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8,942 results for “Prostate”

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ClinicalTrials.gov32/100

The Effects of Testosterone on Prostate Tissue (ACYP-1)

ClinicalTrials.gov study NCT00161486. IPD Sharing: Not stated. Countries: 1. Publications: 11.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov32/100

Saw Palmetto Extract in Benign Prostatic Hyperplasia

ClinicalTrials.gov study NCT00037154. IPD Sharing: Not stated. Countries: 1. Publications: 2.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov32/100

Hypofractionated Radiosurgery for Localised Prostate Cancer

ClinicalTrials.gov study NCT02635256. IPD Sharing: Not stated. Countries: 1. Publications: 2.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov32/100

Brachytherapy in Treating Patients With Prostate Cancer

ClinicalTrials.gov study NCT00003312. IPD Sharing: Not stated. Countries: 2. Publications: 4.

restrictedIPD-UNDECIDEDFeb 2026View details →
dryad32/100

Data from: Peripheral blood mitochondrial DNA copy number is associated with prostate cancer risk and tumor burden

Open the record for dataset details and reuse information.

publicAug 2015View details →
dryad32/100

Data from: Probabilistic interfractional motion carbon ion radiation therapy dose distribution for prostate cancer shows rectum sparing with moderate target coverage degradation

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publicSep 2018View details →
dryad32/100

Prostate-specific deletion of Cdh1 induces murine prostatic inflammation and bladder overactivity

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publicDec 2020View details →
dryad32/100

Harnessing clinical annotations to improve deep learning performance in prostate segmentation

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publicJun 2021View details →
zenodo28/100

Combining genome-wide studies of breast, prostate, ovarian and endometrial cancers maps cross-cancer susceptibility loci and identifies new genetic associations

<p>Data set linked to the paper, &quot;Combining genome-wide studies of breast, prostate, ovarian and endometrial cancers maps cross-cancer susceptibility loci and identifies new genetic associations&quot;.&nbsp; Pre-print of the paper is here: <a href="https://doi.org/10.1101/2020.06.16.146803">https://doi.org/10.1101/2020.06.16.146803</a>.</p> <p>&nbsp;</p> <p>cross_cancer_sum_stats.txt.gz contains summary genome-wide association statistics for susceptibility to single cancers (breast (BR), prostate (PR), ovarian (OV), endometrial (EN), estrogen receptor (ER)-positive breast (POS), ER-negative breast (NEG), and high-grade serous ovarian (HGS) cancers) and from the cross-cancer meta-analysis (main [main] and subtype-focused [sub]). EA in the header refers to the effect allele, OA is the other allele, EAF is the effect allele frequency in the largest of the single cancer data sets (BR), IMPR2 is the imputation quality in the largest of the single cancer data sets (BR), SE is the standard error, PVAL is the P-value, RE2Cs1 is the&nbsp; RE2C statistic mean effect part, RE2Cs2 is the RE2C statistic heterogeneity part, RE2Cp* is the RE2C* P-value.&nbsp; More on RE2Cp* can be found here: <a href="http://software.buhmhan.com/RE2C/index.php?mid=contact&amp;act=dispBoardWrite">http://software.buhmhan.com/RE2C/index.php?mid=contact&amp;act=dispBoardWrite</a> and in&nbsp;&nbsp;&nbsp;&nbsp; <a href="https://academic.oup.com/bioinformatics/article/33/14/i379/3953957">https://academic.oup.com/bioinformatics/article/33/14/i379/3953957</a> SNP names in&nbsp;cross_cancer_sum_stats.txt.gz include the chromosome and build 37 position.</p> <p>&nbsp;</p> <p>main_tetrachoric_corr_matrix.txt and subtype_tetrachoric_corr_matrix.txt provide the tetrachoric correlation matrices used in the main and subtype-focused meta-analyses.&nbsp; These were also used to specify the cryptic.cor argument of the exh.abf function of MetABF.&nbsp; More on MetABF can be found here: <a href="https://github.com/trochet/metabf">https://github.com/trochet/metabf</a> and in <a href="https://onlinelibrary.wiley.com/doi/abs/10.1002/gepi.22202">https://onlinelibrary.wiley.com/doi/abs/10.1002/gepi.22202</a></p> <p>&nbsp;</p> <p>prior_sigmas_for_metabf.txt contains the values used to specify the prior.sigma argument of the exh.abf function in MetABF.</p> <p>&nbsp;</p> <p>The breast cancer data used are described in <a href="https://pubmed.ncbi.nlm.nih.gov/29059683/"><strong>PMID 29059683</strong></a> and can be downloaded from <a href="http://bcac.ccge.medschl.cam.ac.uk/bcacdata/oncoarray/oncoarray-and-combined-summary-result/gwas- summary-results-breast-cancer-risk-2017/">http://bcac.ccge.medschl.cam.ac.uk/bcacdata/oncoarray/oncoarray-and-combined-summary-result/gwas- summary-results-breast-cancer-risk-2017/</a> (this link also includes acknowledgements).&nbsp; The prostate cancer data are described in <a href="https://pubmed.ncbi.nlm.nih.gov/29892016/"><strong>PMID 29892016</strong></a> and can be downloaded from: <a href="http://practical.icr.ac.uk/blog/?page_id=8164">http://practical.icr.ac.uk/blog/?page_id=8164</a> (this link also includes acknowledgements).&nbsp; The ovarian cancer data used are described in <a href="https://pubmed.ncbi.nlm.nih.gov/28346442/"><strong>PMID 28346442</strong></a> and can be downloaded from <a href="https://www.ebi.ac.uk/gwas/studies/GCST004415">https://www.ebi.ac.uk/gwas/studies/GCST004415</a>.&nbsp; The endometrial cancer data are described in <a href="https://pubmed.ncbi.nlm.nih.gov/30093612/"><strong>PMID 30093612</strong></a> and can be downloaded from <a href="https://www.ebi.ac.uk/gwas/studies/GCST006464">https://www.ebi.ac.uk/gwas/studies/GCST006464</a>.&nbsp; These links point to the same data that form the basis of the cross_cancer_sum_stats.txt.gz file.</p> <p>&nbsp;</p> <p><strong>The sample size and precision of the data presented should preclude identification of any individual study participant.&nbsp; However, in downloading these data, you undertake not to attempt to identify individual study participant and not to re-post these data to a third-party website.&nbsp; Please cite the PMIDs highlighted above along with the appropriate acknowledements if you use the cross_cancer_sum_stats.txt.gz file.</strong></p> <p>&nbsp;</p> <p>If you have any questions about this repository, please email Siddhartha Kar at siddhartha dot kar at bristol dot ac dot uk</p>

opencc-by-4.0Jun 2020View details →
dryad28/100

Data from: Identification of intraductal carcinoma of the prostate on tissue specimens using Raman micro-spectroscopy: A diagnostic accuracy case-control study with multicohort validation

<p class="AbstractSummary"><b>Background</b></p> <p class="AbstractSummary">Prostate cancer (PC) is the most frequently diagnosed cancer in North American men. Pathologists are in critical need of accurate biomarkers to characterize PC, particularly to confirm the presence of intraductal carcinoma of the prostate (IDC-P), an aggressive histopathological variant for which therapeutic options are now available. Our aim was to identify IDC-P with Raman micro-spectroscopy and machine learning technology following a protocol suitable for routine clinical histopathology laboratories.</p> <p class="AbstractSummary"><b>Methods and findings</b></p> <p class="AbstractSummary">We used Raman micro-spectroscopy to differentiate IDC-P from PC, as well as PC and IDC-P from benign tissue on formalin-fixed paraffin-embedded first-line radical prostatectomy specimens (embedded in tissue microarrays, TMAs) from 483 patients treated in three Canadian institutions between 1993 and 2013. The main measures were the presence or absence of IDC-P and of PC, regardless of the clinical outcomes. Most of the 483 patients were pT2 stage (44–69%), and pT3a (22–49%) was more frequent than pT3b (9–12%). After approval of the construction of the TMAs by local ethics review board, the diagnostic accuracy study was approved by the Centre hospitalier de l'Université de Montréal (CHUM) ethics review board. Briefly, two consecutive sections of each TMA block were cut. The first section was transferred onto a glass slide to perform immunohistochemistry with H&amp;E counterstaining for cell identification. The second section was placed on an aluminum slide, dewaxed, and then used to acquire an average of 7 Raman spectra per specimen (between 4 and 24 Raman spectra, 4 acquisitions / TMA core). Raman spectra of each cell type were then analyzed to retrieve tissue-specific molecular information and to generate classification models using machine learning technology. <span>Models were trained and cross-validated using data from one institution. Accuracy, sensitivity and specificity were respectively of 87 ± 5%, 86 ± 6% and 89 ± 8% to differentiate PC from benign tissue, and of 95 ± 2%, 96 ± 4% and 94 ± 2% respectively to differentiate IDC-P from PC. The trained models were then tested on data from two independent institutions, reaching accuracies, sensitivities and specificities of 84 and 86%, 84 and 87%, and 81 and 82%, respectively</span><span> to diagnose PC, and of 85 and 91%, 85 and 88%, and 86 and 93% respectively for the identification of IDC-P.</span> IDC-P could further be differentiated from high-grade prostatic intraepithelial neoplasia (HGPIN), a pre-malignant intraductal proliferation which can be mistaken as IDC-P, with accuracies, sensitivities and specificities &gt;95% in both training and testing cohorts. As we used stringent criteria to diagnose IDC-P, the main limitation of our study is the exclusion of borderline, difficult to classify lesions from our datasets.</p> <p class="AbstractSummary"><b>Conclusions</b></p> <p>In this study, we developed classification models for the analysis of Raman micro-spectroscopy data to differentiate IDC-P, PC and benign tissue, including HGPIN. Raman micro-spectroscopy could be a next-generation histopathological technique used to <span>reinforce the identification of high-risk PC patients and lead to more precise diagnosis of IDC-P.</span></p>

opencc-zeroDec 2019View details →
zenodo28/100

Full summary statistics of mixQTL for GTEx v8 Prostate

The mixQTL method is described in paper doi.org/10.1101/2020.04.22.050666. Please cite the original paper if using the data.

opencc-zeroSep 2020View details →
zenodo28/100

Data and code for paper "Reciprocal interactions between tumour cell populations enhance growth and reduce radiation sensitivity in prostate cancer."

<p>This repository contains raw data and code for the manuscript with DOI: 10.1038/s42003-020-01529-5.</p>

opencc-by-4.0Dec 2019View details →
dryad28/100

Isoform specific activities of androgen receptor and its splice variants in prostate cancer cells

<p>Androgen receptor (AR) signaling continues to drive castration resistant prostate cancer (CRPC) in spite of androgen deprivation therapy (ADT). Constitutively active shorter variants of AR, lacking the ligand binding domain, are frequently expressed in CRPC and have emerged as a potential mechanism for prostate cancer to escape ADT.  ARv7 and AR<sup>v567es </sup>are two of the most commonly detected variants of AR in clinical samples of advanced, metastatic prostate cancer. It is not clear if variants of AR merely act as weaker substitutes for AR or can mediate unique isoform specific activities different from AR. In this study, we employed LNCaP prostate cancer cell lines with inducible expression of ARv7 or AR<sup>v567es </sup>to delineate similarities and differences in transcriptomics, metabolomics and lipidomics resulting from the activation of AR, ARv7 or AR<sup>v567es</sup>. While the majority of target genes were similarly regulated by the action of all three isoforms, we found a clear difference in transcriptomic activities of AR versus the variants, and a few differences between ARv7 and AR<sup>v567es</sup>. Some of the target gene regulation by AR isoforms was similar in the VCaP background as well. Differences in downstream activities of AR isoforms were also evident from comparison of the metabolome and lipidome in an LNCaP model. Overall our study implies that shorter variants of AR are capable of mediating unique downstream activities different from AR and some of these are isoform specific.</p>

opencc-zeroJan 2021View details →
dryad28/100

Data from: Predicting classifier performance with limited training data: applications to computer-aided diagnosis in breast and prostate cancer

Clinical trials increasingly employ medical imaging data in conjunction with supervised classifiers, where the latter require large amounts of training data to accurately model the system. Yet, a classifier selected at the start of the trial based on smaller and more accessible datasets may yield inaccurate and unstable classification performance. In this paper, we aim to address two common concerns in classifier selection for clinical trials: (1) predicting expected classifier performance for large datasets based on error rates calculated from smaller datasets and (2) the selection of appropriate classifiers based on expected performance for larger datasets. We present a framework for comparative evaluation of classifiers using only limited amounts of training data by using random repeated sampling (RRS) in conjunction with a cross-validation sampling strategy. Extrapolated error rates are subsequently validated via comparison with leave-one-out cross-validation performed on a larger dataset. The ability to predict error rates as dataset size increases is demonstrated on both synthetic data as well as three different computational imaging tasks: detecting cancerous image regions in prostate histopathology, differentiating high and low grade cancer in breast histopathology, and detecting cancerous metavoxels in prostate magnetic resonance spectroscopy. For each task, the relationships between 3 distinct classifiers (k-nearest neighbor, naive Bayes, Support Vector Machine) are explored. Further quantitative evaluation in terms of interquartile range (IQR) suggests that our approach consistently yields error rates with lower variability (mean IQRs of 0.0070, 0.0127, and 0.0140) than a traditional RRS approach (mean IQRs of 0.0297, 0.0779, and 0.305) that does not employ cross-validation sampling for all three datasets.

opencc-zeroDec 2014View details →
dryad28/100

Data from: Oral contraceptive use is associated with prostate cancer: an ecologic study

INTRODUCTION: Recently there have been several studies suggesting that estrogen exposure may increase the risk of prostate cancer (PCa). In this report we examine associations between PCa incidence and mortality and population-based use of oral contraceptives (OC's). We hypothesized that OC's by-products may cause an environmental contamination leading to an increased low level estrogen exposure and therefore higher PCa incidence and mortality. METHODS: The hypothesis was studied in an ecologic study. We used data from the "international agency for research on cancer" (IACR) to retrieve age-standardized rates of prostate cancer in 2007 and the "United Nations 2007 use of contraceptive report" to retrieve data on contraceptive use. We subsequently used a Pearson correlation and a multivariable linear regression to associate the percentage of women using OC's, intrauterine devices, condoms or vaginal barriers to the age standardized prostate cancer incidence and mortality. We performed these analyses by individual nation and by continent worldwide. RESULTS: OC's use was significantly associated with prostate cancer incidence and mortality in the individual nation world wide (r=0.61 and r=0.53, respectively p&lt;0.05 for all). PCa incidence was also associated with OC's use in Europe (r=0.545 p&lt;0.05) and by continent (r=0.522 p&lt;0.05). All other forms of contraceptives (i.e. intra-uterine devices, condoms or vaginal barriers) were not correlated with prostate cancer incidence or mortality. On multivariable analysis the correlation with OC was independent of nation's wealth. CONCLUSION: In this hypothesis generating ecologic study we have demonstrated a significant association between OC's and PCa. We hypothesize that oral contraceptive effect may be mediated through environmental estrogen levels; this novel concept is worth further investigation.

opencc-zeroDec 2010View details →
zenodo28/100

Prostate Cancer Metastasis Cardiometabolic Diseases Dataset, Meta-Analysis & Systematic Review

Open the record for dataset details and reuse information.

opencc-by-4.0Jun 2024View details →
zenodo28/100

Movies S1: Surgical techniques of the retrotrigonal layer dissection from the posterior approach and bladder neck preservation in a case without prostate enlargement or protrusion. Video S2: Surgical techniques of the retrotrigonal layer dissection from the posterior approach and bladder neck preservation in a case with prostate enlargement.

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opencc-by-4.0Dec 2023View details →
zenodo28/100

Automatic Segmentation of Prostate Cancer using Deep Learning

<p>Demo of Prostate Cancer Segmentation on 3D Magnetic Resonance Imaging using deep learning</p>

openJun 2023View details →
zenodo28/100

Large Language Models and prostate cancer

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opencc-by-4.0May 2024View details →
zenodo28/100

1H-NMR data for prostate cancer and benign prostatic hyperplasia

Open the record for dataset details and reuse information.

opencc-by-4.0Jul 2024View details →

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dandi-nwb
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Last verified 2026-04-30Open record

International Brain Laboratory public data

The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.

ibl
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OpenNeuro

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