109</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143911004078/abstract?rss=yes"><title>Commentary on “Partial orchiectomy for presumed malignancy in patients with a solitary testis due to a prior germ cell tumor: A large North American experience.” Lawrentschuk N, Zuniga A, Grabowksi AC, Rendon RA, Jewett MA, Division of Urology, Department of Surgical Oncology, Princess Margaret Hospital and the University Health Network, University of Toronto, Toronto, Ontario, Canada: J Urol 2011;185:508–13</title><link>http://www.urologiconcology.org/article/PIIS1078143911004078/abstract?rss=yes</link><description>Partial orchiectomy is becoming more accepted for indications such as a metachronous germ cell tumor due to reported oncological control, and minimal functional, physical, and psychological morbidity. Most data originate from Europe. Thus, we reviewed our North American experience with such men who underwent partial orchiectomy for a presumed contralateral testicular malignancy.</description><dc:title>Commentary on “Partial orchiectomy for presumed malignancy in patients with a solitary testis due to a prior germ cell tumor: A large North American experience.” Lawrentschuk N, Zuniga A, Grabowksi AC, Rendon RA, Jewett MA, Division of Urology, Department of Surgical Oncology, Princess Margaret Hospital and the University Health Network, University of Toronto, Toronto, Ontario, Canada: J Urol 2011;185:508–13</dc:title><dc:creator>Jerome P. Richie</dc:creator><dc:identifier>10.1016/j.urolonc.2011.11.003</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Urologic Oncology Survey</prism:section><prism:startingPage>110</prism:startingPage><prism:endingPage>110</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS107814391100408X/abstract?rss=yes"><title>Commentary on “Survival after resection for metastatic testicular nonseminomatous germ cell cancer to the lung or mediastinum.” Kenneth A. Kesler,a Laura E. Kruter,a Susan M. Perkins,b Karen M. Rieger,a Katherine J. Sullivan,a Matthew L. Runyan,a John W. Brown,a Lawrence H. Einhorn,caDepartment of Surgery, Cardiothoracic Division and Medicine, Indiana University Melvin and Bren Simon Cancer Center, Indianapolis, Indiana;bDepartment of Biostatistics, Indiana University Melvin and Bren Simon Cancer Center, Indianapolis, Indiana;cHematology-Oncology Divisions, Indiana University Melvin and Bren Simon Cancer Center, Indianapolis, Indiana: Ann Thorac Surg 2011;91:1085–93</title><link>http://www.urologiconcology.org/article/PIIS107814391100408X/abstract?rss=yes</link><description>Since the advent of cisplatin-based chemotherapy, nonseminomatous germ cell tumors (NSGCT) have been considered one of the most curable solid neoplasms and a model for multimodality cancer therapy. We undertook an institutional review of testicular NSGCT patients who underwent operations to remove lung or mediastinal metastases after chemotherapy in the cisplatin era to determine outcomes.</description><dc:title>Commentary on “Survival after resection for metastatic testicular nonseminomatous germ cell cancer to the lung or mediastinum.” Kenneth A. Kesler,a Laura E. Kruter,a Susan M. Perkins,b Karen M. Rieger,a Katherine J. Sullivan,a Matthew L. Runyan,a John W. Brown,a Lawrence H. Einhorn,caDepartment of Surgery, Cardiothoracic Division and Medicine, Indiana University Melvin and Bren Simon Cancer Center, Indianapolis, Indiana;bDepartment of Biostatistics, Indiana University Melvin and Bren Simon Cancer Center, Indianapolis, Indiana;cHematology-Oncology Divisions, Indiana University Melvin and Bren Simon Cancer Center, Indianapolis, Indiana: Ann Thorac Surg 2011;91:1085–93</dc:title><dc:creator>Jerome P. Richie</dc:creator><dc:identifier>10.1016/j.urolonc.2011.11.004</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Urologic Oncology Survey</prism:section><prism:startingPage>110</prism:startingPage><prism:endingPage>111</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143911004091/abstract?rss=yes"><title>Commentary on “Screening for testicular cancer: U.S. Preventive Services Task Force reaffirmation recommendation statement.” Collaborators (18), U.S. Preventive Services Task Force: Ann Intern Med 2011 Apr 5;154:483–6</title><link>http://www.urologiconcology.org/article/PIIS1078143911004091/abstract?rss=yes</link><description>Reaffirmation of the 2004 U.S. Preventive Services Task Force (USPSTF) recommendation statement on screening for testicular cancer.   The USPSTF performed a targeted literature search for benefits and harms of screening for testicular cancer in asymptomatic males and found no new studies.</description><dc:title>Commentary on “Screening for testicular cancer: U.S. Preventive Services Task Force reaffirmation recommendation statement.” Collaborators (18), U.S. Preventive Services Task Force: Ann Intern Med 2011 Apr 5;154:483–6</dc:title><dc:creator>Jerome P. Richie</dc:creator><dc:identifier>10.1016/j.urolonc.2011.11.005</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Urologic Oncology Survey</prism:section><prism:startingPage>111</prism:startingPage><prism:endingPage>111</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143911004108/abstract?rss=yes"><title>Commentary on “Successful treatment of post-chemotherapy azoospermia with microsurgical testicular sperm extraction: The Weill Cornell experience.” Hsiao W, Stahl PJ, Osterberg EC, Nejat E, Palermo GD, Rosenwaks Z, Schlegel PN, Weill Cornell Medical College, James Buchanan Brady Foundation, New York, New York: J Clin Oncol 2011;29:1607–11</title><link>http://www.urologiconcology.org/article/PIIS1078143911004108/abstract?rss=yes</link><description>Advances in chemotherapy have led to greater longevity and paternity may be an important consideration for post-chemotherapy survivors of childhood cancers. While traditionally considered sterile, men who are azoospermic after chemotherapy can be treated with microdissection testicular sperm extraction (TESE) and intracytoplasmic sperm injection (ICSI).</description><dc:title>Commentary on “Successful treatment of post-chemotherapy azoospermia with microsurgical testicular sperm extraction: The Weill Cornell experience.” Hsiao W, Stahl PJ, Osterberg EC, Nejat E, Palermo GD, Rosenwaks Z, Schlegel PN, Weill Cornell Medical College, James Buchanan Brady Foundation, New York, New York: J Clin Oncol 2011;29:1607–11</dc:title><dc:creator>Jerome P. Richie</dc:creator><dc:identifier>10.1016/j.urolonc.2011.11.006</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Urologic Oncology Survey</prism:section><prism:startingPage>112</prism:startingPage><prism:endingPage>112</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS107814391100411X/abstract?rss=yes"><title>Commentary on “Adverse prognostic factors for testicular cancer-specific survival: A population-based study of 27,948 patients.” Fosså SD, Cvancarova M, Chen L, Allan AL, Oldenburg J, Peterson DR, Travis LB, Oslo University Hospital, University of Oslo, Norway: J Clin Oncol 2011;29:963–70</title><link>http://www.urologiconcology.org/article/PIIS107814391100411X/abstract?rss=yes</link><description>The prognostic significance of age at testicular cancer (TC) diagnosis, socioeconomic status (SES), race, and marital status on TC-specific mortality is not well-characterized. In a cancer that is so curable, it is important to identify any influence that confers an increased risk of TC-specific mortality.</description><dc:title>Commentary on “Adverse prognostic factors for testicular cancer-specific survival: A population-based study of 27,948 patients.” Fosså SD, Cvancarova M, Chen L, Allan AL, Oldenburg J, Peterson DR, Travis LB, Oslo University Hospital, University of Oslo, Norway: J Clin Oncol 2011;29:963–70</dc:title><dc:creator>Jerome P. Richie</dc:creator><dc:identifier>10.1016/j.urolonc.2011.11.007</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Urologic Oncology Survey</prism:section><prism:startingPage>112</prism:startingPage><prism:endingPage>113</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143911004121/abstract?rss=yes"><title>Commentary on “Management of rectal injury during robotic radical prostatectomy.” Kheterpal E, Bhandari A, Siddiqui S, Pokala N, Peabody J, Menon M, Vattikuti Urology Institute, Henry Ford Health System, Henry Ford Hospital, Detroit, Michigan: Urology 2011;77:976–9</title><link>http://www.urologiconcology.org/article/PIIS1078143911004121/abstract?rss=yes</link><description>To review the incidence and management of rectal injury in 4,400 consecutive cases of robotic radical prostatectomy at a single institution.   From September 2001 to September 2009, 4,400 patients underwent robotic radical prostatectomy. We reviewed the intraoperative and postoperative data from patients with rectal injuries. Once recognized, the rectal injuries were closed in 2 layers. Clear liquids were started the day after surgery. Healing of the vesicourethral anastomosis was confirmed by cystography 5–14 days postoperatively.</description><dc:title>Commentary on “Management of rectal injury during robotic radical prostatectomy.” Kheterpal E, Bhandari A, Siddiqui S, Pokala N, Peabody J, Menon M, Vattikuti Urology Institute, Henry Ford Health System, Henry Ford Hospital, Detroit, Michigan: Urology 2011;77:976–9</dc:title><dc:creator>Christopher Kane</dc:creator><dc:identifier>10.1016/j.urolonc.2011.11.008</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Urologic Oncology Survey</prism:section><prism:startingPage>113</prism:startingPage><prism:endingPage>113</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143911004133/abstract?rss=yes"><title>Commentary on “Posterior reconstruction before vesicourethral anastomosis in patients undergoing robot-assisted laparoscopic prostatectomy leads to earlier return to baseline continence.” Brien JC, Barone B, Fabrizio M, Given R, Department of Urology, Eastern Virginia Medical School, Norfolk, Virginia: J Endourol 2011;25:441–5</title><link>http://www.urologiconcology.org/article/PIIS1078143911004133/abstract?rss=yes</link><description>Reapproximation of Denonvilliers' fascia adjacent to bladder neck to the rectourethralis, or posterior reconstruction (PR), has been suggested to improve continence in post-prostatectomy patients. We examined the impact of the PR on postoperative urinary and other quality-of-life (QoL) outcomes in patients undergoing robot-assisted laparoscopic prostatectomy (RALP).</description><dc:title>Commentary on “Posterior reconstruction before vesicourethral anastomosis in patients undergoing robot-assisted laparoscopic prostatectomy leads to earlier return to baseline continence.” Brien JC, Barone B, Fabrizio M, Given R, Department of Urology, Eastern Virginia Medical School, Norfolk, Virginia: J Endourol 2011;25:441–5</dc:title><dc:creator>Christopher Kane</dc:creator><dc:identifier>10.1016/j.urolonc.2011.11.009</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Urologic Oncology Survey</prism:section><prism:startingPage>114</prism:startingPage><prism:endingPage>114</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143911004145/abstract?rss=yes"><title>Commentary on “Posterior rhabdosphincter reconstruction during robotic assisted radical prostatectomy: Results from a phase II randomized clinical trial.” Sutherland DE, Linder B, Guzman AM, Hong M, Frazier HA II, Engel JD, Bianco FJ Jr., Department of Urology, George Washington University, Washington, DC: J Urol 2011;185:1262–7</title><link>http://www.urologiconcology.org/article/PIIS1078143911004145/abstract?rss=yes</link><description>Posterior rhabdosphincter reconstruction following radical prostatectomy was designed to improve early urinary continence. We executed a randomized clinical trial to test this conjecture in men undergoing robotic radical prostatectomy.</description><dc:title>Commentary on “Posterior rhabdosphincter reconstruction during robotic assisted radical prostatectomy: Results from a phase II randomized clinical trial.” Sutherland DE, Linder B, Guzman AM, Hong M, Frazier HA II, Engel JD, Bianco FJ Jr., Department of Urology, George Washington University, Washington, DC: J Urol 2011;185:1262–7</dc:title><dc:creator>Christopher Kane</dc:creator><dc:identifier>10.1016/j.urolonc.2011.11.010</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Urologic Oncology Survey</prism:section><prism:startingPage>114</prism:startingPage><prism:endingPage>115</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143911004157/abstract?rss=yes"><title>Commentary on “Outcomes of robotic partial nephrectomy for renal masses with nephrometry score of ≥7.” White MA, Haber GP, Autorino R, Khanna R, Hernandez AV, Forest S, Yang B, Altunrende F, Stein RJ, Kaouk JH, Department of Surgery, Center for Laparoscopic and Robotic Surgery, Glickman Urological and Kidney Institute, Cleveland, Ohio: Urology 2011;77:809–13</title><link>http://www.urologiconcology.org/article/PIIS1078143911004157/abstract?rss=yes</link><description>To evaluate the safety and feasibility of robotic partial nephrectomy for patients with complex renal masses.   We reviewed the data for 164 consecutive patients who had undergone transperitoneal robotic partial nephrectomy at a tertiary care center from February 2007 to June 2010. Of the 112 patients who had available imaging studies to review, 67 were identified and classified as having a moderately or highly complex renal mass according to the R.E.N.A.L. nephrometry score (≥7) (tumor size-[R]adius, location and depth-[E]xophytic or endophytic; nearness to the renal sinus fat or collecting system [N]; anterior or posterior position [A], and polar vs. non-polar location [L]). The preoperative, perioperative, pathologic, and functional outcomes data were analyzed.</description><dc:title>Commentary on “Outcomes of robotic partial nephrectomy for renal masses with nephrometry score of ≥7.” White MA, Haber GP, Autorino R, Khanna R, Hernandez AV, Forest S, Yang B, Altunrende F, Stein RJ, Kaouk JH, Department of Surgery, Center for Laparoscopic and Robotic Surgery, Glickman Urological and Kidney Institute, Cleveland, Ohio: Urology 2011;77:809–13</dc:title><dc:creator>Christopher Kane</dc:creator><dc:identifier>10.1016/j.urolonc.2011.11.011</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Urologic Oncology Survey</prism:section><prism:startingPage>115</prism:startingPage><prism:endingPage>116</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143911004169/abstract?rss=yes"><title>Commentary on “Surgery-related complications of robot-assisted radical cystectomy with intracorporeal urinary diversion.” Schumacher MC, Jonsson MN, Hosseini A, Nyberg T, Poulakis V, Pardalidis NP, John H, Wiklund PN, Department of Molecular Medicine and Surgery, Division of Urology, Karolinska Institutet, Stockholm, Sweden: Urology 2011;77:871–6</title><link>http://www.urologiconcology.org/article/PIIS1078143911004169/abstract?rss=yes</link><description>To assess the surgery-related complications at robot-assisted radical cystectomy with total intracorporeal urinary diversion during our learning curve in treating 45 patients with bladder cancer.</description><dc:title>Commentary on “Surgery-related complications of robot-assisted radical cystectomy with intracorporeal urinary diversion.” Schumacher MC, Jonsson MN, Hosseini A, Nyberg T, Poulakis V, Pardalidis NP, John H, Wiklund PN, Department of Molecular Medicine and Surgery, Division of Urology, Karolinska Institutet, Stockholm, Sweden: Urology 2011;77:871–6</dc:title><dc:creator>Christopher Kane</dc:creator><dc:identifier>10.1016/j.urolonc.2011.11.012</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>Urologic Oncology Survey</prism:section><prism:startingPage>116</prism:startingPage><prism:endingPage>116</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143911004704/abstract?rss=yes"><title>The Society of Urologic Oncology's reply to the US Preventative Services Task Force's recommendation on PSA testing</title><link>http://www.urologiconcology.org/article/PIIS1078143911004704/abstract?rss=yes</link><description>
The United States Preventative Services Task Force (USPSTF) recently published its preliminary recommendation against PSA testing. There have been a variety of highly vocal critics and supporters of this recommendation whose opinions have appeared in the lay press, blogs, etc. The Society of Urologic Oncology requested a committee chaired by Gerald Andriole of Washington University (St. Louis), and consisting of Peter Albertsen (University of Connecticut), Peter Carroll (UCSK), Eric Klein (Cleveland Clinic) and myself (Edward Messing) (with input from other SUO members) to write a reply to the Task Force's recommendation. The following letter was submitted to the USPSTF's website, responding to their request for such comments.
November 8, 2011</description><dc:title>The Society of Urologic Oncology's reply to the US Preventative Services Task Force's recommendation on PSA testing</dc:title><dc:creator>Edward M. Messing, Peter Albertsen, Gerald L. Andriole, Peter R. Carroll, Eric A. Klein</dc:creator><dc:identifier>10.1016/j.urolonc.2011.12.010</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section>News and Topics</prism:section><prism:startingPage>117</prism:startingPage><prism:endingPage>119</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143911004819/abstract?rss=yes"><title>Information for Authors</title><link>http://www.urologiconcology.org/article/PIIS1078143911004819/abstract?rss=yes</link><description></description><dc:title>Information for Authors</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1078-1439(11)00481-9</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 30, 1 (2012)</dc:source><dc:date>2012-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2012-01-01</prism:publicationDate><prism:volume>30</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(11)X0008-X</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>120</prism:startingPage><prism:endingPage>120</prism:endingPage></item></rdf:RDF>
