Gail P. Risbridger

ORCID: 0000-0003-3089-4028
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About
Contact & Profiles
Research Areas
  • Prostate Cancer Treatment and Research
  • TGF-β signaling in diseases
  • Sperm and Testicular Function
  • Hormonal and reproductive studies
  • Estrogen and related hormone effects
  • Epigenetics and DNA Methylation
  • Prostate Cancer Diagnosis and Treatment
  • Cancer, Lipids, and Metabolism
  • Testicular diseases and treatments
  • Cancer Cells and Metastasis
  • Kruppel-like factors research
  • Sexual Differentiation and Disorders
  • Urinary Bladder and Prostate Research
  • Immunotherapy and Immune Responses
  • Heat shock proteins research
  • Metabolism, Diabetes, and Cancer
  • Phytoestrogen effects and research
  • Urological Disorders and Treatments
  • Ubiquitin and proteasome pathways
  • Reproductive Biology and Fertility
  • Cancer Mechanisms and Therapy
  • Urologic and reproductive health conditions
  • Molecular Biology Techniques and Applications
  • Cancer Research and Treatments
  • Peptidase Inhibition and Analysis

Monash University
2016-2025

The University of Melbourne
2006-2025

Peter MacCallum Cancer Centre
2013-2025

Australian Regenerative Medicine Institute
2005-2024

Discovery Institute
2018-2024

Cabrini Hospital
2022-2024

John Wiley & Sons (United States)
2015-2021

Johns Hopkins University
2019-2021

Johns Hopkins Medicine
2019-2021

Sidney Kimmel Comprehensive Cancer Center
2019-2021

In recent years the Illumina HumanMethylation450 (HM450) BeadChip has provided a user-friendly platform to profile DNA methylation in human samples. However, HM450 lacked coverage of distal regulatory elements. have now released MethylationEPIC (EPIC) BeadChip, with new content specifically designed target these regions. We used and whole-genome bisulphite sequencing (WGBS) perform critical evaluation EPIC array platform. covers over 850,000 CpG sites, including >90 % CpGs from an additional...

10.1186/s13059-016-1066-1 article EN cc-by Genome biology 2016-10-07
Fredrick R. Schumacher Ali Amin Al Olama Sonja I. Berndt Sara Benlloch Mahbubl Ahmed and 95 more Edward J. Saunders Tokhir Dadaev Daniel Leongamornlert Ezequiel Anokian Clara Cieza-Borrella Chee Goh Mark N. Brook Xin Sheng Laura Fachal Joe Dennis Jonathan P. Tyrer Kenneth Muir Artitaya Lophatananon Victoria L. Stevens Susan M. Gapstur Brian D. Carter Catherine M. Tangen Phyllis J. Goodman Ian M. Thompson Jyotsna Batra Suzanne K. Chambers Leire Moya Judith A. Clements Lisa G. Horvath Wayne D. Tilley Gail P. Risbridger Henrik Grönberg Markus Aly Tobias Nordström Paul D.P. Pharoah Nora Pashayan Johanna Schleutker Teuvo L.J. Tammela Csilla Sipeky Anssi Auvinen Demetrius Albanes Stephanie J. Weinstein Alicja Wolk Niclas Håkansson Catharine West Alison M. Dunning N.G. Burnet Lorelei A. Mucci Edward Giovannucci Gerald L. Andriole Olivier Cussenot Géraldine Cancel‐Tassin Stella Koutros Laura E. Beane Freeman Karina D. Sørensen Torben F. Ørntoft Michael Borre Lovise Mæhle Eli Marie Grindedal David E. Neal Jenny Donovan Freddie C. Hamdy Richard M. Martin Ruth C. Travis Timothy J. Key Robert J. Hamilton Neil E. Fleshner Antonio Finelli Sue A. Ingles Mariana C. Stern Barry S. Rosenstein Sarah L. Kerns Harry Ostrer Yong‐Jie Lu Hong-Wei Zhang Ninghan Feng Xueying Mao Xin Guo Guomin Wang Zan Sun Graham G. Giles Melissa C. Southey Robert J. MacInnis Liesel M. FitzGerald Adam S. Kibel Bettina F. Drake Ana Vega Antonio Gómez‐Caamaño Robert Szulkin Martin Eklund Manolis Kogevinas Javier Llorca Gemma Castaño‐Vinyals Kathryn L. Penney Meir J. Stampfer Jong Y. Park Thomas A. Sellers Hui‐Yi Lin Janet L. Stanford Cezary Cybulski

10.1038/s41588-018-0142-8 article EN Nature Genetics 2018-06-08

Prostate cancers (PCs) with loss of the potent tumor suppressors TP53 and RB1 exhibit poor outcomes. also influence cell plasticity are frequently lost in PCs neuroendocrine (NE) differentiation. Therapeutic strategies that address these aggressive variant urgently needed. Using deep genomic profiling 410 metastatic biopsies, we determine relationships between combined PC phenotypes. Notably, 40% TP53/RB1-deficient tumors classified as AR-active adenocarcinomas, indicating NE differentiation...

10.1016/j.celrep.2020.107669 article EN cc-by-nc-nd Cell Reports 2020-05-01

Abstract Germline mutations in the BRCA2 tumour suppressor are associated with both an increased lifetime risk of developing prostate cancer (PCa) and aggressive disease. To understand this aggression, here we profile genomes methylomes localized PCa from 14 carriers deleterious germline ( -mutant PCa). We show that harbour genomic instability a mutational more closely resembles metastastic than shows epigenomic dysregulation MED12L / MED12 axis, which is frequently dysregulated metastatic...

10.1038/ncomms13671 article EN cc-by Nature Communications 2017-01-09
Anqi Wang Jiayi Shen Alex A Rodriguez Edward J. Saunders Fei Chen and 95 more Rohini Janivara Burcu F. Darst Xin Sheng Yili Xu Alisha Chou Sara Benlloch Tokhir Dadaev Mark N. Brook Anna Plym Ali Sahimi Thomas J Hoffman Atushi Takahashi Koichi Matsuda Yukihide Momozawa Masashi Fujita Triin Laisk Jéssica Figuerêdo Kenneth Muir Shuji Ito Xiaoxi Liu Yuji Uchio Michiaki Kubo Yoichiro Kamatani Artitaya Lophatananon Peggy Wan Caroline Andrews Adriana Lori Parichoy Pal Choudhury Johanna Schleutker Teuvo L.J. Tammela Csilla Sipeky Anssi Auvinen Graham G. Giles Melissa C. Southey Robert J. MacInnis Cezary Cybulski Dominika Wokołorczyk Jan Lubiński Christopher T. Rentsch Kelly Cho Benjamin H. McMahon David E. Neal Jenny L. Donovan Freddie C. Hamdy Richard M. Martin Børge G. Nordestgaard Sune F. Nielsen Maren Weischer Stig E. Bojesen Martin Andreas Røder Hein Vincent Stroomberg Jyotsna Batra Suzanne K. Chambers Lisa G. Horvath Judith A. Clements Wayne Tilly Gail P. Risbridger Henrik Grönberg Markus Aly Robert Szulkin Martin Eklund Tobias Nordström Nora Pashayan Alison M. Dunning Maya Ghoussaini Ruth C. Travis Timothy J. Key Elio Ríboli Jong Y. Park Thomas A. Sellers Hui-Yi Lin Demetrius Albanes Stephanie J. Weinstein Michael B. Cook Lorelei A. Mucci Edward Giovannucci Sara Lindstrӧm Peter Kraft David J. Hunter Kathryn L. Penney Constance Turman Catherine M. Tangen Phyllis J. Goodman Ian M. Thompson Robert J. Hamilton Neil E. Fleshner Antonio Finelli Marie‐Élise Parent Janet L. Stanford Elaine A. Ostrander Stella Koutros Laura E. Beane Freeman Meir Stampfer Alicja Wolk Niclas Håkansson

10.1038/s41588-023-01534-4 article EN Nature Genetics 2023-11-09

It was recently demonstrated that antiestrogens prevented prostate cancer (PRCA) in men. The source of estradiol (E2) contributes to carcinogenesis, as well the selected estrogen receptor (ER) signaling pathway, is unknown. To evaluate estrogen's effects we developed a new model PRCA utilizing testosterone and E2 stimulate PRCA. determine whether local situ production affected incidence PRCA, aromatase-knockout (ArKO) mice were evaluated. In contrast wild-type mice, ArKO had reduced...

10.1096/fj.07-9526com article EN The FASEB Journal 2007-11-30

Prostate cancer (PCa) and benign prostatic hyperplasia (BPH) are androgen-dependent diseases commonly treated by inhibiting androgen action. However, ablation or castration fail to target androgen-independent cells implicated in disease etiology recurrence. Mechanistically different castration, this study shows beneficial proapoptotic actions of estrogen receptor–β (ERβ) BPH PCa. ERβ agonist induces apoptosis stromal, luminal castrate-resistant basal epithelial estrogen-deficient aromatase...

10.1073/pnas.0905524107 article EN Proceedings of the National Academy of Sciences 2010-02-01

Tissue-specific aromatase production is significant in breast cancer and osteoporosis. Prostatic expression has been equivocal, any local actions of estrogens are considered secondary to centrally mediated androgen suppression. We examine estrogen biosynthesis the human prostate. Pure samples stroma epithelia from biopsy tissues were isolated by laser capture microdissection. Aromatase protein was detected Western blot analysis, mRNA RT-PCR, enzyme activity tritiated water assay, whereas...

10.1210/jc.2003-030933 article EN The Journal of Clinical Endocrinology & Metabolism 2004-05-01

Abstract Background: Epigenetic alterations are common in prostate cancer, yet how these modifications contribute to carcinogenesis is poorly understood. We investigated whether specific histone prognostic for cancer relapse, and the expression of epigenetic genes altered tumorigenesis. Methods: Global levels H3 lysine-18 acetylation (H3K18Ac) lysine-4 dimethylation (H3K4diMe) were assessed immunohistochemically a cohort 279 cases. gene was silico by analysis microarray data from 23 primary...

10.1158/1055-9965.epi-10-0555 article EN Cancer Epidemiology Biomarkers & Prevention 2010-10-01

The growth and progression of solid tumors involves dynamic cross-talk between cancer epithelium the surrounding microenvironment. To date, molecular profiling has largely been restricted to epithelial component tumors; therefore, features underpinning persistent protumorigenic phenotype tumor microenvironment are unknown. Using whole-genome bisulfite sequencing, we show for first time that cancer-associated fibroblasts (CAFs) from localized prostate display remarkably distinct enduring...

10.1101/gr.229070.117 article EN cc-by-nc Genome Research 2018-04-12

In prostate cancer, cancer-associated fibroblasts (CAF) exhibit contrasting biological properties to non-malignant (NPF) and promote tumorigenesis. Resolving intercellular signaling pathways between CAF tumor epithelium may offer novel opportunities for research translation. To this end, the proteome phosphoproteome of four pairs patient-matched NPF were characterized identify discriminating proteomic signatures. Samples analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS)...

10.1074/mcp.ra119.001496 article EN cc-by Molecular & Cellular Proteomics 2019-05-07

Although androgens are the main steroids controlling growth of mammalian prostate, increasing evidence demonstrates that estrogens also regulate prostate development and growth. This study describes effects estrogen deficiency using aromatase knockout mice (ArKO) with targeted disruption cyp19 gene. Serum tissue testosterone 5α-dihydrotestosterone as well serum PRL levels significantly (P < 0.05) elevated in mature male ArKO mice. Histological, stereological, immunohistochemical studies...

10.1210/endo.142.6.8079 article EN Endocrinology 2001-06-01
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