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    <title>Montironi, R.</title>
    <link>http://repub.eur.nl/res/aut/26956/</link>
    <description>List of Publications</description>
    <language>en</language>
    <image>
      <url>http://repub.eur.nl/static-eur/img/logo.png</url>
      <title>RePub, Erasmus University Rotterdam</title>
      <link>http://repub.eur.nl</link>
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    <item>
      <title>Comparison of incidentally detected prostate cancer with screen-detected prostate cancer treated by prostatectomy (Article)</title>
      <link>http://repub.eur.nl/res/pub/32008/</link>
      <pubDate>2012-01-01T00:00:00Z</pubDate>
      <description>BACKGROUND The prostate may often harbor a prostate cancer (PC) which will not cause morbidity if left untreated. Screening for PC leads to increased detection of these insignificant cancers. Objective of this study is to compare PC detected by PSA screening at subsequent screening rounds and treated by radical prostatectomy (RP) with PC incidentally found in cystoprostatectomy specimens. METHODS Radical prostatectomy specimens of 617 screen-detected PC were compared with 123 PC identified in cystoprostatectomy specimens. Surgical specimens were systematically examined and stage, grade, tumor volume were recorded. Next, we classified PC as clinically significant or insignificant (i.e., tumor volume &lt;0.5 cm3, absence of Gleason pattern 4/5, organ confined). Pathological features of incidentally detected PC were compared with PC detected in subsequent screening rounds and with screen-detected T1c PC. RESULTS Screen-detected PC overall were more often multifocal, larger in volume, more advanced in tumor stage and of higher grade, while the frequency of insignificant PC was lower as compared to those in cystoprostatectomy specimens. This effect became more pronounced during subsequent screening rounds. Screen-detected T1c PC were also more often multifocal (73% vs. 37%) in average fivefold larger (0.85 cm3vs. 0.16 cm3), less often organ confined (81% vs. 94%), and less frequently clinically insignificant (33% vs. 81%). CONCLUSIONS: Screen-detected (T1c) PC treated with RP shows more aggressive features than incidentally found PC. This PSA screening-related selection seems to be mainly driven by tumor volume and-in later screening rounds-by the preferential treatment by prostatectomy of more aggressive PC. Copyright </description>
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      <title>The controversial relationship between benign prostatic hyperplasia and prostate cancer: The role of inflammation (Article)</title>
      <link>http://repub.eur.nl/res/pub/33851/</link>
      <pubDate>2011-07-01T00:00:00Z</pubDate>
      <description>Context: Prostate cancer (PCa) is the most common cancer in the adult male, and benign prostatic hyperplasia (BPH) represents the most frequent urologic diagnosis in elderly males. Recent data suggest that prostatic inflammation is involved in the pathogenesis and progression of both conditions. Objective: This review aims to evaluate the available evidence on the role of prostatic inflammation as a possible common denominator of BPH and PCa and to discuss its possible clinical implication for the management, prevention, and treatment of both diseases. Evidence acquisition: The National Library of Medicine Database was searched for the following Patient population, Intervention, Comparison, Outcome (PICO) terms: male, inflammation, benign prostatic hyperplasia, prostate cancer, diagnosis, progression, prognosis, treatment, and prevention. Basic and clinical studies published in the past 10 yr were reviewed. Additional references were obtained from the reference list of full-text manuscripts. Evidence synthesis: The histologic signature of chronic inflammation is a common finding in benign and malignant prostate tissue. The inflammatory infiltrates are mainly represented by CD3+T lymphocytes (70-80%, mostly CD4), CD19 or CD20 B lymphocytes (10-15%), and macrophages (15%). Bacterial infections, urine reflux, dietary factors, hormones, and autoimmune response have been considered to cause inflammation in the prostate. From a pathophysiologic standpoint, tissue damage associated with inflammatory response and subsequent chronic tissue healing may result in the development of BPH nodules and proliferative inflammatory atrophy (PIA). The loss of glutathione S-transferase P1 (GSTP1) may be responsible in patients with genetic predisposition for the transition of PIA into high-grade intraepithelial neoplasia (HGPIN) and PCa. Although there is growing evidence of the association among inflammatory response, BPH, and PCa, we can only surmise on the immunologic mechanisms involved, and further research is required to better understand the role of prostatic inflammation in the initiation of BPH and PCa. There is not yet proof that targeting prostate inflammation with a pharmacologic agent results in a lower incidence and progression or regression of either BPH or PCa. Conclusions: Evidence in the peer-reviewed literature suggested that chronic prostatic inflammation may be involved in the development and progression of chronic prostatic disease, such as BPH and PCa, although there is still no evidence of a causal relation. Inflammation should be considered a new domain in basic and clinical research in patients with BPH and PCa. </description>
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      <title>Optimizing performance and interpretation of prostate biopsy: A critical analysis of the literature (Article)</title>
      <link>http://repub.eur.nl/res/pub/21729/</link>
      <pubDate>2010-12-01T00:00:00Z</pubDate>
      <description>Context: The number and location of biopsy cores and the interpretation of prostate biopsy in different clinical settings remain the subjects of continuing debate. Objective: Our aim was to review the current evidence regarding the performance and interpretation of initial, repeat, and saturation prostatic biopsy. Evidence acquisition: A comprehensive Medline search was performed using the Medical Subject Heading search terms prostate biopsy, prostate cancer, detection, transrectal ultrasound (TRUS), nomogram, and diagnosis. Results were restricted to the English language, with preference given to those published within the last 3 yr. Evidence synthesis: At initial biopsy, a minimum of 10 but not &gt;18 systematic cores are recommended, with 14-18 cores in glands ≥50 cm3. Biopsies should be directed laterally, and transition zone (TZ) cores are not recommended in the initial biopsy setting. Further biopsy sets, either as an extended repeat or as a saturation biopsy (≥20 cores) including the TZ, are warranted in young and fit men with a persistent suspicion of prostate cancer. An immediate repeat biopsy is not indicated for prior high-grade prostatic intraepithelial neoplasia diagnosis given an adequate extended initial biopsy. Conversely, biopsies with atypical glands that are suspicious but not diagnostic of cancer should be repeated within 3-6 mo. Overall recommendations for further biopsy sets (a third set or more) cannot be made. Transrectal ultrasound-guided systematic biopsies represent the standard-of-care method of prostate sampling. However, transperineal biopsies are an up-to-standard alternative. Conclusions: The optimal prostatic biopsy regimen should be based on the individualized clinical setting of the patient and should follow the minimum standard requirements reported in this paper.</description>
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      <title>Variability in diagnostic opinion among pathologists for single small atypical foci in prostate biopsies (Article)</title>
      <link>http://repub.eur.nl/res/pub/27766/</link>
      <pubDate>2010-02-01T00:00:00Z</pubDate>
      <description>Pathologists are increasingly exposed to prostate biopsies with small atypical foci, requiring differentiation between adenocarcinoma, atypical small acinar proliferation suspicious for malignancy, and a benign diagnosis. We studied the level of agreement for such atypical foci among experts in urologic pathology and all-round reference pathologists of the European Randomized Screening study of Prostate Cancer (ERSPC). For this purpose, we retrieved 20 prostate biopsies with small (most &lt;1 mm) atypical foci. Hematoxylin and eosin-stained slides, including 10 immunostained slides were digitalized for virtual microscopy. The lesional area was not marked. Five experts and 7 ERSPC pathologists examined the cases. Multirater κ statistics was applied to determine agreement and significant differences between experts and ERSPC pathologists. The κ value of experts (0.39; confidence interval, 0.29-0.49) was significantly higher than that of ERSPC pathologists (0.21; confidence interval, 0.14-0.27). Full (100%) agreement was reached by the 5 experts for 7 of 20 biopsies. Experts and ERSPC pathologists rendered diagnoses ranging from benign to adenocarcinoma on the same biopsy in 5 and 9 biopsies, respectively. Most of these lesions comprised between 2 and 5 atypical glands. The experts diagnosed adenocarcinoma (49%) more often than the ERSPC pathologists (32%) (P&lt;0.001). As agreement was particularly poor for foci comprising &lt;6 glands, we would encourage pathologists to obtain intercollegial consultation of a specialized pathologist for these lesions before a carcinoma diagnosis, whereas clinicians may consider to perform staging biopsies before engaging on deferred or definite therapy. Copyright </description>
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