<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>10(3)</volume><submitter>Van Hemelrijck M</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Signs of disease progression (28%) and conversion to active treatment without evidence of disease progression (13%) are the main reasons for discontinuation of active surveillance (AS) in men with localised prostate cancer (PCa). We aimed to develop a nomogram to predict disease progression in these patients.&lt;h4>Methods&lt;/h4>As a first step in the development of a nomogram, using data from Movembers' GAP3 Consortium (n=14,380), we assessed heterogeneity between centres in terms of risk of disease progression. We started with assessment of baseline hazards for disease progression based on grouping of centres according to follow-up protocols [high: yearly; intermediate: ~2 yearly; and low: at year 1, 4 &amp; 7 (i.e., PRIAS)]. We conducted cause-specific random effect Cox propor</pubmed_abstract><journal>Translational andrology and urology</journal><pagination>1102-1109</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8039580</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>A first step towards a global nomogram to predict disease progression for men on active surveillance.</pubmed_title><pmcid>PMC8039580</pmcid><pubmed_authors>de Jonge C</pubmed_authors><pubmed_authors>Tolosa E</pubmed_authors><pubmed_authors>Auvinen A</pubmed_authors><pubmed_authors>Patil D</pubmed_authors><pubmed_authors>Guo W</pubmed_authors><pubmed_authors>Olivier J</pubmed_authors><pubmed_authors>Gnanapragasam V</pubmed_authors><pubmed_authors>Buzza M</pubmed_authors><pubmed_authors>Xinge J</pubmed_authors><pubmed_authors>Carter B</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Lophatananon A</pubmed_authors><pubmed_authors>Benfante N</pubmed_authors><pubmed_authors>Helleman J</pubmed_authors><pubmed_authors>Lehmann K</pubmed_authors><pubmed_authors>Hirama H</pubmed_authors><pubmed_authors>Mamedov A</pubmed_authors><pubmed_authors>Sugimoto M</pubmed_authors><pubmed_authors>Hugosson J</pubmed_authors><pubmed_authors>Rancati T</pubmed_authors><pubmed_authors>Kouspou M</pubmed_authors><pubmed_authors>van der Linden W</pubmed_authors><pubmed_authors>Logothetis C</pubmed_authors><pubmed_authors>Chung BH</pubmed_authors><pubmed_authors>Kattan M</pubmed_authors><pubmed_authors>Dasgupta P</pubmed_authors><pubmed_authors>Movember Foundation’s Global Action Plan Prostate Cancer Active Surveillance (GAP3) Consortium</pubmed_authors><pubmed_authors>Fahey M</pubmed_authors><pubmed_authors>Crump T</pubmed_authors><pubmed_authors>Lofgren A</pubmed_authors><pubmed_authors>Hefermehl L</pubmed_authors><pubmed_authors>van der Kwast T</pubmed_authors><pubmed_authors>Filson C</pubmed_authors><pubmed_authors>van Bochove K</pubmed_authors><pubmed_authors>Carroll P</pubmed_authors><pubmed_authors>Roobol MJ</pubmed_authors><pubmed_authors>Bjartell A</pubmed_authors><pubmed_authors>Stavrinides V</pubmed_authors><pubmed_authors>Kakehi Y</pubmed_authors><pubmed_authors>Trock B</pubmed_authors><pubmed_authors>Obbink H</pubmed_authors><pubmed_authors>Kim J</pubmed_authors><pubmed_authors>Hulsen T</pubmed_authors><pubmed_authors>Kimberly-Duffell J</pubmed_authors><pubmed_authors>Roobol M</pubmed_authors><pubmed_authors>Klotz L</pubmed_authors><pubmed_authors>Bangma C</pubmed_authors><pubmed_authors>Pickles T</pubmed_authors><pubmed_authors>Van Hemelrijck M</pubmed_authors><pubmed_authors>Rannikko A</pubmed_authors><pubmed_authors>Lee LS</pubmed_authors><pubmed_authors>Hyndman E</pubmed_authors><pubmed_authors>Rubio-Briones J</pubmed_authors><pubmed_authors>Steyerberg E</pubmed_authors><pubmed_authors>Nieboer D</pubmed_authors><pubmed_authors>Ehdaie B</pubmed_authors><pubmed_authors>Muir K</pubmed_authors><pubmed_authors>Villers A</pubmed_authors><pubmed_authors>LaPointe V</pubmed_authors><pubmed_authors>Lin CH</pubmed_authors><pubmed_authors>Haider M</pubmed_authors><pubmed_authors>Cowan J</pubmed_authors><pubmed_authors>Frydenberg M</pubmed_authors><pubmed_authors>Kattan MW</pubmed_authors><pubmed_authors>Perry A</pubmed_authors><pubmed_authors>Gledhill S</pubmed_authors><pubmed_authors>Bruinsma S</pubmed_authors><pubmed_authors>Lee KS</pubmed_authors><pubmed_authors>Shiong LL</pubmed_authors><pubmed_authors>Jenster G</pubmed_authors><pubmed_authors>Ji X</pubmed_authors><pubmed_authors>Ahlgren H</pubmed_authors><pubmed_authors>Mascaros J</pubmed_authors><pubmed_authors>Morgan T</pubmed_authors><pubmed_authors>Moore C</pubmed_authors><pubmed_authors>Santaolalla A</pubmed_authors><pubmed_authors>Valdagni R</pubmed_authors><pubmed_authors>Kim TK</pubmed_authors></additional><is_claimable>false</is_claimable><name>A first step towards a global nomogram to predict disease progression for men on active surveillance.</name><description>&lt;h4>Background&lt;/h4>Signs of disease progression (28%) and conversion to active treatment without evidence of disease progression (13%) are the main reasons for discontinuation of active surveillance (AS) in men with localised prostate cancer (PCa). We aimed to develop a nomogram to predict disease progression in these patients.&lt;h4>Methods&lt;/h4>As a first step in the development of a nomogram, using data from Movembers' GAP3 Consortium (n=14,380), we assessed heterogeneity between centres in terms of risk of disease progression. We started with assessment of baseline hazards for disease progression based on grouping of centres according to follow-up protocols [high: yearly; intermediate: ~2 yearly; and low: at year 1, 4 &amp; 7 (i.e., PRIAS)]. We conducted cause-specific random effect Cox propor</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Mar</publication><modification>2025-04-27T00:07:25.947Z</modification><creation>2025-04-06T17:48:29.327Z</creation></dates><accession>S-EPMC8039580</accession><cross_references><pubmed>33850745</pubmed><doi>10.21037/tau-20-1082</doi></cross_references></HashMap>