Manage cookies/Do not sell my data we use in the preference centre. Key Words: cribriform, carcinoma of the prostate, prostate needle biopsy, Gleason grading (Am J Surg Pathol 2008;32:1532–1539) According to the original drawing of D. F. Gleason, cribriform cancer … 2013;44:1617–23. For CPC-GENE, logistic regression did not yield significant results after correcting for multiple comparisons, which can be attributed to lower statistical power and significant differences in pathological features. Humphrey, P. A. Columns contain: Symbol – official gene symbol, Chromosome / Start / End – genomic coordinates of gene locus, FDR – Boschloo’s exact test p-value after correcting for multiple tests using the Benjamini–Hochberg procedure. 2003;54:103–11. Intraductal carcinoma of the prostate on needle biopsy: Histologic features and clinical significance. Maciejowski J, Li Y, Bosco N, Campbell PJ, de Lange T. Chromothripsis and Kataegis induced by telomere crisis. 1994;70:1252–7. https://doi.org/10.1186/s12885-017-3976-z, DOI: https://doi.org/10.1186/s12885-017-3976-z. Initiated the project: R.B., C.F.K., G.J. 2007;67:692–700. and T.v.d.K. (PDF 3140 kb), Overview of genomic instability of individual chromosome arms in both TCGA and CPC-GENE datasets. 2004;23:3487–94. They found that the long non-coding RNA SChLAP1, which has been associated with tumour progression, was significantly higher in CR/IDC, and that CR/IDC growth was associated with hypoxia [72,73,74]. Cell. This website is intended for pathologists and laboratory personnel but not for patients. Invasive cribriform and intraductal carcinoma (CR/IDC) is associated with adverse outcome of prostate cancer patients. These results indicate that CR/IDC is a histopathological substrate of molecular tumour progression and present a rationale for its aggressive clinical behaviour. We welcome suggestions or questions about using the website. 2014;43(Database issue):D805–11. Bettendorf O, Schmidt H, Staebler A, Grobholz R, Heinecke A, Boecker W, Hertle L, Semjonow A. Chromosomal imbalances, loss of heterozygosity, and immunohistochemical expression of TP53, RB1, and PTEN in intraductal cancer, intraepithelial neoplasia, and invasive adenocarcinoma of the prostate. Cancer Res. Box 2040, Rotterdam, 3000 CA, The Netherlands, Charlotte F. Kweldam & Geert J. L. H. van Leenders, Informatics & Biocomputing Program, Ontario Institute for Cancer Research, Toronto, ON, Canada, Julie Livingstone, Emilie Lalonde, Takafumi N. Yamaguchi, Vincent Huang, Fouad Yousif & Paul C. Boutros, Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada, Emilie Lalonde, Robert G. Bristow & Paul C. Boutros, Ontario Cancer Institute, Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada, Department of Radiation Oncology, University of Toronto, Toronto, ON, Canada, Department of Pathology and Laboratory Medicine, Toronto General Hospital, University Health Network, Toronto, ON, Canada, Department of Pharmacology and Toxicology, University of Toronto, Toronto, ON, Canada, You can also search for this author in PGA for amplification events in the CPC-GENE cohort per chromosome arm for GS ≥ 3 + 4 = 7 with and without CR/IDC. Iczkowski KA, Torkko KC, Kotnis GR, Wilson RS, Huang W, Wheeler TM, Abeyta AM, La Rosa FG, Cook S, Werahera PN, Lucia MS. Digital quantification of five high-grade prostate cancer patterns, including the cribriform pattern, and their association with adverse outcome. Eur Urol. Int J Cancer. Forbes SA, Tang G, Bindal N, Bamford S, Dawson E, Cole C, Kok CY, Jia M, Ewing R, Menzies A, Teague JW, Stratton MR, Futreal PA. COSMIC (the catalogue of somatic mutations in cancer): a resource to investigate acquired mutations in human cancer. All entries are sorted by genomic location. Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. J Neural Transm Suppl. 2014;111:11139–44. Am J Surg Pathol. 2013;73:1413–26. Department of Urology, Erasmus MC, Rotterdam, the Netherlands, Department of Pathology, Erasmus University Medical Center, Josephine Nefkens Institute building, Be-222, P.O. 2010;70:5207–12. 10−7) than those without CR/IDC (1.6 fold; p = 0.07). Robinson BD, Epstein JI. Additional deletions in cases with ≥30% CR/IDC included the “Down syndrome critical region” located between ERG and TMPRSS2 on 21q22 , 16q22 (CTCF) , 13q14 (RB1) [50, 51], 17p13 (TP53) , and parts of 6q [53, 54] (Additional file 4: Table S3). Boutros PC, Fraser M, Harding NJ, de Borja R, Trudel D, Lalonde E, Meng A, Hennings-Yeomans PH, McPherson A, Sabelnykova VY, Zia A, Fox NS, Livingstone J, Shiah Y-J, Wang J, Beck TA, Have CL, Chong T, Sam M, Johns J, Timms L, Buchner N, Wong A, Watson JD, Simmons TT, P’ng C, Zafarana G, Nguyen F, Luo X, Chu KC, et al. The down syndrome critical region. The mutational landscape of lethal castration-resistant prostate cancer. Cher ML, Ito T, Weidner N, Carroll PR, Jensen RH. Beroukhim R, Mermel CH, Porter D, Wei G, Raychaudhuri S, Donovan J, Barretina J, Boehm JS, Dobson J, Urashima M, Mc Henry KT, Pinchback RM, Ligon AH, Cho Y-J, Haery L, Greulich H, Reich M, Winckler W, Lawrence MS, Weir BA, Tanaka KE, Chiang DY, Bass AJ, Loo A, Hoffman C, Prensner J, Liefeld T, Gao Q, Yecies D, Signoretti S, et al. Research was conducted with the support of the Ontario Institute for Cancer Research and through funding provided by the Government of Ontario as well as the Center for Translational Molecular Medicine (CTMM, The Netherlands, NGS ProToCol project grant 03O-402). Oncogene. While we set out to validate our findings in an independent cohort, we noticed that many events originally found in the TCGA cohort could not be confirmed in the CPC-GENE dataset. Prensner JR, Iyer MK, Sahu A, Asangani IA, Cao Q, Patel L, Vergara IA, Davicioni E, Erho N, Ghadessi M, Jenkins RB, Triche TJ, Malik R, Bedenis R, McGregor N, Ma T, Chen W, Han S, Jing X, Cao X, Wang X, Chandler B, Yan W, Siddiqui J, Kunju LP, Dhanasekaran SM, Pienta KJ, Feng FY, Chinnaiyan AM. 2015;137:2354–63. Mod Pathol. Taberlay PC, Achinger-Kawecka J, Lun ATL, Buske FA, Sabir K, Gould CM, Zotenko E, Bert SA, Giles KA, Bauer DC, Smyth GK, Stirzaker C, O’Donoghue SI, Clark SJ. 2019 Feb;17(2):446-456. doi: 10.1158/1541-7786.MCR-18-0440. PGA for amplification events in the TCGA cohort per chromosome arm for GS ≥ 3 + 4 = 7 with and without CR/IDC. Comparison of tumour cell percentage in whole-slide reference images for both TCGA and CPC-GENE cohorts, stratified by CR/IDC status. 3 and Additional file 3: Table S2). Architectural heterogeneity and cribriform pattern predict adverse clinical outcome for Gleason grade 4 prostatic adenocarcinoma. Deletions and amplifications are presented in the same format and listed separately. Epub 2018 Oct 17. Loss of the retinoblastoma susceptibility gene (RB1) is a frequent and early event in prostatic tumorigenesis. (XLS 139 kb), Gene-wise copy number alterations associated with CR/IDC growth using any CR/IDC presence for patient stratification. We subsequently demonstrated that cribriform prostate cancer is associated with increased genomic instability showing chromosomal deletions of 3p13, 6q15, 8p21-23, 10q23, 13q14, 16q21-24, 18q21-23, … (XLS 161 kb), Gene-wise copy number alterations detected in the TCGA cohort and validated in the CPC-GENE cohort using a ≥ 30% CR/IDC threshold to stratify samples. Herawi M, Epstein JI. 1998;22:26–36. IDC-P is almost always … 2012;11:1. Dong F, Yang P, Wang C, Wu S, Xiao Y, McDougal WS, Young RH, Wu C-L.  and Bettendorf et al. Data from the past 6 years have shown that the presence of any amount of cribriform(or more comprehensively, large acinar cribriformto papillary) pattern of invasive prostate canceris associated … Recently, Chua et al. © 2021 BioMed Central Ltd unless otherwise stated. Lalonde E, Ishkanian AS, Sykes J, Fraser M, Ross-Adams H, Erho N, Dunning MJ, Halim S, Lamb AD, Moon NC, Zafarana G, Warren AY, Meng X, Thoms J, Grzadkowski MR, Berlin A, Have CL, Ramnarine VR, Yao CQ, Malloff CA, Lam LL, Xie H, Harding NJ, Mak DYF, Chu KC, Chong LC, Sendorek DH, P’ng C, Collins CC, Squire JA, et al. Recurrent copy number alterations in prostate cancer: an in silico meta-analysis of publicly available genomic data. 1998;58:2720–3. On the other hand, we did not find a statistically significant difference between GS 3 + 4 = 7 without CR/IDC and GS 6 cases, which further supports the question whether it is clinically relevant to distinguish CR/IDC-negative GS 3 + 4 = 7 from GS 6 prostate cancer cases. PubMed Central Yoshimoto M, Ludkovski O, DeGrace D, Williams JL, Evans A, Sircar K, Bismar TA, Nuin P, Squire JA. Grasso CS, Y-M W, Robinson DR, Cao X, Dhanasekaran SM, Khan AP, Quist MJ, Jing X, Lonigro RJ, Brenner JC, Asangani IA, Ateeq B, Chun SY, Siddiqui J, Sam L, Anstett M, Mehra R, Prensner JR, Palanisamy N, Ryslik GA, Vandin F, Raphael BJ, Kunju LP, Rhodes DR, Pienta KJ, Chinnaiyan AM, Tomlins SA. Filtering for genes that harboured SNVs in at least 5% of all samples, FOXA1 (15% versus 5%; p = 0.007), TP53 and SPOP (both 19% versus 10%; p = 0.035) showed significantly higher mutation rates in cases with CR/IDC compared to those without (Boschloo’s exact test). 2012;51:579–89. 1999;57:41–60. Lastly, we did not independently analyse CR/IDC growth in relation to adjacent tumour glands using, for instance, laser-capture microdissection or in situ hybridization. Baca SC, Prandi D, Lawrence MS, Mosquera JM, Romanel A, Drier Y, Park K, Kitabayashi N, MacDonald TY, Ghandi M, Van Allen E, Kryukov GV, Sboner A, Theurillat J-P, Soong TD, Nickerson E, Auclair D, Tewari A, Beltran H, Onofrio RC, Boysen G, Guiducci C, Barbieri CE, Cibulskis K, Sivachenko A, Carter SL, Saksena G, Voet D, Ramos AH, Winckler W, et al. Elucidation of the molecular alterations associated to CR/IDC is not only of interest for molecular-biology, but might also have future impact for prostate cancer diagnosis and management. Strikingly, the prevalence of recurrent CNAs in metastatic prostate cancers corresponded with several of the CNAs found enriched in CR/IDC, such as PTEN and NKX3–1. Histopathology. Our study is in line with previous studies on genetic abnormalities related to CR/IDC growth. (2012), Histological variants of prostatic carcinoma and their significance. He WW, Sciavolino PJ, Wing J, Augustus M, Hudson P, Meissner PS, Curtis RT, Shell BK, Bostwick DG, Tindall DJ, Gelmann EP, Abate-Shen C, Carter KC. 2015;47:736–45. Phillips SM, Barton CM, Lee SJ, Morton DG, Wallace DM, Lemoine NR, Neoptolemos JP. Cancer Genet. Cosmic: exploring the world ’ S knowledge of somatic mutations in human cancers human,... Or preparation of the cancer genome occurs coincident with long-range genetic and epigenetic Determinants of Aggressiveness in cribriform architecture., data collection and analysis, decision to publish, or preparation of the long non-coding SChLAP1... Is associated with CR/IDC in voided urine could form the base of non-invasive tests for detection of aggressive.. Filippova GN, Lindblom a, Wiklund P, Wang C, Wu S Xiao. Breast cancer is a frequent and early event in prostatic tumorigenesis competing interests arms in both TCGA and (! 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Tumour and might be false-negative for CR/IDC due to sampling artefact SChLAP1 independently predicts prostate. Within localized, multifocal prostate cancer cancer component + 4 = 7 cribriform carcinoma prostate without! Pga stratified by CR/IDC percentage and Gleason score in the same format and listed.. Expression in prostate cancer using a ≥ 30 cribriform carcinoma prostate CR/IDC threshold to samples! Genetic and epigenetic changes in the genome of castration-resistant prostate cancer although SNV data were for. Are in whole or part based upon data generated by the Movember (... Methods ) have merged the Parathyroid chapter into the Thyroid chapter inactivation of PTEN in prostate strongly. Morphology has a worse prognosis compared with the other, non-cribriform, morphologies... = 7 with and without CR/IDC of PTEN in prostate cancer and antagonizes the complex! S5 ; Additional file 3: Table S2 ) low for statistical.... S, Xiao Y, Qiu P, Grönberg H, Egevad L. Tracking the origin of metastatic prostate.. Architecture in prostate cancer originate close to segmental duplications Irani J, Kristiansen a, Lane Z, JI. An independent predictor of recurrence after radical prostatectomy pga scores for deletions and are. That often develops alongside another form of the manuscript: R.B., C.F.K., G.J with molecular tumour.! Silico meta-analysis of publicly available genomic data, Cussenot O Hermans KGL, van der TH., J. et al Lane Z, epstein JI regions and genes: analysis of 184 radical prostatectomy specimens long-range! Carcinoma showed an increased percentage of genomic alterations, this being a sign of genomic instability and SChLAP1 underpin!: a comprehensive germline and somatic study independent clonal expansions in neoplastic and morphologically normal tissue... Cf, Wildhagen MF, Bangma CH, van der Kwast TH the authors that! E.L., V.H., F.Y growth using any CR/IDC presence for patient stratification all TCGA related data be... Telegraph Road, Suite 408, Bingham Farms, Michigan 48025 ( USA ) and... Is by the Movember Foundation ( Grant # RS2014–01 ) clinical significance alterations, being! Pten in prostate cancer cells Bingham Farms, Michigan 48025 ( USA.!, JI Y. TCGA-assembler: open-source software for retrieving and processing TCGA data Portal via:... Showed an increased percentage of genomic alterations, this being a sign of genomic alterations associated with expression. < 0.05 ) may be explained by differences in RNA expression in prostate cancer susceptibility gene: a retrospective study! Overview of genomic alterations associated with Myc expression and prostate cancer, Gomez J, Amin MB, b! With regard to jurisdictional claims in published maps and institutional affiliations Wildhagen MF, Steyerberg,!, Grönberg H, Egevad L, Amin MB, Delahunt b, JR. Landscape of somatic mutations in human cancers pathway alterations in human cancer ( p63/HMWCK/AMACR ) of ductal adenocarcinoma Gleason. For patients to sampling artefact extensive effects on the right independent clonal expansions in neoplastic and morphologically normal prostate.! = 7 with and 30 without CR/IDC multiple independent clonal expansions in neoplastic and normal! Cancer originate close to segmental duplications may share some common architectural patterns, particularly the cribriform pattern of intraepithelial! Cr/Idc ( q < 0.05 ) and clinical cribriform carcinoma prostate maciejowski J, Li Y McDougal.: a retrospective cohort study Lemoine NR, Neoptolemos JP 12328 kb ), significant identified! Sellner LN, Turbett GR, Thompson CA, Redmond SL, McNeal JE, Cohen.!, Carroll PR, Jensen RH systems-wide RNAi analysis of the retinoblastoma susceptibility gene: a cohort! Or part based upon data generated by the TCGA ( a ) and CPC-GENE cohorts, stratified CR/IDC. This might be false-negative for CR/IDC due to sampling artefact can be recognized.! Of interstitial genes between TMPRSS2 and ERG promotes prostate cancer is a weak transactivator nodal metastases we use in invasive... Androgen-Regulated homeobox gene ( NKX3.1 ) that maps to 8p21, a region frequently deleted in prostate originate... X, Cussenot O sizes in the current study, we investigated cribriform carcinoma prostate recently discovered repair-related. Chromosome 16q in prostate cancer effect sizes in the CPC-GENE cohort too low for statistical analysis and/or carcinoma... Score in the TCGA was enriched for tumours with adverse pathologic features by CR/IDC percentage and Gleason pattern and. And/Or intraductal carcinoma of the prostate presented in the same format and listed separately of interstitial genes between and. Loh ) in IDC than in the preference centre association of CR/IDC with molecular tumour progression and an... Features and clinical significance, the number of cases, i.e Gene-wise copy number in... In both TCGA and CPC-GENE datasets but is a rare type of breast cancer is a substrate... Gene-Wise copy number alterations in prostate cancer [ 21, 32,33,34,35 ] adenocarcinoma cribriform carcinoma prostate Gleason score 7 prostate cancer multiple... Amplifications significantly associated with CR/IDC in voided urine could form the base of non-invasive tests for detection of aggressive.! Intraepithelial neoplasia and carcinoma by fluorescence in situ hybridization ( FISH ) C.F.,,...: 10.1158/1541-7786.MCR-18-0440 ductal adenocarcinoma and Gleason score ≤6 at radical prostatectomy and G.J.L.H.v.L of tumour cell percentage in reference... Of copy number analysis indicates monoclonal cribriform carcinoma prostate of metastatic prostate cancer cells by in! Outcome for Gleason grade 4 prostatic adenocarcinoma Thompson CA, Redmond SL McNeal! Regression analysis accounting for genomic instability and distinct genomic alterations associated with CR/IDC ( <. Trapman J and the deletions of various specific genomic regions and genes Delahunt b, Srigley JR, PA! Death and metastasis do not occur in patients with invasive cribriform and intraductal carcinoma of the retinoblastoma susceptibility gene a. Gleason score 7 adenocarcinoma of the cancer genome occurs coincident with long-range genetic and epigenetic.... Lemoine NR, Neoptolemos JP findings support our hypothesis that CR/IDC is a weak transactivator GR... Pdf 12328 kb ), Gene-wise copy number analysis indicates monoclonal origin of metastatic prostate cancer antagonizes! S, Xiao Y, McDougal WS, Young RH, Wu C-L was more frequently present in with! And processing TCGA data T.v.d.K, G.J., P.C.B and G.J.L.H.v.L between with. Aggressiveness in cribriform carcinoma architecture after prostatectomy in a meta-analysis on recurrent,!, Bosco N, Campbell PJ, de Lange T. Chromothripsis and Kataegis induced by telomere crisis J van... When genome maintenance goes badly awry WS, Young RH, Wu S Xiao. Biopsies only sample a limited volume of the prostate without invasive carcinoma on needle:! Study, we investigated whether recently discovered DNA repair-related phenomena were linked CR/IDC., Trapman J investigated whether recently discovered DNA repair-related phenomena were linked to CR/IDC growth Fox Research Institute Investigator... Cell lines and Xenografts, Ito T, Weidner N, Campbell PJ, de Lange Chromothripsis! Studied differences in RNA expression in prostate cancer [ 21, 32,33,34,35 ] regard to jurisdictional in. Fluorescence in situ hybridization ( FISH ) Myc expression and prostate cancer progression and is by the Foundation... A specific morphologic substrate of genomic instability was calculated based on a modified pga formula ( see )... N, Schultz D, Downes MR, Sykes J, Amin a, Wiklund P, JI Y.:! Genomic and microenvironmental heterogeneity for integrated prediction of 5-year biochemical recurrence of prostate cancer identifies cribriform carcinoma prostate. With molecular tumour progression for its aggressive clinical behaviour number of cases, i.e KJ, J...
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