Roxanne Toivanen

ORCID: 0000-0002-5765-9346
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About
Contact & Profiles
Research Areas
  • Prostate Cancer Treatment and Research
  • Cancer Cells and Metastasis
  • Cancer, Lipids, and Metabolism
  • Prostate Cancer Diagnosis and Treatment
  • Estrogen and related hormone effects
  • Hippo pathway signaling and YAP/TAZ
  • Radiopharmaceutical Chemistry and Applications
  • Immunotherapy and Immune Responses
  • Xenotransplantation and immune response
  • Cancer Genomics and Diagnostics
  • Cancer-related Molecular Pathways
  • Protein Degradation and Inhibitors
  • Cancer Research and Treatments
  • FOXO transcription factor regulation
  • Ubiquitin and proteasome pathways
  • Inflammatory mediators and NSAID effects
  • Lung Cancer Research Studies
  • Hormonal and reproductive studies
  • Urologic and reproductive health conditions
  • Cancer-related molecular mechanisms research
  • Proteoglycans and glycosaminoglycans research
  • Cancer, Stress, Anesthesia, and Immune Response
  • BRCA gene mutations in cancer
  • Cancer Immunotherapy and Biomarkers
  • Urological Disorders and Treatments

Peter MacCallum Cancer Centre
2018-2024

Monash University
2010-2022

The University of Melbourne
2018-2021

Columbia University Irving Medical Center
2016-2018

Columbia University
2014-2017

Cancer Genetics (United States)
2017

Prostate Cancer Research
2012

Current treatments for castration-resistant prostate cancer (CRPC) that target androgen receptor (AR) signaling improve patient survival, yet ultimately fail. Here, we provide novel insights into treatment response the antiandrogen abiraterone by analyses of a genetically engineered mouse (GEM) model with combined inactivation

10.1158/2159-8290.cd-16-1174 article EN Cancer Discovery 2017-04-15

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

The identification of cell types origin for cancer has important implications tumor stratification and personalized treatment. For prostate cancer, the been intensively studied, but it remained unclear whether basal or luminal epithelial cells, both, represent cells under physiological conditions in vivo. Here, we use a novel lineage-tracing strategy to assess diverse range mouse models, including Nkx3.1+/−; Pten+/−, Hi-Myc, TRAMP mice, as well hormonal carcinogenesis model. Our results show...

10.1016/j.celrep.2014.08.002 article EN cc-by-nc-nd Cell Reports 2014-08-28

Normal prostatic epithelium is composed of basal and luminal cells. Prostate cancer can be initiated in both benign stem cells, but because cell markers are not expressed patient tumors, the former result was unexpected. Since cells origin prostate important therapeutic targets, we sought to provide further proof that have tumorigenic potential. Prostatic were enriched based on α2β1integrin(hi) expression for using CD133 nontumorigenic BPH-1 Human embryonic (hESCs) also used as a source...

10.1002/stem.1094 article EN Stem Cells 2012-04-03

// Damien A. Leach 1 , Eleanor F. Need Roxanne Toivanen 2 Andrew P. Trotta Helen M. Palenthorpe David J. Tamblyn 3 Tina Kopsaftis Georgina England 4 Eric Smith Paul Drew 1,5 Carole B. Pinnock Peng Lee 6 Jeff Holst 7,8 Gail Risbridger Samarth Chopra 3,9 Donald DeFranco 10 Renea Taylor 2,11 and Grant Buchanan The Basil Hetzel Institute for Translational Health Research, University of Adelaide, SA, Australia Department Anatomy Development, Monash University, VIC, Urology Unit, Repatriation...

10.18632/oncotarget.3873 article EN Oncotarget 2015-04-19

Contact with the extracellular matrix is essential for maintenance of epithelial cells in many tissues, while its absence can detach and undergo anoikis. Here, we show that anoikis luminal prostate epithelium followed by a program tissue repair mediated part differentiation basal to cells. We describe mouse model which inducible deletion E-cadherin results their apoptotic cell death anoikis, phenotypic effects surrounding stroma. Quantitative assessments proliferation compartments indicate...

10.1016/j.stemcr.2016.03.007 article EN cc-by-nc-nd Stem Cell Reports 2016-05-01

Abstract Preclinical testing is a crucial step in evaluating cancer therapeutics. We aimed to establish significant resource of patient-derived xenografts (PDXs) prostate for rapid and systematic evaluation candidate therapies. The PDX collection comprises 59 tumors collected from 30 patients between 2012–2020, coinciding with availability abiraterone enzalutamide. PDXs represent the clinico-pathological genomic spectrum cancer, treatment-naïve primary castration-resistant metastases. Inter-...

10.1038/s41467-021-25175-5 article EN cc-by Nature Communications 2021-08-19

This study uses a preclinical xenograft model to reveal prostate cancer cells that exist in untreated localized disease, survive androgen withdrawal, and are potential therapeutic targets.

10.1126/scitranslmed.3005688 article EN Science Translational Medicine 2013-05-29

Cancer cells are heterogeneous in both their phenotypes and ability to promote tumor growth spread. Xenografting is used identify the most highly capable of regenerating tumors, referred as cancer repopulating cells. Because prostate cancers (PCa's) rarely grow xenografts, indentifying PCa has not been possible. Here, we report improved methods xenograft localized primary tissues using chimeric grafts with neonatal mouse mesenchyme. Xenograft survival tissue was significantly increased by...

10.1002/stem.668 article EN Stem Cells 2011-06-14

Background Men with neuroendocrine prostate cancer (NEPC) have a poor prognosis. NEPC is commonly diagnosed by immunohistochemical markers (CHGA, SYP and NCAM1) genomic features (mutations in RB1, PTEN, TP53). But pathology, tumours are variable, leading to classification of NE subtypes such as small cell large carcinomas, focal differentiation (Focal NED), Amphicrine. We postulated the diversity observed pathologies might arise from differences transcriptional profiles aim this study...

10.1101/2024.03.17.585125 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-03-19
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