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<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 2.531, 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>5</prism:number><prism:publicationDate>September 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/PIIS1078143910001997/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143910002000/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143910002012/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909004207/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143910000062/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143910000359/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS107814390800389X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909003676/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143908002652/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143908002664/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS107814390800313X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143908003207/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143908003438/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909002634/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143908003888/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143908003906/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909000891/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143910001572/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143910001560/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143910000025/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143910001961/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143909004220/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143910000748/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143910002085/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143910001596/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143910001602/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143910001614/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143910001626/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143910001638/abstract?rss=yes"/><rdf:li rdf:resource="http://www.urologiconcology.org/article/PIIS1078143910002103/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143910001997/abstract?rss=yes"><title>Masthead</title><link>http://www.urologiconcology.org/article/PIIS1078143910001997/abstract?rss=yes</link><description></description><dc:title>Masthead</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1078-1439(10)00199-7</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</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/PIIS1078143910002000/abstract?rss=yes"><title>Editorial Board</title><link>http://www.urologiconcology.org/article/PIIS1078143910002000/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1078-1439(10)00200-0</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</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/PIIS1078143910002012/abstract?rss=yes"><title>Contents</title><link>http://www.urologiconcology.org/article/PIIS1078143910002012/abstract?rss=yes</link><description></description><dc:title>Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1078-1439(10)00201-2</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</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/PIIS1078143909004207/abstract?rss=yes"><title>Understanding the agreement of histology of familial testicular tumors</title><link>http://www.urologiconcology.org/article/PIIS1078143909004207/abstract?rss=yes</link><description>A recent article, by Mai et al.  reported clinicopathologic features of familial testicular germ cell tumors (TGCTs) collected in the auspices of the International Testicular Cancer Linkage Consortium (ITCLC) composed of more than 20 centers from 14 countries. The patients included 985 men with TGCTs from 461 families, of which 266 families with 2 cases had detailed histology information for both cases. The results indicated that there was no evidence of the concordance of the two main histologic types, seminoma and nonseminoma, of TGCTs within-family, the overall measure of concordance, κ was 0.15. No evidence of histologic concordance was observed among son–father pairs, fraternal pairs, cousins, or other kindred; the κ ranging from 0.16 to 0.38. These are agreeably modest κ values, but no P values were given. According to other types of epidemiologic studies, similar incidence trends in seminoma and nonseminoma have been suggested to imply sharing of etiologic factors between the histologic types .</description><dc:title>Understanding the agreement of histology of familial testicular tumors</dc:title><dc:creator>Hao Liu, Jan Sundquist, Kari Hemminki</dc:creator><dc:identifier>10.1016/j.urolonc.2009.12.010</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-05-20</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-05-20</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Letter</prism:section><prism:startingPage>465</prism:startingPage><prism:endingPage>465</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143910000062/abstract?rss=yes"><title>T1 bladder cancer: Advocating early cystectomy to improve oncologic control</title><link>http://www.urologiconcology.org/article/PIIS1078143910000062/abstract?rss=yes</link><description>Treating bladder cancer is challenging. Even with efforts to promote early detection and close surveillance, nearly 50% of patients undergoing cystectomy die of metastatic disease . This alarming rate has remained relatively unchanged despite advances in bladder cancer detection, staging, use of intravesical therapy, and surgical technique. T1 bladder cancer accounts for up to 45% of superficial bladder tumors and more than 90% of these tumors are high grade . Of these, 30% progress to muscle-invasive disease within 5 years of diagnosis when treated with transurethral resection (TUR) alone. Although traditionally referred to as superficial disease, T1 bladder cancer is unique compared with Ta and carcinoma in situ (CIS). T1 disease either develops or inherently possesses the genetic capability to invade the bladder wall, penetrating the basement membrane into the lamina propria and often the associated muscularis mucosa, with the risk of tumor progression and metastasis if not effectively eliminated.</description><dc:title>T1 bladder cancer: Advocating early cystectomy to improve oncologic control</dc:title><dc:creator>Jeffrey S. Montgomery, Alon Z. Weizer, James E. Montie</dc:creator><dc:identifier>10.1016/j.urolonc.2010.01.003</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-05-10</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-05-10</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>News and Topics</prism:section><prism:startingPage>466</prism:startingPage><prism:endingPage>468</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143910000359/abstract?rss=yes"><title>Defining sexual function after radical retropubic prostatectomy</title><link>http://www.urologiconcology.org/article/PIIS1078143910000359/abstract?rss=yes</link><description>While the prevalence of erectile dysfunction (ED) as a direct sequela of radical retropubic prostatectomy (RRP) is universally recognized, statistics regarding the frequency of ED following RRP are widely disparate . As Wang aptly remarked in a 2007 review, “currently published clinical studies produce poorly interpretable and inconsistent determinations of erection outcome following the treatment of clinically localized prostate cancer” . Unfortunately, this fact hinders the ability of the urologist not only to counsel patients, but also to optimize postoperative therapies and, consequently, maximize patient recovery of sexual function. Such an environment requires urologic oncologists and urologists with an expertise in sexual medicine to establish an integrated approach to the pre- and postoperative evaluation, diagnosis, and management of patients undergoing pelvic surgery that is based on a common understanding of sexual function in the post-prostatectomy patient. Developing clear definitions for sexual function in this population would subsequently lay the groundwork for universal standards of both counseling and treatment of patients undergoing pelvic surgery.</description><dc:title>Defining sexual function after radical retropubic prostatectomy</dc:title><dc:creator>Moira E. Dwyer, Ajay Nehra</dc:creator><dc:identifier>10.1016/j.urolonc.2010.01.007</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-05-10</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-05-10</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>News and Topics</prism:section><prism:startingPage>469</prism:startingPage><prism:endingPage>472</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS107814390800389X/abstract?rss=yes"><title>The epithelial-mesenchymal transition-inducing factor TWIST is an attractive target in advanced and/or metastatic bladder and prostate cancers</title><link>http://www.urologiconcology.org/article/PIIS107814390800389X/abstract?rss=yes</link><description>Abstract: Purpose: Metastasis remains the main cause of death in both bladder (BCa) and prostate (PCa) cancers. The results of chemotherapy did not show any significant improvement of the survival the past years. Cancer research has led to the identification of signaling pathways involved and molecular targets that could change the natural history. The epithelial-mesenchymal transition (EMT), critical during embryonic development, becomes potentially destructive in many epithelial tumors progression where it is inappropriately activated. The cell-cell and cell-extracellular matrix interactions are altered to release cancer cells, which are able to migrate toward metastatic sites. Hallmarks of EMT include the down-regulation of E-cadherin expression, which is the main component of the adherens junctions. The protein TWIST is a transcriptional repressor of E-cadherin, tumor progression, and metastasis, and could be used as a molecular target to restore the chemosensitivity in BCa and PCa.Materials and methods: We selected the last 5-year basic research literature on EMT and TWIST but also clinical studies on BCa and PCa in which TWIST is overexpressed and could be considered as an efficient prognostic marker and molecular target.Results: TWIST is considered as a potential oncogene promoting the proliferation and inhibiting the apoptosis. TWIST promotes the synthesis of the pro-angiogenic factor, vascular endothelial growth factor (VEGF) involved in tumor progression and metastasis. Apoptosis and angiogenesis are two essential cancer progression steps in many epithelial tumors, including BCa and PCa.Conclusions: With the targeted therapy, oncology has entered into a new era, which is going to be critical in cancer treatment in combination with traditional anticancer drugs.</description><dc:title>The epithelial-mesenchymal transition-inducing factor TWIST is an attractive target in advanced and/or metastatic bladder and prostate cancers</dc:title><dc:creator>Hervé Wallerand, Grégoire Robert, Gilles Pasticier, Alain Ravaud, Philippe Ballanger, Robert E. Reiter, Jean-Marie Ferrière</dc:creator><dc:identifier>10.1016/j.urolonc.2008.12.018</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2009-03-09</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2009-03-09</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Review Articles</prism:section><prism:startingPage>473</prism:startingPage><prism:endingPage>479</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909003676/abstract?rss=yes"><title>Robot-assisted radical cystectomy: An expert panel review of the current status and future direction</title><link>http://www.urologiconcology.org/article/PIIS1078143909003676/abstract?rss=yes</link><description>Abstract: Objective: At the 9th Annual Meeting of the Society of Urologic Oncology (SUO), an expert panel discussed the current status of robot-assisted radical cystectomy (RARC).Materials and methods: The presentations were derived from: (1) review of published literature, unpublished addendums, and SUO abstracts, (2) initial abstract data of pooled results of 528 patients from the International Robot-Assisted Cystectomy Consortium (IRCC), and (3) an internet-based survey of the SUO membership (n = 54) on training and practice patterns related to RARC.Results: Using pathologic assessment of surgical margins as a surrogate for cancer control, the results are favorable with organ confined disease, with select expert series showing no positive margins and the IRCC group reporting 4%. In non-organ-confined disease, select expert series also show no positive margins, while for the IRCC group it was 15%. The median lymph node yield in all series is 12–19 with 5%–33% positive. The S-model robot is preferred for an extended node dissection to the aortic bifurcation. In experienced hands, estimated blood loss is &lt;500 cc, and hospital discharge by postoperative d 4–5. Complications appear similar to open and decrease with experience. In one study comparing RARC to open, pain scales were similar but morphine use was consistently lower for RARC. The technique is most often applied to the bladder and lymph nodes only with a mini-laparotomy for the diversion; technical considerations for female patients were described. The membership surveys showed that 37% of respondents have attempted RARC, but &lt; 20% received robot console training during fellowship. The greatest area of concern was the adequacy of the lymph node dissection in the higher regions—common iliac to peri-caval/aortic.Conclusions: Initial reports of RARC demonstrate feasibility of technique, early oncologic outcomes, and learning curve experiences. Surgeons learning RARC should select patients without clinical evidence of locally advanced disease, and consider a second look open node dissection. Experienced surgeons have demonstrated the possibility of reduced blood loss, opiate requirement, and hospital stay. Moving forward, an international consortium has been organized to address the unmet needs of prospective comparisons with long-term oncologic outcomes, standardized complication reporting, and quality of life.</description><dc:title>Robot-assisted radical cystectomy: An expert panel review of the current status and future direction</dc:title><dc:creator>John W. Davis, Erik P. Castle, Raj S. Pruthi, David K. Ornstein, Khurshid A. Guru</dc:creator><dc:identifier>10.1016/j.urolonc.2009.11.014</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</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>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Review Articles</prism:section><prism:startingPage>480</prism:startingPage><prism:endingPage>486</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143908002652/abstract?rss=yes"><title>Is residual neurovascular tissue on prostatectomy specimens associated with surgeon intent at nerve-sparing and postoperative quality of life measures?</title><link>http://www.urologiconcology.org/article/PIIS1078143908002652/abstract?rss=yes</link><description>Abstract: Objectives: Preservation of periprostatic neurovascular tissue at the time of radical prostatectomy has been correlated with subsequent erectile function and urinary continence. We evaluated whether the amount of neurovascular tissue identified on prostatectomy specimens correlated with surgeon's intention of nerve-sparing and/or predicted quality of life outcomes.Materials and methods: Radical prostatectomy specimens from 60 patients were evaluated by 2 pathologists for residual neurovascular bundle tissue. Reviewable pathology was available for 17, 19, and 19 patients with bilateral, unilateral, and non-nerve-sparing radical prostatectomy, respectively. The patients completed the Expanded Prostate Cancer Index Composite, a validated quality of life questionnaire. Differences between neurovascular tissue thickness, surgeon's intent at nerve-sparing, and quality of life among patients in each group were analyzed using standard statistical software.Results: Neurovascular tissue thickness identified on radical prostatectomy specimens did not correlate with surgeon's intent at performing a nerve-sparing procedure, nor was it found to be predictive of postoperative quality of life. Surgeon's intent at neurovascular preservation, however, was associated with improved sexual and urinary function scores at 1 year (both P &lt; 0.05).Conclusions: Surgeon intent, regardless of the amount of neurovascular tissue identified on radical prostatectomy specimen, is predictive of postoperative sexual-related and urinary quality of life. This suggests that factors other than the amount of neurovascular tissue spared contribute to postoperative sexual and urinary function.</description><dc:title>Is residual neurovascular tissue on prostatectomy specimens associated with surgeon intent at nerve-sparing and postoperative quality of life measures?</dc:title><dc:creator>Timothy J. Bradford, Alon Z. Weizer, Scott M. Gilbert, Rodney L. Dunn, Kirk Wojno, Rajal Shah, David P. Wood</dc:creator><dc:identifier>10.1016/j.urolonc.2008.09.042</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2008-12-29</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2008-12-29</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>487</prism:startingPage><prism:endingPage>491</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143908002664/abstract?rss=yes"><title>The International Testicular Cancer Linkage Consortium: A clinicopathologic descriptive analysis of 461 familial malignant testicular germ cell tumor kindred</title><link>http://www.urologiconcology.org/article/PIIS1078143908002664/abstract?rss=yes</link><description>Abstract: Objectives: Familial aggregation of testicular germ cell tumor (TGCT) has been reported, but it is unclear if familial TGCT represents a unique entity with distinct clinicopathologic characteristics. Here we describe a collection of familial TGCT cases from an international consortium, in an effort to elucidate any clinical characteristics that are specific to this population.Materials and methods: Families with ≥2 cases of TGCT enrolled at 18 of the sites participating in the International Testicular Cancer Linkage Consortium were included. We analyzed clinicopathologic characteristics of 985 cases from 461 families.Results: A majority (88.5%) of families had only 2 cases of TGCT. Men with seminoma (50% of cases) had an older mean age at diagnosis than nonseminoma cases (P = 0.001). Among individuals with a history of cryptorchidism, TGCT was more likely to occur in the ipsilateral testis (κ = 0.65). Cousin pairs appeared to represent a unique group, with younger age at diagnosis and a higher prevalence of cryptorchidism than other families.Conclusions: Clinicopathologic characteristics in these familial TGCT cases were similar to those generally described for nonfamilial cases. However, we observed a unique presentation of familial TGCT among cousin pairs. Additional studies are needed to further explore this observation.</description><dc:title>The International Testicular Cancer Linkage Consortium: A clinicopathologic descriptive analysis of 461 familial malignant testicular germ cell tumor kindred</dc:title><dc:creator>Phuong L. Mai, Michael Friedlander, Kathy Tucker, Kelly-Anne Phillips, David Hogg, Michael A.S. Jewett, Radka Lohynska, Gedske Daugaard, Stéphane Richard, Catherine Bonaïti-Pellié, Axel Heidenreich, Peter Albers, Istvan Bodrogi, Lajos Geczi, Edith Olah, Peter A. Daly, Parry Guilford, Sophie D. Fosså, Ketil Heimdal, Ludmila Liubchenko, Sergei A. Tjulandin, Hans Stoll, Walter Weber, Douglas F. Easton, Darshna Dudakia, Robert Huddart, Michael R. Stratton, Lawrence Einhorn, Larissa Korde, Katherine L. Nathanson, D. Timothy Bishop, Elizabeth A. Rapley, Mark H. Greene</dc:creator><dc:identifier>10.1016/j.urolonc.2008.10.004</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (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>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>492</prism:startingPage><prism:endingPage>499</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS107814390800313X/abstract?rss=yes"><title>Are patients with hematuria appropriately referred to Urology? A multi-institutional questionnaire based survey</title><link>http://www.urologiconcology.org/article/PIIS107814390800313X/abstract?rss=yes</link><description>Abstract: Introduction: Hematuria is a common finding that may be a sign of serious underlying urologic disease. Thus, the AUA guidelines (written in conjunction with the American Academy of Family Practice) recommend urologic evaluation for patients with both microscopic and gross hematuria. We sought to evaluate practice patterns of the evaluation of hematuria by primary care physicians (PCPs) in two locations in the United States.Methods: Anonymous questionnaires regarding use of urinalysis (UA) and evaluation of hematuria were mailed to 586 PCPs in Miami, Florida and 1,915 in Dallas, Texas. Surveys were mailed to physicians who identified themselves as practitioners of internal medicine, family practice, primary care, or obstetrics and gynecology.Results: Surveys were completed by 788 PCPs including 270 (46%) and 518 (26%) PCPs in Miami and Dallas, respectively. Screening UAs were obtained on all patients by 77% and 64%, of physicians in Miami and Dallas, respectively. In both Miami and Dallas, only 36% of PCPs reported referring patients with microscopic hematuria to an urologist. In patients with gross hematuria, referral rates were 77% and 69% in Miami and Dallas, respectively.Conclusions: While many PCPs use UA in many of their patients routinely, few PCPs automatically refer their patients with microscopic hematuria to urology and not all patients with gross hematuria are referred. Further investigations regarding why and when patients are referred to urology is warranted. Increasing awareness of the complete and timely evaluation of hematuria may be beneficial in preventing a delay in bladder cancer.</description><dc:title>Are patients with hematuria appropriately referred to Urology? A multi-institutional questionnaire based survey</dc:title><dc:creator>Alan M. Nieder, Yair Lotan, Geoffrey R. Nuss, Joshua P. Langston, Sachin Vyas, Murugesan Manoharan, Mark S. Soloway</dc:creator><dc:identifier>10.1016/j.urolonc.2008.10.018</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2008-12-22</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2008-12-22</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>500</prism:startingPage><prism:endingPage>503</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143908003207/abstract?rss=yes"><title>Complications of open primary and post-chemotherapy retroperitoneal lymph node dissection for testicular cancer</title><link>http://www.urologiconcology.org/article/PIIS1078143908003207/abstract?rss=yes</link><description>Abstract: Objective: Treatment decisions regarding the use of retroperitoneal lymph node dissection (RPLND) for low-stage and advanced testicular cancer may be influenced by the morbidity of the procedure. We sought to compare the complication profile of primary (P-) and post-chemotherapy (PC-) RPLND using a standardized complication grading scale.Materials and methods: A retrospective analysis was conducted of 112 and 96 patients who underwent P-RPLND and PC-RPLND, respectively, between 1982 and 2007 for perioperative outcomes and late complications. Postoperative complications were graded using a 5-tiered scale based on the severity and/or level of intervention required for resolution.Results: P-RPLND patients had rates of 5%, 24%, and 7% for intraoperative, postoperative, and late complications, respectively. For PC-RPLND, these rates were 12%, 32%, and 7%, respectively (P = 0.11, 0.19, and 1, respectively). Major postoperative complications (grades III–V) were observed in 3 (3%) P-RPLND and 8 (8%) PC-RPLND patients (P = 0.15), including 1 fatal pulmonary embolus in a PC-RPLND patient. Ileus accounted for 63% and 45% of postoperative complications of P-RPLND and PC-RPLND, respectively. PC-RPLND was associated with significantly greater operative times, blood loss, and transfusion rates (P &lt; 0.001). Compared with PC-RPLND after first-line chemotherapy for advanced NSGCT, there were no significant differences in perioperative outcomes for PC-RPLND performed in other settings.Conclusions: P-RPLND and PC-RPLND are associated with low rates of serious short- and long-term complications and negligible mortality, without significant differences between the 2 procedures. The safe morbidity profile of RPLND performed by fellowship-trained urologic oncologists should be considered during treatment decision-making for low-stage and advanced testicular cancer.</description><dc:title>Complications of open primary and post-chemotherapy retroperitoneal lymph node dissection for testicular cancer</dc:title><dc:creator>Vairavan S. Subramanian, Carvell T. Nguyen, Andrew J. Stephenson, Eric A. Klein</dc:creator><dc:identifier>10.1016/j.urolonc.2008.10.026</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2008-12-22</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2008-12-22</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>504</prism:startingPage><prism:endingPage>509</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143908003438/abstract?rss=yes"><title>Sequential intravesical gemcitabine and mitomycin C chemotherapy regimen in patients with non-muscle invasive bladder cancer</title><link>http://www.urologiconcology.org/article/PIIS1078143908003438/abstract?rss=yes</link><description>Abstract: Objectives: Currently, there are few options other than cystectomy for the management of BCG refractory non-muscle invasive bladder cancer. We report our experience with intravesical combination chemotherapy using gemcitabine and MMC in such patients.Materials and methods: We identified all patients with non-muscle invasive bladder cancer who were BCG refractory or intolerant and had been treated with intravesical gemcitabine and MMC at our institution. Patients were treated with a combination of intravesical gemcitabine (1000 mg in 50 ml sterile water) followed sequentially by intravesical MMC (40 mg in 20 ml sterile water) every week for 6 weeks (induction). Induction therapy was followed by a maintenance regimen using the same dose of gemcitabine and MMC once a month for 12 months. Data regarding patient demographics and disease information such as previous intravesical therapy, previous cystoscopy, cytology results, time to recurrence, and side effect profile were collected.Results: A total of 10 patients (6 male and 4 female) aged 48 to 85 years (median 67 years) underwent treatment with a median follow-up of 26.5 months (4–34 months). Six patients were recurrence free and have maintained their response at a median of 14 months (4–34 months). Four patients had biopsy proven recurrence. Median time to recurrence was 6 months (range 4–13 months). The therapy was well tolerated in all patients. There were no major complications. Two patients experienced irritative lower urinary tract symptoms, which did not require cessation of therapy and one experienced a maculopapillary rash that improved with benadryl.Conclusions: In patients with recurrent BCG refractory bladder cancer, intravesical combination chemotherapy with gemcitabine and MMC appears to be well tolerated and yields a response in a good proportion number of patients.</description><dc:title>Sequential intravesical gemcitabine and mitomycin C chemotherapy regimen in patients with non-muscle invasive bladder cancer</dc:title><dc:creator>Benjamin N. Breyer, Jared M. Whitson, Peter R. Carroll, Badrinath R. Konety</dc:creator><dc:identifier>10.1016/j.urolonc.2008.11.019</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2009-01-27</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2009-01-27</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>510</prism:startingPage><prism:endingPage>514</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909002634/abstract?rss=yes"><title>Abnormalities of thyroid function in Japanese patients with metastatic renal cell carcinoma treated with sorafenib: A prospective evaluation</title><link>http://www.urologiconcology.org/article/PIIS1078143909002634/abstract?rss=yes</link><description>Abstract: The objective of this study was to characterize features of thyroid dysfunction in Japanese patients with metastatic renal cell carcinoma (RCC) who were treated with sorafenib. We performed a prospective observational study including 69 Japanese patients who were diagnosed as having metastatic RCC refractory to cytokine therapy and subsequently treated with sorafenib for at least 12 weeks. Thyroid function was assessed before and every 4 weeks after the initiation of sorafenib treatment. Of the 69 patients, 23 (33.3%) did not show any biochemical thyroid abnormality, while the remaining 46 (67.7%) developed hypothyroidism. However, 11 (23.9%) of these 46 hypothyroid patients initially had a suppressed thyroid-stimulating hormone (TSH) value accompanying the increase in free triiodothyronine (T3) and/or free thyroxine (T4) before developing hypothyroidism, suggesting sorafenib-induced thyroiditis. During the observation period of this study, 4 patients (5.8%) demonstrated severe clinical symptoms caused by hypothyroidism and received thyroid hormone replacement. Among several factors examined, only age was significantly associated with the risk for hypothyroidism. These findings suggest that although the incidence of clinically significant hypothyroidism requiring thyroid hormone replacement therapy was not very high, biochemical thyroid abnormality was frequently observed in Japanese RCC patients treated with sorafenib. Accordingly, regular surveillance of thyroid function by the measurement of TSH, free T3, and T4 is warranted during sorafenib treatment in Japanese RCC patients.</description><dc:title>Abnormalities of thyroid function in Japanese patients with metastatic renal cell carcinoma treated with sorafenib: A prospective evaluation</dc:title><dc:creator>Hideaki Miyake, Toshifumi Kurahashi, Kazuki Yamanaka, Yutaka Kondo, Mototsugu Muramaki, Atsushi Takenaka, Taka-aki Inoue, Masato Fujisawa</dc:creator><dc:identifier>10.1016/j.urolonc.2009.08.011</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (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>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>515</prism:startingPage><prism:endingPage>519</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143908003888/abstract?rss=yes"><title>The therapeutic potential of recombinant BCG expressing the antigen S1PT in the intravesical treatment of bladder cancer</title><link>http://www.urologiconcology.org/article/PIIS1078143908003888/abstract?rss=yes</link><description>Abstract: Purpose: Bacillus Calmette-Guerin (BCG) continues to be employed as the most effective immunotherapy against superficial bladder cancer. We have developed an rBCG-S1PT strain that induces a stronger cellular immune response than BCG. This preclinical study was designed to test the potential of rBCG-S1PT as an immunotherapeutic agent for intravesical bladder cancer therapy.Materials and methods: A tumor was induced in C57BL/6 mice after chemical cauterization of the bladder and inoculation of the tumor cell line MB49. Next, mice were treated by intravesical instillation with BCG, rBCG-S1PT, or PBS once a week for 4 weeks. After 35 days, the bladders were removed and weighed, Th1 (IL-2, IL-12, INOS, INF-γ, TNF-α), and Th2 (IL-5, IL-6, IL-10, TGF-β) cytokine mRNA responses in individual mice bladders were measured by quantitative real time PCR, and the viability of MB49 cells in 18-hour coculture with splenocytes from treated mice was assessed. In an equivalent experiment, animals were observed for 60 days to quantify their survival.Results: Both BCG and rBCG-S1PT immunotherapy resulted in bladder weight reduction, and rBCG-S1PT increased survival time compared with the control group. There were increases in TNF-α in the BCG treated group, as well as increases in TNF-α and IL-10 mRNA in the rBCG-S1PT group. The viability of MB49 cells cocultured with splenocytes from rBCG-S1PT-treated mice was lower than in both the BCG and control groups.Conclusions: rBCG-S1PT therapy improved outcomes and lengthened survival times. These results indicate that rBCG could serve as a useful substitute for wild-type BCG.</description><dc:title>The therapeutic potential of recombinant BCG expressing the antigen S1PT in the intravesical treatment of bladder cancer</dc:title><dc:creator>Priscila M. Andrade, Daher C. Chade, Ricardo C. Borra, Ivan P. Nascimento, Fabiola E. Villanova, Luciana C.C. Leite, Enrico Andrade, Miguel Srougi</dc:creator><dc:identifier>10.1016/j.urolonc.2008.12.017</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2009-03-09</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2009-03-09</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>520</prism:startingPage><prism:endingPage>525</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143908003906/abstract?rss=yes"><title>p21 Expression by human urothelial carcinoma cells modulates the phenotypic response to BCG</title><link>http://www.urologiconcology.org/article/PIIS1078143908003906/abstract?rss=yes</link><description>Abstract: Purpose: The direct phenotypic effects of BCG on human urothelial carcinoma (UC) cells include cell cycle arrest, apoptotic resistance, and caspase-independent cell death. These effects are associated with increased expression of the cyclin dependant kinase inhibitor (CDKI) p21. This study assessed the role of p21 expression in mediating the phenotypic effects observed in response to BCG.Materials and methods: Inducible systems for the autocrine expression of p21, or the blockade of p21 expression in response to BCG, were established in the human UC line T24. The effect of increasing or inhibiting p21 expression on tumor phenotype was assessed using assays for cell cycle compartmentalization (flow cytometry), apoptotic sensitivity (caspase 3 activation), and cytotoxicity (vital dye exclusion).Results: p21 Overexpression resulted in cell cycle arrest with an increase in the percentage of the cell in G0/G1 phase when compared with the untreated group. p21 Expression decreased basal caspase-3 expression compared with the untreated group, and reversed camptothecin-induced caspase-3 activity compared with camptothecin alone group. p21 Overexpression increased BCG's direct cytotoxicity. shRNA-mediated inhibition of p21 expression in response to BCG failed to reverse BCG-induced changes in cell cycle compartmentalization. p21 Inhibition partially reversed the antiapoptotic effect of BCG. The expression of p21 was required for the direct cytotoxic effect of BCG.Conclusions: p21 Expression is sufficient but not necessary for BCG-induced cell cycle arrest. It is both sufficient and necessary for the full antiapoptotic effect of BCG. p21 Expression alone is not sufficient for caspase-independent cytotoxicity but is necessary for BCG's direct cytotoxic effect.</description><dc:title>p21 Expression by human urothelial carcinoma cells modulates the phenotypic response to BCG</dc:title><dc:creator>William A. See, Guangjian Zhang, Fanghong Chen, Yanli Cao</dc:creator><dc:identifier>10.1016/j.urolonc.2008.12.023</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2009-05-18</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2009-05-18</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>526</prism:startingPage><prism:endingPage>533</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909000891/abstract?rss=yes"><title>The expression of syndecan-1 and -2 is associated with Gleason score and epithelial-mesenchymal transition markers, E-cadherin and β-catenin, in prostate cancer</title><link>http://www.urologiconcology.org/article/PIIS1078143909000891/abstract?rss=yes</link><description>Abstract: The epithelial-mesenchymal transition (EMT) is considered a key step in tumor progression, where the invasive cancer cells change from epithelial to mesenchymal phenotype. During this process, a decrease or loss in adhesion molecules expression and an increase in migration molecules expression are observed. The aim of this work was to determine the expression and cellular distribution of syndecan-1 and -2 (migration molecules) and E-cadherin and β-catenin (adhesion molecules) in different stages of prostate cancer progression. A quantitative immunohistochemical study of these molecules was carried out in tissue samples from benign prostatic hyperplasia and prostate carcinoma, with low and high Gleason score, obtained from biopsies archives of the Clinic Hospital of the University of Chile and Dipreca Hospital. Polyclonal specific antibodies and amplification system of estreptavidin-biotin peroxidase and diaminobenzidine were used. Syndecan-1 was uniformly expressed in basolateral membranes of normal epithelium, changing to a granular cytoplasmatic expression pattern in carcinomas. Syndecan-2 was observed mainly in a cytoplasmatic granular pattern, with high immunostaining intensity in areas of low Gleason score. E-cadherin was detected in basolateral membrane of normal epithelia showing decreased expression in high Gleason score samples. β-Catenin was found in cell membranes of normal epithelia changing its distribution toward the nucleus and cytoplasm in carcinoma samples. We concluded that changes in expression and cell distribution of E-cadherin and β-catenin correlated with the progression degree of prostate adenocarcinoma, suggesting a role of these molecules as markers of progression and prognosis. Furthermore, changes in the pattern expression of syndecan-1 and -2 indicate that both molecules may be involved in the EMT and tumor progression of prostate cancer.</description><dc:title>The expression of syndecan-1 and -2 is associated with Gleason score and epithelial-mesenchymal transition markers, E-cadherin and β-catenin, in prostate cancer</dc:title><dc:creator>Hector R. Contreras, Rodrigo A. Ledezma, Jorge Vergara, Federico Cifuentes, Cristina Barra, Pablo Cabello, Ivan Gallegos, Bernardo Morales, Christian Huidobro, Enrique A. Castellón</dc:creator><dc:identifier>10.1016/j.urolonc.2009.03.018</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2009-05-18</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2009-05-18</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>534</prism:startingPage><prism:endingPage>540</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143910001572/abstract?rss=yes"><title>Proceeding of the 2009 Society of Urologic Oncology Spring Meeting</title><link>http://www.urologiconcology.org/article/PIIS1078143910001572/abstract?rss=yes</link><description>In this issue of the Seminars, we summarize highlights of the Annual Spring Meeting of the Society of Urologic Oncology, held on April 25, 2009 in Chicago, Illinois, immediately prior to the American Urological Association 2009 Annual Meeting. The Society meeting encompassed a broad range of topics related to the care of urologic cancer patients. As is usually the case, the speakers made outstanding presentations and offered thoughtful, unique, and occasionally divergent opinions on disease management. While the content of the meeting was broad, I have selected a few representative topics for presentation in this SUO Proceedings issue of the Seminars, which I believe embody the spirit of the meeting.</description><dc:title>Proceeding of the 2009 Society of Urologic Oncology Spring Meeting</dc:title><dc:creator>Samir S. Taneja</dc:creator><dc:identifier>10.1016/j.urolonc.2010.05.013</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Seminar Section Introduction</prism:section><prism:startingPage>541</prism:startingPage><prism:endingPage>541</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143910001560/abstract?rss=yes"><title>Deciding whom to biopsy</title><link>http://www.urologiconcology.org/article/PIIS1078143910001560/abstract?rss=yes</link><description>Abstract: Biopsy results from the Prostate Cancer Prevention Trial (PCPT) showed that prostate cancer exists at all PSA levels and that a significant number of men with “normal” PSA levels have high grade cancer. These findings and the low specificity of total PSA in discriminating cancer from benign disease have added to the debate about how best to use PSA in selecting men for prostate biopsy. Lower PSA thresholds for consideration of biopsy, particularly in younger men, are advocated by some. PSA velocity measurements may assist in the identification of men most likely to harbor cancer, and lower PSA velocity thresholds may be more appropriate in younger men. A more individualized approach using a predictive model developed from PCPT biopsy results is promoted by others. While able to incorporate risk variables other than PSA, including new markers, this risk calculator does not include PSA velocity since this variable was not found to have independent predictive value in this model. This article will present differing viewpoints on selecting men for prostate biopsy, one advocating the use of a PSA cut-off or PSA velocity measure (Dr. Catalona) and the other arguing for the routine use of established risk nomograms (Dr. Klein).</description><dc:title>Deciding whom to biopsy</dc:title><dc:creator>Christopher L. Amling, William J. Catalona, Eric A. Klein</dc:creator><dc:identifier>10.1016/j.urolonc.2010.05.012</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Seminar Articles</prism:section><prism:startingPage>542</prism:startingPage><prism:endingPage>545</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143910000025/abstract?rss=yes"><title>Limitations of a contemporary prostate biopsy: The blind march forward</title><link>http://www.urologiconcology.org/article/PIIS1078143910000025/abstract?rss=yes</link><description>Abstract: In an attempt to reduce morbidity, focal targeted therapies and active surveillance have become increasingly popular treatment choices for localized prostate cancer. However, these modalities rely heavily on accurate and reliable tumor localization information provided by a prostate biopsy. Evidence that our contemporary biopsy techniques can do little more than detect some prostate cancers is notably lacking. What is meant by the accuracy and reliability of a prostate biopsy and why they are such important concepts to focal therapy and active surveillance are discussed.</description><dc:title>Limitations of a contemporary prostate biopsy: The blind march forward</dc:title><dc:creator>John T. Wei</dc:creator><dc:identifier>10.1016/j.urolonc.2009.12.022</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Seminar Articles</prism:section><prism:startingPage>546</prism:startingPage><prism:endingPage>549</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143910001961/abstract?rss=yes"><title>Focal therapy for prostate cancer: Fact or fiction?</title><link>http://www.urologiconcology.org/article/PIIS1078143910001961/abstract?rss=yes</link><description>Abstract: Prostate cancer is the commonest male cancer diagnosed in men in the UK, and the treatment of organ confined prostate cancer is a subject of much debate. Focal therapy for prostate cancer intends to treat the cancer within the prostate, whilst sparing the majority of the benign prostate tissue. In addition, the intention is to avoid treatment effects in the surrounding structures, the damage of which leads to the side effects commonly associated with radical whole gland therapies. This relies on accurate localization of the prostate cancer by biopsy and imaging followed by treatment using a modality capable of delivery to a focal area within the prostate. Focal therapy lies between the current extremes of radical whole gland treatment and active surveillance. There have been many articles reviewing the concept of focal therapy for organ confined prostate cancer, but with a paucity of data available for analysis. This is being addressed with an increase in the published data on focal therapy, using a number of different modalities. In this review, we address the question of whether the data currently published does in fact support the further development of the focal therapy approach, or whether it is a concept best relegated to the realms of fiction.</description><dc:title>Focal therapy for prostate cancer: Fact or fiction?</dc:title><dc:creator>Emilie Lecornet, Caroline Moore, Hashim Uddin Ahmed, Mark Emberton</dc:creator><dc:identifier>10.1016/j.urolonc.2010.08.004</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Seminar Articles</prism:section><prism:startingPage>550</prism:startingPage><prism:endingPage>556</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143909004220/abstract?rss=yes"><title>What is the optimal management of high risk, clinically localized prostate cancer?</title><link>http://www.urologiconcology.org/article/PIIS1078143909004220/abstract?rss=yes</link><description>Abstract: Objectives: To summarize the presentations and debate regarding the optimal treatment of localized high-risk prostate cancer as presented at the 2009 Spring Meeting of the Society of Urologic Oncology.Materials and methods: The debate was centered on presentations arguing for radical prostatectomy (RP) or radiotherapy as the optimal treatment for this condition. The meeting presentations are summarized by their respective presenters herein.Results: Dr. James Eastham presents the varied definitions for “high-risk” prostate cancer as strongly influencing which patients end up in this cohort. Based upon this, between 3% and 38% of patients with high-risk features could be defined as “high-risk”. Despite that, these men do not have a uniformly poor prognosis after RP, and attention to surgical principles as outlined improve outcomes. Disease-specific survival at 12 years is excellent and up to one-half of these men may not need adjuvant or salvage therapies, depending on their specific disease characteristics. Adjuvant or salvage radiotherapies improve outcomes and are part of a sequential approach to treating these patients. Dr. Anthony Zietman presented radiotherapy as the gold-standard based upon large, randomized clinical trials of intermediate- and high-risk prostate cancer patients. Compared with androgen deprivation alone, the addition of radiotherapy provided a 12% cancer-specific survival advantage and 10% overall survival advantage. Dose escalation seems to confer further improvements in cancer control without significant escalation of toxicities, with more data forthcoming.Conclusions: There are no randomized trials comparing RP to radiotherapy for any risk category. In high-risk prostate cancer patients, both approaches have potential benefits and cumulative toxicities that must be matched to disease characteristics and patient expectations in selecting a treatment course.</description><dc:title>What is the optimal management of high risk, clinically localized prostate cancer?</dc:title><dc:creator>James A. Eastham, Christopher P. Evans, Anthony Zietman</dc:creator><dc:identifier>10.1016/j.urolonc.2009.12.012</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Seminar Articles</prism:section><prism:startingPage>557</prism:startingPage><prism:endingPage>567</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143910000748/abstract?rss=yes"><title>Impact of nephron sparing on kidney function and non-oncologic mortality</title><link>http://www.urologiconcology.org/article/PIIS1078143910000748/abstract?rss=yes</link><description>Abstract: The surgical management of kidney tumors has significantly evolved over the past decade. Partial nephrectomy and nephron sparing surgery have emerged as the treatments of choice for most newly diagnosed kidney tumors at tertiary care centers. The trend towards an organ sparing approach is largely due to an improved understanding of the global importance of kidney function as well as the impact that kidney surgery may have on non-oncologic morbidity and mortality. In addition to reviewing the methods of evaluating kidney function, this article discusses the effectiveness of various nephron sparing techniques in preserving kidney function and improving non-oncologic outcomes.</description><dc:title>Impact of nephron sparing on kidney function and non-oncologic mortality</dc:title><dc:creator>William C. Huang</dc:creator><dc:identifier>10.1016/j.urolonc.2010.03.018</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Seminar Articles</prism:section><prism:startingPage>568</prism:startingPage><prism:endingPage>574</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143910002085/abstract?rss=yes"><title>Survey Section Editorial Board</title><link>http://www.urologiconcology.org/article/PIIS1078143910002085/abstract?rss=yes</link><description></description><dc:title>Survey Section Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1078-1439(10)00208-5</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>575</prism:startingPage><prism:endingPage>575</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143910001596/abstract?rss=yes"><title>Commentary on “Prospective randomized controlled trial of robotic vs. open radical cystectomy for bladder cancer: Perioperative and pathologic results” Jeff Nix, Angela Smith, Raj Kurpad, Matthew E. Nielsen, Eric M. Wallen, Raj S. Pruthi, Division of Urologic Surgery, University of North Carolina at Chapel Hill, Chapel Hill, NC</title><link>http://www.urologiconcology.org/article/PIIS1078143910001596/abstract?rss=yes</link><description>Eur Uroljavascript:AL_get(this, ‘jour’, ‘Eur Urol.’); 2010;57:196–201 (Epub 2009 Oct 20)   Eur Urol 2010;57:202–3; author reply 203–4 http://www.ncbi.nlm.nih.gov/pubmed/19931975?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract</description><dc:title>Commentary on “Prospective randomized controlled trial of robotic vs. open radical cystectomy for bladder cancer: Perioperative and pathologic results” Jeff Nix, Angela Smith, Raj Kurpad, Matthew E. Nielsen, Eric M. Wallen, Raj S. Pruthi, Division of Urologic Surgery, University of North Carolina at Chapel Hill, Chapel Hill, NC</dc:title><dc:creator>Sean P. Stroup, Christopher J. Kane</dc:creator><dc:identifier>10.1016/j.urolonc.2010.06.002</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Urologic Oncology Survey</prism:section><prism:startingPage>576</prism:startingPage><prism:endingPage>576</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143910001602/abstract?rss=yes"><title>Commentary on “Cost analysis of robotic vs. open radical cystectomy for bladder cancer” Angela Smith, Raj Kurpad, Anjana Lal, Matthew E. Nielsen, Eric M. Wallen, Raj S. Pruthi, Division of Urologic Surgery, The University of North Carolina at Chapel Hill, Chapel Hill, NC</title><link>http://www.urologiconcology.org/article/PIIS1078143910001602/abstract?rss=yes</link><description>J Urol 2010;183:505–9 (Epub 2009 Dec 14)   J Urol 2010;183:509</description><dc:title>Commentary on “Cost analysis of robotic vs. open radical cystectomy for bladder cancer” Angela Smith, Raj Kurpad, Anjana Lal, Matthew E. Nielsen, Eric M. Wallen, Raj S. Pruthi, Division of Urologic Surgery, The University of North Carolina at Chapel Hill, Chapel Hill, NC</dc:title><dc:creator>Christopher J. Kane</dc:creator><dc:identifier>10.1016/j.urolonc.2010.06.003</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Urologic Oncology Survey</prism:section><prism:startingPage>577</prism:startingPage><prism:endingPage>577</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143910001614/abstract?rss=yes"><title>Commentary on “Robot assisted partial nephrectomy vs. laparoscopic partial nephrectomy for renal tumors: A multi-institutional analysis of perioperative outcomes” Brian M. Benway, Sam B. Bhayani, Craig G. Rogers, Lori M. Dulabon, Manish N. Patel, Michael Lipkin, Agnes J. Wang, Michael D. Stifelman, Division of Urologic Surgery, Department of Surgery, Washington University School of Medicine, St. Louis, MO</title><link>http://www.urologiconcology.org/article/PIIS1078143910001614/abstract?rss=yes</link><description>J Urol 2009;182:866–72 (Epub 2009 Jul 17)   J Urol 2009;182:828–9</description><dc:title>Commentary on “Robot assisted partial nephrectomy vs. laparoscopic partial nephrectomy for renal tumors: A multi-institutional analysis of perioperative outcomes” Brian M. Benway, Sam B. Bhayani, Craig G. Rogers, Lori M. Dulabon, Manish N. Patel, Michael Lipkin, Agnes J. Wang, Michael D. Stifelman, Division of Urologic Surgery, Department of Surgery, Washington University School of Medicine, St. Louis, MO</dc:title><dc:creator>Christopher J. Kane</dc:creator><dc:identifier>10.1016/j.urolonc.2010.06.004</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Urologic Oncology Survey</prism:section><prism:startingPage>577</prism:startingPage><prism:endingPage>578</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143910001626/abstract?rss=yes"><title>Commentary on “Laparoendoscopic single-site surgery: Early experience with tumor nephrectomy” Jens-Uwe Stolzenburg, Giles Hellawell, Panagiotis Kallidonis, Minh Do, Tim Haefner, Anja Dietel, Evangelos N. Liatsikos, Department of Urology, University of Leipzig, Leipzig, Germany</title><link>http://www.urologiconcology.org/article/PIIS1078143910001626/abstract?rss=yes</link><description>J Endourol 2009;23:1287–92   Laparoendoscopic single-site surgery (LESS) represents the closest surgical technique to scar-free surgery. We performed LESS for renal tumor nephrectomy in 8 patients to assess feasibility and perioperative outcome.</description><dc:title>Commentary on “Laparoendoscopic single-site surgery: Early experience with tumor nephrectomy” Jens-Uwe Stolzenburg, Giles Hellawell, Panagiotis Kallidonis, Minh Do, Tim Haefner, Anja Dietel, Evangelos N. Liatsikos, Department of Urology, University of Leipzig, Leipzig, Germany</dc:title><dc:creator>Christopher J. Kane</dc:creator><dc:identifier>10.1016/j.urolonc.2010.06.005</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Urologic Oncology Survey</prism:section><prism:startingPage>578</prism:startingPage><prism:endingPage>579</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143910001638/abstract?rss=yes"><title>Commentary on “Preoperative superselective transarterial embolization in laparoscopic partial nephrectomy: Technique, oncologic, and functional outcomes” Giuseppe Simone, Rocco Papalia, Salvatore Guaglianone, Ester Forestiere, Michele Gallucci, Department of Urology, Regina Elena National Cancer Institute, Rome, Italy</title><link>http://www.urologiconcology.org/article/PIIS1078143910001638/abstract?rss=yes</link><description>J Endourol 2009;23:1473–8   We report the mid-term oncologic and functional results of a series of 110 patients treated with transperitoneal laparoscopic partial nephrectomy (LPN) after superselective arterial embolization (SEA).</description><dc:title>Commentary on “Preoperative superselective transarterial embolization in laparoscopic partial nephrectomy: Technique, oncologic, and functional outcomes” Giuseppe Simone, Rocco Papalia, Salvatore Guaglianone, Ester Forestiere, Michele Gallucci, Department of Urology, Regina Elena National Cancer Institute, Rome, Italy</dc:title><dc:creator>Christopher J. Kane</dc:creator><dc:identifier>10.1016/j.urolonc.2010.06.006</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section>Urologic Oncology Survey</prism:section><prism:startingPage>579</prism:startingPage><prism:endingPage>579</prism:endingPage></item><item rdf:about="http://www.urologiconcology.org/article/PIIS1078143910002103/abstract?rss=yes"><title>Information for Authors</title><link>http://www.urologiconcology.org/article/PIIS1078143910002103/abstract?rss=yes</link><description></description><dc:title>Information for Authors</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1078-1439(10)00210-3</dc:identifier><dc:source>Urologic Oncology: Seminars and Original Investigations 28, 5 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Urologic Oncology: Seminars and Original Investigations</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>28</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1078-1439(10)X0005-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>IBC</prism:startingPage><prism:endingPage>IBC</prism:endingPage></item></rdf:RDF>