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 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 2.662, 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> © 2010 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>28</prism:volume><prism:number>1</prism:number><prism:publicationDate>January 2010</prism:publicationDate><prism:copyright> © 2010 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/PIIS1078143909003792/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909003809/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909003810/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909002737/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143908002834/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143908001580/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143908001579/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143908001609/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909002373/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143908001555/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143908003281/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143908001592/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909003755/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909000374/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909000908/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909001914/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909002026/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909000635/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909001896/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909000933/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909001471/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909001045/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909001392/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909003846/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909003792/abstract?rss=yes"><title>Masthead</title><link>http://www.urologiconcology.org/article/PIIS1078143909003792/abstract?rss=yes</link><description></description><dc:title>Masthead</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1078-1439(09)00379-2</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>IFC</prism:startingPage><prism:endingPage>IFC</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909003809/abstract?rss=yes"><title>Editorial Board</title><link>http://www.urologiconcology.org/article/PIIS1078143909003809/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1078-1439(09)00380-9</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>i</prism:startingPage><prism:endingPage>i</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909003810/abstract?rss=yes"><title>Contents</title><link>http://www.urologiconcology.org/article/PIIS1078143909003810/abstract?rss=yes</link><description></description><dc:title>Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1078-1439(09)00381-0</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>ii</prism:startingPage><prism:endingPage>iv</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909002737/abstract?rss=yes"><title>Regionalizing urologic cancer care: Appropriate health care policy?</title><link>http://www.urologiconcology.org/article/PIIS1078143909002737/abstract?rss=yes</link><description>Health care spending dominates current political discussion. Recently, President Barak Obama has lobbied heavily for reform of our patchwork quilt of private payers and government programs, including Medicare and Medicaid. Health care spending in the United States now totals over $7,000 per person per year compared with Canadians, who spend about $4,000, and the British, who spend slightly less than $3,000 per person per year . Public sector spending averages $2,000– $3,000 per person per year in most Western countries, including the United States, but with the exception of the U.S., health care coverage in most Western countries extends to all citizens.</description><dc:title>Regionalizing urologic cancer care: Appropriate health care policy?</dc:title><dc:creator>Peter Albertsen</dc:creator><dc:identifier>10.1016/j.urolonc.2009.08.016</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2009-11-16</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2009-11-16</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>News and Topics</prism:section><prism:startingPage>1</prism:startingPage><prism:endingPage>3</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143908002834/abstract?rss=yes"><title>MicroRNAs and cancer: Current state and future perspectives in urologic oncology</title><link>http://www.urologiconcology.org/article/PIIS1078143908002834/abstract?rss=yes</link><description>Abstract: MicroRNAs (miRNAs) are small non-protein coding RNAs that regulate basic cellular processes and are associated with cancer characteristics. It is the aim of this review to describe the basics of the biogenesis and function of miRNAs, provide their role in tumorigenesis, and demonstrate their clinical potential in general and especially in urologic oncology. For that purpose, a PubMed search up to August 2008 was conducted using the Medical Subject Heading (MeSH) terms for miRNAs alone and the urological carcinomas of kidney, prostate, bladder, testis, and penis combined with the Boolean operator “AND”. Until August 2008, about 3,500 miRNA publications were included in the PubMed database. It has been estimated that about 1,500 would be published in 2008 alone. Several miRNA expression studies and corresponding functional experiments in various cancers showed the important role of miRNAs in cancer initiation and progression and proved their potential as diagnostic, prognostic, and predictive biomarkers and as basis for novel therapeutic strategies. However, in uro-oncology, only a few miRNA related articles (22 for prostate, 4 for kidney, 3 for bladder, and 6 for testis) were published. Cancer-specific expressions of miRNA patterns were shown, but the limited and partly inconsistent data underscore that we are at an early stage regarding this topic in urology. In spite of the obvious significance of miRNAs in malignant tumors, the relatively sparse data on miRNAs in uro-oncology clearly advocate that this area should be more intensively studied. Detailed understanding of the characteristic miRNA abnormalities could contribute to novel approaches in diagnosis and treatment of urological tumors.</description><dc:title>MicroRNAs and cancer: Current state and future perspectives in urologic oncology</dc:title><dc:creator>Annika Schaefer, Monika Jung, Glen Kristiansen, Michael Lein, Mark Schrader, Kurt Miller, Carsten Stephan, Klaus Jung</dc:creator><dc:identifier>10.1016/j.urolonc.2008.10.021</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2009-01-05</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2009-01-05</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Review Article</prism:section><prism:startingPage>4</prism:startingPage><prism:endingPage>13</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143908001580/abstract?rss=yes"><title>Combined modality treatment with bladder preservation for muscle invasive bladder cancer</title><link>http://www.urologiconcology.org/article/PIIS1078143908001580/abstract?rss=yes</link><description>Abstract: Objective: To evaluate the 5-year results of the following trimodal therapy for treatment of some selected cases of muscle invasive bladder cancer.Materials and Methods: In this prospective study, we included 104 patients with transitional cell carcinoma (TCC) (T2 and T3a, N0, M0) who were amenable to complete transurethral resection. All patients received adjuvant chemo-radiotherapy (CRT) in the form of gemcitabine and cisplatin and conventional radiotherapy after the maximum resection of their tumors. Two weeks later, all cases had radiologic and cystoscopic evaluation. The patients who showed no evidence of the bladder tumors [complete response (CR)] went on to complete the CRT, while those with recurrent invasive tumors did not receive any more CRT and were assigned to have salvage cystectomy. Thereafter, all patients were subjected to a regular follow-up.Results: This trimodal therapy was well tolerated in most of cases with no severe acute toxicities. Complete response was achieved in 78.8% of cases after the initial CRT, and tumor grade was found to be the most significant risk factor to predict this response (P = 0.004). With a median follow-up of 71 months for patients with initial CR, 16.2% of cases showed muscle invasive recurrences, and multifocality was the only significant risk factor for their development (P = 0.003). Meanwhile, superficial recurrences were detected in 8.1% of cases with initial CR and were successfully treated with transurethral resection and intravesical bacillus Calmette-Guerin (BCG). On the other hand, we reported distant metastasis in 24.3% of patients with initial CR, and tumor grade, stage and multifocality were the most significant risk factors for this complication (P = 0.002, 0.031, 0.006). No cases of contracted bladder or late gastrointestinal complications were demonstrated in this series. The 5-year overall survival rate for patients with initial CR was 67.6%, and for all the patients in this study it was 59.4%.Conclusions: This trimodal therapy can be considered as a treatment option for patients with localized muscle invasive TCC. The best candidates for such therapy are those with solitary T2, low grade tumors that are amenable to complete transurethral resection.</description><dc:title>Combined modality treatment with bladder preservation for muscle invasive bladder cancer</dc:title><dc:creator>Magdy A. Sabaa, Osama M. El-Gamal, Mohamed Abo-Elenen, Amr Khanam</dc:creator><dc:identifier>10.1016/j.urolonc.2008.07.005</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2008-09-26</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2008-09-26</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>14</prism:startingPage><prism:endingPage>20</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143908001579/abstract?rss=yes"><title>Safety and efficacy of sorafenib in patients with castrate resistant prostate cancer: A Phase II study</title><link>http://www.urologiconcology.org/article/PIIS1078143908001579/abstract?rss=yes</link><description>Abstract: Purpose: We determined the safety and efficacy of sorafenib in patients with castrate resistant prostate cancer (CRPC).Methods: Sixty-four chemotherapy and radiotherapy naïve patients with CRPC received 400 mg sorafenib orally twice daily in 6-week cycles. All patients had bone metastasis, while 16 had lymph node-, 9 had liver-, and 10 had lung metastases. Treatment was continued until disease progression or excessive toxicity.Results: All patients were assessable for response. A median of 6.4 consecutive cycles was administered per patient. Median overall survival for all patients was 14.6 months (confidence interval [CI], 8.2–22.2). No complete response (CR) occurred. Of the 35 patients with measurable extraosseous disease, 7 (20%) had a partial response. Overall, 13 patients (20.3%; 95% CI, 4%–32%) achieved a 50% or greater reduction (partial response [PR]) in prostate-specific antigen (PSA) level after two cycles. The median response duration was 2.5 months (95% CI, 1.4 to 4.8), and the median time to progression was 5.9 months (95% CI 3.6 to 7.6). There was no treatment-related death. Toxicities were well tolerated.Conclusions: Sorafenib demonstrated some antitumor activity. Further studies are necessary to determine a subgroup of patients who would likely respond better to sorafenib.</description><dc:title>Safety and efficacy of sorafenib in patients with castrate resistant prostate cancer: A Phase II study</dc:title><dc:creator>Mohammad Reza Safarinejad</dc:creator><dc:identifier>10.1016/j.urolonc.2008.06.003</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2008-09-15</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2008-09-15</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>21</prism:startingPage><prism:endingPage>27</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143908001609/abstract?rss=yes"><title>Extramammary Paget's disease of scrotum—report of 25 cases and literature review</title><link>http://www.urologiconcology.org/article/PIIS1078143908001609/abstract?rss=yes</link><description>Abstract: Objectives: We evaluate the clinical manifestations, management, and prognostic characteristics of scrotal extramammary Paget's disease (EMPD).Methods: The study comprised 25 patients with scrotal EMPD at our institute from January 1982 to February 2005, with all available clinical and pathological data reviewed.Results: Of these 25 patients, 1 received radiotherapy and 24 received local wide excisions. In 24 operated patients, 7 had local recurrence and/or metastasis of groin lymph node. Five of the 7 with recurrence had a positive surgical margin postoperatively and they received a second local extensive excision. One of the 7 with recurrence and metastasis of the groin lymph node had a second local extensive excision with groin lymphadenectomy, and the last one who only had metastasis of the groin lymph node had a groin lymphadenectomy. Four of 13 patients with dermal invasion by Paget's cell had metastasis. None of the other 12 patients without dermal invasion had metastasis. However, there was no statistical metastasis rate difference (P = 0.096) between the patients with dermal invasion by Paget's cell and without. There was no statistical difference (P = 0.947) in mean delay time from onset of symptoms to diagnosis between the 2 groups either. The follow-up duration varies from 17 to 243 months (mean 119 + 86.2 months). One patient with stage D died of EMPD of the scrotum.Conclusions: We found that EMPD of the scrotum is usually a slow progressive disease, mainly seen in elderly patients, and has a good prognosis when there is noninvasive disease. The primary treatment for EMPD of the scrotum is wide surgical excision. The key to decreasing tumor recurrence, however, is a precise, preoperative histological examination to define the range of the lesion.</description><dc:title>Extramammary Paget's disease of scrotum—report of 25 cases and literature review</dc:title><dc:creator>Ning Zhang, Kan Gong, Xiaodong Zhang, Yong Yang, Yanqun Na</dc:creator><dc:identifier>10.1016/j.urolonc.2008.07.002</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2008-09-22</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2008-09-22</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>28</prism:startingPage><prism:endingPage>33</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909002373/abstract?rss=yes"><title>Juxtaglomerular cell tumor of the kidney—a new classification scheme</title><link>http://www.urologiconcology.org/article/PIIS1078143909002373/abstract?rss=yes</link><description>Abstract: Objective: To introduce a new classification scheme of juxtaglomerular cell tumor (JCT) of the kidney for differential diagnosis of hypertension and renal cell carcinoma.Methods: Five cases of JCT have been diagnosed and treated surgically in our hospital during the last 4 years. Through a search in PubMed, we incorporated 7 large series of case reports of JCT into a review of 71 cases previously published in the literature. Clinical presentations (blood pressure), laboratory examinations [serum potassium, plasma renin activity (PRA), aldosterone (ALD), and renal venous sampling for renin assay], and imaging examinations [ultrasonography, computerized tomography (CT), excretory urography, and selective renal angiography] were summarized.Results: The 71 cases of JCTs can be classified into 3 types, which are typical type, atypical type, and non-functioning type. The 57 typical cases had the typical characteristics of hypertension, hypokalemia, hyperaldosteronism, and high renin. The 12 atypical cases had hypertension with normal potassium levels, and the 2 non-functioning cases had normal blood pressure and normal potassium levels.Conclusions: The classification of typical, atypical, and non-functioning JCTs depends on blood pressure and serum potassium. JCT of the kidney should be considered in patients with hypertension and renal tumor, and nephron-sparing surgery is the first choice.</description><dc:title>Juxtaglomerular cell tumor of the kidney—a new classification scheme</dc:title><dc:creator>Dexin Dong, Hanzhong Li, Weigang Yan, Weifeng Xu</dc:creator><dc:identifier>10.1016/j.urolonc.2009.08.003</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2009-11-16</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2009-11-16</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>34</prism:startingPage><prism:endingPage>38</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143908001555/abstract?rss=yes"><title>A microRNA expression ratio defining the invasive phenotype in bladder tumors</title><link>http://www.urologiconcology.org/article/PIIS1078143908001555/abstract?rss=yes</link><description>Abstract: Objective: The goal of this study was to identify a microRNA (miRNA) signature in bladder cancer capable of differentiating superficial from invasive disease.Methods: Expression profiling of 343 miRNAs was performed in a microarray format using noninvasive and invasive bladder carcinoma cell lines with differential expression confirmed using a single molecule detection platform assay. miR-21 and miR-205 expression levels were determined in 53 bladder tumors (28 superficial and 25 invasive). Sensitivity, specificity, and a ROC curve were calculated to determine the discriminatory power of the miRNA ratio to predict invasion. Knockdown and forced expression of miRNAs was performed to evaluate their role in invasion.Results: Expression profiling of 343 miRNAs, using noninvasive and invasive bladder cell lines, revealed significant differential expression of 9 miRNAs. Cell lines characterized as invasive showed a miR-21:miR-205 ratio at least 10-fold higher than the quantitative ratio obtained from non-invasive cell lines. The same expression ratio was determined in 53 bladder tumors. From these results, we recorded a sensitivity and specificity of 100% and 78%, respectively, using a cutoff of 1.79 to predict an invasive lesion. The area under the receiver operator characteristic curve was 0.89. Using in vitro invasion assays, we have demonstrated a role for miR-21 in establishing the invasive phenotype of bladder carcinoma cells.Conclusion: In this study, we identified a miR-21:miR-205 expression ratio that has the ability to distinguish between invasive and noninvasive bladder tumors with high sensitivity and specificity, with the potential to identify superficial lesions at high risk to progress.</description><dc:title>A microRNA expression ratio defining the invasive phenotype in bladder tumors</dc:title><dc:creator>Lori A. Neely, Kimberly M. Rieger-Christ, Brasil Silva Neto, Alexey Eroshkin, Joanne Garver, Sonal Patel, Nu Ai Phung, Stephen McLaughlin, John A. Libertino, Duncan Whitney, Ian C. Summerhayes</dc:creator><dc:identifier>10.1016/j.urolonc.2008.06.006</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2008-09-17</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2008-09-17</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>39</prism:startingPage><prism:endingPage>48</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143908003281/abstract?rss=yes"><title>Testis cancer cells have a genetic determination for a high sensitivity to apoptosis inducing stimuli</title><link>http://www.urologiconcology.org/article/PIIS1078143908003281/abstract?rss=yes</link><description>Abstract: Objective: The effect of cytotoxic therapy in testicular tumors (TGCT) has been shown to be mediated mainly by the induction of apoptosis. So far, it is not known which genes play a role for this inherent sensitivity to apoptosis inducing drugs. The aim of this study was to investigate the differential gene expression of apoptosis regulating genes in testicular tumors and in normal testis tissue using a quantitative method. As a premature S-phase entry was shown to induce apoptosis, genes controlling the G1/S-phase checkpoint were also investigated.Material and Methods: Gene expression levels of a representative subset of 19 genes involved in apoptosis and cell cycle control were investigated in vivo in 19 TGCTs using real-time quantitative PCR. Measurements were performed in tumor tissues of both tumor entities, seminomatous and non-seminomatous tumors (SGCT and NSGCT), and in corresponding biopsies from the unaffected site of the resected testis.Results: There was an up-regulation of genes that play a role in facilitating apoptosis, such as FasL, TRAIL, and Bax in both tumor entities. Genes inhibiting apoptosis, such as Bcl-2 were predominantly down-regulated. Regarding cell cycle regulators, a gene expression profile was found that corresponds to a premature S phase entry and subsequent apoptosis induction.Conclusion: This study for the first time identified in vivo a panel of genes that give TGCT an inherent sensitivity to apoptotic stimuli after exposure to DNA damaging agents. Studies on these genes in therapy-refractory cancers should provide further insight into the mechanisms of chemotherapy resistance. Furthermore, these genes are promising targets for a future targeted therapy of testis cancer.</description><dc:title>Testis cancer cells have a genetic determination for a high sensitivity to apoptosis inducing stimuli</dc:title><dc:creator>Hans U. Schmelz, Matthias Port, Markus Stockinger, Christian Ruf, Andreas Martinscheck, Christoph Sparwasser, Wolfgang Weidner, Michael Abend</dc:creator><dc:identifier>10.1016/j.urolonc.2008.11.003</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2009-01-23</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2009-01-23</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>49</prism:startingPage><prism:endingPage>58</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143908001592/abstract?rss=yes"><title>Radiosensitivity of prostate cancer cells is enhanced by EGFR inhibitor C225</title><link>http://www.urologiconcology.org/article/PIIS1078143908001592/abstract?rss=yes</link><description>Abstract: Purpose: To determine the direct effects of the epidermal growth factor receptor (EGFR) inhibitor C225 on the radiosensitivity of human prostate cancer cells.Experimental design: Human prostate cancer DU145 cells were irradiated with 60Co (1.953 Gy/min) at various doses in the presence or absence of C225. The cellular proliferation and cell-survival rate were evaluated by MTT and colony-forming assays after irradiation. The cell-cycle distribution, cell apoptosis, and MAPK expression were investigated using FCM. The expression of Cyclin D1, CDK2, CDK4, and Survivin were determined by RT-PCR.Results: The RBE in the C225 group compared with that in the control group was 1.39. Cells treated with C225 and irradiated at 4 Gy predominantly exhibited G0/G1 phase arrest and significant decrease in the fraction of cells in the S phase in comparison with those in the control cells, respectively. An evidently higher apoptosis rate on irradiation at 4 Gy was observed in C225-treated cells compared with that in the control cells. Decreased cell proliferation and increased cell death were further supported by the down-regulation of cyclin D1, CDK2, CDK4, and survivin in C225-treated DU145 cells, as determined by RT-PCR. Furthermore, C225 significantly inhibited the phosphorylation of P38-MAPK in DU145 cells.Conclusions: The EGFR inhibitor C225 increased the radiosensitivity of DU145 cells through antiproliferative effect, inhibition of clonal growth, G0/G1 phase arrest, apoptosis induction, and inhibition of EGFR-signaling pathways by the down-regulation of MAPK activation.</description><dc:title>Radiosensitivity of prostate cancer cells is enhanced by EGFR inhibitor C225</dc:title><dc:creator>Feng Liu, Jun-Jie Wang, Zhen-Yu You, Ying-Dong Zhang, Yong Zhao</dc:creator><dc:identifier>10.1016/j.urolonc.2008.07.001</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2008-09-17</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2008-09-17</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>59</prism:startingPage><prism:endingPage>66</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909003755/abstract?rss=yes"><title>Overview of SUO Winter 2008 proceedings</title><link>http://www.urologiconcology.org/article/PIIS1078143909003755/abstract?rss=yes</link><description>The 9th Annual Meeting of the Society of Urologic Oncology was held at the Natcher Conference Center, the National Institutes of Health, Bethesda, Maryland, December 4–5, 2008. At this meeting, clinical and basic investigators met to discuss recent developments in urologic cancers. Speakers discussed recent advances in the diagnosis, prevention, and treatment of patients with prostate, bladder, and kidney cancer.</description><dc:title>Overview of SUO Winter 2008 proceedings</dc:title><dc:creator>Seth P. Lerner, Bernard Bochner, W. Marston Linehan, Eric Klein, Michael Cookson</dc:creator><dc:identifier>10.1016/j.urolonc.2009.11.022</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Seminar Section Introduction</prism:section><prism:startingPage>67</prism:startingPage><prism:endingPage>68</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909000374/abstract?rss=yes"><title>Neoadjuvant treatment of renal cell carcinoma</title><link>http://www.urologiconcology.org/article/PIIS1078143909000374/abstract?rss=yes</link><description>Abstract: Renal cell carcinoma is a potentially devastating cancer, and when metastatic, remains incurable with currently available systemic therapy. Surgical nephrectomy remains the only proven modality which can offer curative options for patients with resectable disease. Further, cytoreductive nephrectomy continues to play a role in the metastatic disease setting. The use of targeted therapy as an adjunct to surgical resection is beginning to be explored in both of these clinical scenarios. Immediate questions regarding preoperative treatment with VEGF pathway targeted therapy include issues surrounding the safety of these agents in use in the perioperative time period, the expectations for response in the primary tumor, the optimal duration of therapy, and the clinical settings in which this therapy may be most beneficial. This review will discuss the current experience with neoadjuvant or preoperative therapy in locally advanced or metastatic renal cell carcinoma and will overview the challenges and opportunities which lie ahead for this form of multimodality therapy.</description><dc:title>Neoadjuvant treatment of renal cell carcinoma</dc:title><dc:creator>W. Kimryn Rathmell, Raj Pruthi, Eric Wallen</dc:creator><dc:identifier>10.1016/j.urolonc.2009.02.001</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Kidney</prism:section><prism:startingPage>69</prism:startingPage><prism:endingPage>73</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909000908/abstract?rss=yes"><title>Robotic partial nephrectomy: A comparison to current techniques</title><link>http://www.urologiconcology.org/article/PIIS1078143909000908/abstract?rss=yes</link><description>Abstract: The bar has been set high for nephron sparing surgery by experts in both open and laparoscopic approaches. Robotic partial nephrectomy has emerged as an option for minimally invasive nephron sparing surgery. We discuss the current literature for robotic partial nephrectomy in the context of reported outcomes for open and laparoscopic partial nephrectomy.</description><dc:title>Robotic partial nephrectomy: A comparison to current techniques</dc:title><dc:creator>Manish N. Patel, Mani Menon, Craig G. Rogers</dc:creator><dc:identifier>10.1016/j.urolonc.2009.03.020</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Kidney</prism:section><prism:startingPage>74</prism:startingPage><prism:endingPage>76</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909001914/abstract?rss=yes"><title>Converting from open to robotic prostatectomy: Key concepts</title><link>http://www.urologiconcology.org/article/PIIS1078143909001914/abstract?rss=yes</link><description>Abstract: Robotic-assisted laparoscopic prostatectomy (RALP) is rapidly becoming the surgical procedure of choice for treating localized prostate cancer. Although a learning curve does exist, RALP can readily be adopted by surgeons with minimal training in laparoscopy. Monitoring short- and long-term patient outcomes is the key to the individual surgeon improving this procedure for his/her patients. Although both open radical prostatectomy (ORP) and RALP can provide excellent patient outcomes, recent trends indicate that demand for RALP will continue to increase, and it is in the interest of the open surgeon to adopt this technique and aim to continuously improve patient outcomes after RALP.</description><dc:title>Converting from open to robotic prostatectomy: Key concepts</dc:title><dc:creator>Emilie K. Johnson, David P. Wood</dc:creator><dc:identifier>10.1016/j.urolonc.2009.06.009</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Prostate</prism:section><prism:startingPage>77</prism:startingPage><prism:endingPage>80</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909002026/abstract?rss=yes"><title>Transition from pure laparoscopic to robotic-assisted radical prostatectomy: A single surgeon institutional evolution</title><link>http://www.urologiconcology.org/article/PIIS1078143909002026/abstract?rss=yes</link><description>Abstract: Purpose: To review a single surgeon experience of transitioning to a robotic-assisted laparoscopic prostatectomy program (RALP) with prior pure laparoscopic radical prostatectomy (LRP) experience.Materials and methods: A retrospective review of surgical results from a single surgeon performing LRP transitioning to RALP was performed. Two hundred five patients undergoing RALP by a single, fellowship-trained, urologic oncologist were analyzed and compared with 45 patients undergoing LRP by the same surgeon. Operative, pathologic, and functional outcomes were evaluated. Validated questionnaires, including the International Prostate Symptom Score (IPSS) and International Index of Erectile Function (IIEF), were utilized for assessing urinary and sexual parameters.Results: Preoperative parameters (age, PSA, Gleason score) were similar in both RALP and LRP groups. Operative time (190 vs. 299 minutes), estimated blood loss (253 vs. 299 ml), and length of stay (1.6 vs. 2.6 days) were reduced in RALP vs. LRP. Although not statistically significant, there was a trend toward fewer transfusions with RALP (2.0% vs. 4.4%) as well as a lower positive margin rate in organ-confined (pT2) disease (9.8%, RALP vs. 20%, LRP). Continence at 12 months was 94% following RALP as opposed to 82% after LRP. In preoperatively potent men undergoing bilateral nerve sparing procedures, RALP conferred 81% potency at 12 months as opposed to only 62% following LRP.Conclusions: The transition from LRP to RALP, in concert with an institutional commitment to a successful robotic surgery program, has yielded superior operative, oncologic, and functional results.</description><dc:title>Transition from pure laparoscopic to robotic-assisted radical prostatectomy: A single surgeon institutional evolution</dc:title><dc:creator>Edouard J. Trabulsi, Joseph C. Zola, Leonard G. Gomella, Costas D. Lallas</dc:creator><dc:identifier>10.1016/j.urolonc.2009.07.002</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Prostate</prism:section><prism:startingPage>81</prism:startingPage><prism:endingPage>85</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909000635/abstract?rss=yes"><title>The second decade of prostate brachytherapy: Evidence and cost based outcomes</title><link>http://www.urologiconcology.org/article/PIIS1078143909000635/abstract?rss=yes</link><description>Abstract: Permanent prostate brachytherapy (PPB) is an established and successful treatment option for localized prostate cancer. Under ultrasound guidance, the procedure can be performed in the ambulatory setting and represents a conformal, ablative technique. For low-risk patients, PSA control is expected in over 90% with outcomes now reported past 12 years. High-risk patients can benefit from PPB as part of a program that may include external beam therapy and androgen ablation. Morbidity tends to center on urinary function, but with modern adaptive techniques, this can be minimized. Sexual functioning is likely disturbed less with PPB than with surgery or external beam radiation therapy. Finally, cost benefit analysis confirms PPB as the most attractive radiation option. With the incidence of prostate cancer still rising, PPB remains a key treatment option in the successful management of prostate cancers.</description><dc:title>The second decade of prostate brachytherapy: Evidence and cost based outcomes</dc:title><dc:creator>Philip Vigneri, Amin S. Herati, Louis Potters</dc:creator><dc:identifier>10.1016/j.urolonc.2009.02.003</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Prostate</prism:section><prism:startingPage>86</prism:startingPage><prism:endingPage>90</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909001896/abstract?rss=yes"><title>Bladder cancer: Novel molecular characteristics, diagnostic, and therapeutic implications</title><link>http://www.urologiconcology.org/article/PIIS1078143909001896/abstract?rss=yes</link><description>Abstract: Bladder cancer (BC) comes in two flavors: as non-muscle invasive (NMI) and as muscle invasive (MI) disease. These two subtypes differ in their genetic aberrations. In NMI-BC mutations in the FGFR3 oncogene are found with a frequency of 75%, whereas mutations in the TP53 tumor suppressor gene prevail in MI-BC. Mutations in the RAS genes occur in 15% of BC of all stages and are mutually exclusive with FGFR3 mutations. Mutations in the PIK3CA gene are found in about 13% and these almost exclusively co-occur with FGFR3 mutations. NMI-BC with FGFR3 mutations are genetically stable, but FGFR3 wild type NMI-BC and MI tumors are genetically unstable. In this paper, we discuss the use of these genetic aberrations in relation to recurrence, progression, surveillance, and therapeutic options. As of yet, there is no biomarker that can predict recurrences or the rate of recurrences when they occur. We show that FGFR3 mutations are associated with a decreased risk of progression, and a better survival both in BC and in upper urinary tract cancer. Microsatellite analysis (MA) in order to detect loss-of-heterozygosity can be used to detect recurrences in urinary cells of patients under surveillance. The results of a Dutch randomized trial show that consecutive positive MA results are a strong predictor for future recurrences. Using FGFR3 mutation analysis for those patients who have an FGFR3 mutant tumor will enhance performance of urine-based surveillance. Although FGFR3 mutations occur in only 20% of MI tumors, these tumors often have a high expression of the FGFR3 protein. This suggests that this receptor could present a target for adjuvant therapy in MI-BC. However, whether the FGFR3 pathway is active in these tumors remains to be established.</description><dc:title>Bladder cancer: Novel molecular characteristics, diagnostic, and therapeutic implications</dc:title><dc:creator>Lucie C. Kompier, Angela A.G. van Tilborg, Ellen C. Zwarthoff</dc:creator><dc:identifier>10.1016/j.urolonc.2009.06.007</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Bladder (Cancer Assessment)</prism:section><prism:startingPage>91</prism:startingPage><prism:endingPage>96</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909000933/abstract?rss=yes"><title>Role of biomarkers to predict outcomes and response to therapy</title><link>http://www.urologiconcology.org/article/PIIS1078143909000933/abstract?rss=yes</link><description>Abstract: Molecular markers are not established in management of bladder cancer. There is, however, a limit to the ability of clinical and pathological parameters to predict patients at high risk for urothelial carcinoma of the bladder (UCB) recurrence or mortality. The assessment of molecular biomarkers in surgical UCB specimens offers additional information on the biology of the disease, and might improve the prediction of oncologic end points. There is also a potential for molecular biomarkers to predict the response to adjuvant or neoadjuvant therapies. Furthermore, markers may guide targeted therapy. Prospective trials are needed to validate the clinical benefit of assessing expression patterns of molecular biomarkers.</description><dc:title>Role of biomarkers to predict outcomes and response to therapy</dc:title><dc:creator>Yair Lotan</dc:creator><dc:identifier>10.1016/j.urolonc.2009.03.017</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Bladder (Cancer Assessment)</prism:section><prism:startingPage>97</prism:startingPage><prism:endingPage>101</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909001471/abstract?rss=yes"><title>Are nomograms needed in the management of bladder cancer?</title><link>http://www.urologiconcology.org/article/PIIS1078143909001471/abstract?rss=yes</link><description>Abstract: Bladder cancer has a remarkably variable natural history. Noninvasive, low-grade (TaLG) lesions have a propensity to recur but pose little threat to the patient's longevity. Non-muscle-invasive, high-grade (Ta-TIS-T1HG) lesions can be effectively treated with intravesical BCG, but a subset may progress to muscle-invasive and metastatic bladder cancer. Muscle-invasive cancers (T2-T3) are uniformly lethal if inadequately treated, and subsets of patients benefit from perioperative chemotherapy and some may be adequately treated with bladder preservation strategies. The ability to accurately predict this variable natural history is essential to optimize treatment. At each stage of disease, the prognosis is often influenced by multiple parameters (e.g., tumor grade and stage, age, comorbidity) and treatments (e.g., radical cystectomy vs. BCG), and different endpoints are relevant based on the stage of disease (recurrence for TaLG, progression for Ta-TIS-T1HG, survival for T2-T4a). Historically, prediction of these endpoints for decision-making has been accomplished with physician judgment and/or basic decision aids such as risk classification systems. However, such methods of risk estimation are unable to fully account for the complex tumor biology and behavior of bladder cancer, potentially leading to inaccurate predictions and inappropriate treatment assignment. Nomograms are capable of incorporating multiple variables and generating accurate risk estimates tailored to the individual patient which may greatly facilitate patient counseling and treatment selection. Although their use has become more widespread, bladder cancer nomograms remain a relatively nascent field of study, and further development of novel nomograms that can account for all clinical stages of bladder cancer is needed.</description><dc:title>Are nomograms needed in the management of bladder cancer?</dc:title><dc:creator>Carvell T. Nguyen, Andrew J. Stephenson, Michael W. Kattan</dc:creator><dc:identifier>10.1016/j.urolonc.2009.04.020</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Bladder (Cancer Treatment)</prism:section><prism:startingPage>102</prism:startingPage><prism:endingPage>107</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909001045/abstract?rss=yes"><title>Novel intravesical therapies for non-muscle-invasive bladder cancer refractory to BCG</title><link>http://www.urologiconcology.org/article/PIIS1078143909001045/abstract?rss=yes</link><description>Abstract: The definitive treatment for patients with non-muscle-invasive bladder cancer (NMIBC) who fail to respond to intravesical BCG is cystectomy. When a patient is deemed BCG-refractory and cannot or will not undergo cystectomy, alternative intravesical therapy may be the most effective way to minimize recurrence and progression. A number of immunotherapeutic and chemotherapeutic agents have been given intravesically over the years, and several recently and currently investigated novel agents appear to be particularly promising for the management of BCG-refractory NMIBC. The most effective treatments in the future will likely utilize targeted therapies based on the underlying genetic mutations associated with each individual diagnosis of NMIBC.</description><dc:title>Novel intravesical therapies for non-muscle-invasive bladder cancer refractory to BCG</dc:title><dc:creator>LaMont J. Barlow, Catherine M. Seager, Mitchell C. Benson, James M. McKiernan</dc:creator><dc:identifier>10.1016/j.urolonc.2009.03.029</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Bladder (Cancer Treatment)</prism:section><prism:startingPage>108</prism:startingPage><prism:endingPage>111</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909001392/abstract?rss=yes"><title>Analysis of gender differences in early perioperative complications following radical cystectomy at a tertiary cancer center using a standardized reporting methodology</title><link>http://www.urologiconcology.org/article/PIIS1078143909001392/abstract?rss=yes</link><description>Abstract: Objectives: Gender differences in perioperative complications following radical cystectomy (RC) are under-studied, but suggest a tendency for higher blood loss and/or transfusion in females. Variability in reporting methodologies may affect findings; therefore, we utilized a standardized reporting methodology to evaluate for gender differences in perioperative complications at a tertiary cancer center.Materials and methods: A retrospective review of the Memorial Sloan-Kettering Cancer Center (MSKCC) RC database between 1995 and 2005 was performed. All complications within 90 days of surgery were recorded and classified using a 5-grade modification of the Clavien system.Results: Of 1,142 study patients, 280 (25%) were female. Preoperatively, females were more likely to have multiple co-morbidities (39% vs. 27%, P &lt; 0.001), a prior abdominal surgery (64% vs. 42%, P &lt; 0.001), and to be slightly less obese than men. Females had longer operative times (mean 413 vs. 391 minutes; P = 0.005), higher blood loss (mean 1,322 cc vs. 1,151 cc, P = 0.002), and higher transfusion rates (&gt;4 units red blood cells: 13% vs. 8%; P = 0.025). Although females were significantly more likely than males to experience a complication within 90 days of surgery (72% vs. 62%; P = 0.003); we did not find any important differences in the rate, grade, type, or timing of complications between genders. Additionally, females were less likely than males to receive a continent diversion (25% vs. 40%, P &lt; 0.001) or a pelvic lymph node dissection (90% vs. 96%, P &lt; 0.001).Conclusions: Females in our cohort had significantly higher blood loss, more transfusions, and a higher rate of complications. Females were also less likely to undergo a node dissection or continent diversion, for reasons not totally attributable to patient or disease characteristics, implying patient or surgeon preference played a role.</description><dc:title>Analysis of gender differences in early perioperative complications following radical cystectomy at a tertiary cancer center using a standardized reporting methodology</dc:title><dc:creator>Timothy Siegrist, Caroline Savage, Ahmad Shabsigh, Angel Cronin, S. Machele Donat</dc:creator><dc:identifier>10.1016/j.urolonc.2009.04.012</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Bladder (Cancer Treatment)</prism:section><prism:startingPage>112</prism:startingPage><prism:endingPage>117</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909003846/abstract?rss=yes"><title>Information for Authors</title><link>http://www.urologiconcology.org/article/PIIS1078143909003846/abstract?rss=yes</link><description></description><dc:title>Information for Authors</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1078-1439(09)00384-6</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 1 (2010)</dc:source><dc:date>2010-01-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-01-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1078-1439(09)X0007-4</prism:issueIdentifier><prism:section>Bladder (Cancer Treatment)</prism:section><prism:startingPage>IBC</prism:startingPage><prism:endingPage>IBC</prism:endingPage></item></rdf:RDF>