Dr Ryan Duchatel
Chadtough Defeat DIPG Fellow
School of Biomedical Sciences and Pharmacy (Medical Biochemistry)
- Email:ryan.duchatel@newcastle.edu.au
- Phone:(02) 49854489
Targeting the path of most resistance
Dr Ryan Duchatel, a Postdoctoral Fellow with the University’s School of Biomedical Sciences and Pharmacy, is on a mission to identify combination therapies that inhibit a rare but deadly form of childhood brain cancer.
In the second half of 2017, Dr Ryan Duchatel was finishing up his PhD in experimental pharmacology with a focus on schizophrenia. Looking around for a new challenge, Ryan took a position beside established researcher Dr Matt Dun and turned his focus to fighting leukemia.
Soon after, the focus of Ryan’s new team turned to diffuse intrinsic pontine glioma (DIPG). A childhood cancer with a median diagnosis age of 6-7, DIPG has a 1% survival rate at two years from discovery, and is uniformly fatal. It manifests as a tumour of the brain stem, ultimately destroying messaging that controls movement, hearing, speech and finally, breathing.
Discovering that current treatment in the form of radiation therapy only offers transient, short acting benefits, Ryan set about developing new targets for chemotherapy based on identifying proteins that control how DIPG cells grow and survive.
Roadblocks to survival pathways
Moving away from the scattergun approach of radiation therapy, Ryan is using proteomics to look for DIPG specific gene mutations and protein pathways to target with novel drug treatments.
“We’ve spent probably 18 months non-stop, doing long hours of research seven days a week, trying to come up with different treatment paradigms”, Ryan explains.
Recent large scale sequencing studies on DIPG donor tumours have identified a genetic mutation called H3K27M, which drives disease initiation. This detection has provided vital clues as to which co-occurring protein pathways may be vulnerable to inhibition. Ryan is working on inhibiting one specific growth and survival protein pathway called Phosphoinositide 3-kinase (PI3K), which is over expressed in more than 80% of DIPG patients.
Perpetually aggressive, DIPG cells eventually adapt to the inhibitors, changing the proteins they use to grow, and bypassing pathways initially blocked by targeted drug therapies.
“Cells are able to make themselves resistant. But we are trying to identify those main drug protein pathways that cells can use and inhibiting all of their different options – essentially putting in roadblocks to their growth. Hopefully that'll one day lead to killing the tumours”.
“We've been able to identify new drug combinations, to synergistically target together. So instead of two plus two equals four, two plus two equals eight. And you can only really do that by utilising this type of protein analysis.”
From the lab to the clinic
Using donor tissue and animal models, Ryan examines the impact of combination therapies not just on the targeted cells, but the entire system.
“There are lots of different drugs that you can use to kill DIPG cells in a Petri dish. But that doesn't necessarily mean that they'll work in a patient. So, animal models work as our pseudo patients.”
To ensure the efficacy of possible treatments, Ryan also cultures cells to directly test the ability of combination therapies to cross the blood brain barrier, a physical barrier in the brain which prevents toxins, but also helpful chemotherapies, from crossing into the brain.
This work on new combinations of therapies is already being translated into clinical practice.
“The data we've got has helped put a PI3K inhibitor called paxalisib into clinical trials for DIPG in the United States. It was first developed for the use in an aggressive adult brain cancer called glioblastoma, but now those trials have seen paxalisib gain a rare disease designation by the FDA to treat patients with DIPG.”
Collaboration and supports
Ryan has been instrumental in assisting Dr Matt Dun in the development of The Cancer Research Signalling Group at HMRI. Initially reliant on donations and support from global experts and local community such as local charity RUN DIPG (www.rundipg.org), and although still in its infancy, the DIPG program is already informing global therapies, sharing lab materials and data with the best fellow DIPG researchers in the world.
A close bond with the brain cancer community and awareness of the demographic he is working to save, means Ryan is more motivated than ever to pinpoint effective therapies.
Ryan credits Stanford University researcher Associate Professor Michelle Monje, who runs one of the largest DIPG research labs in the world, with facilitating their initial lab work through the donation of tissue samples and cell lines.
“Working on DIPG is an amazing collaborative experience,” Ryan explains.
“We get emails all hours of the night from different people all around the world. We share data and samples and compare results.”
“It's good to know via feedback from the international DIPG research community, that the research we're doing is on the right track to make a real difference.”
Targeting the path of most resistance
Dr Ryan Duchatel, a Postdoctoral Fellow with the University’s School of Biomedical Sciences and Pharmacy, is on a mission to identify combination therapies that inhibit a rare but deadly form of childhood brain cancer.
Career Summary
Biography
Dr Ryan John Duchatel is an Early Career Researcher, achieving his PhD in Experimental Pharmacology in November 2018. This work examined the neurobiology, and immune and genetic fingerprints underpinning schizophrenia contributing to the understanding of the development of schizophrenia, through alterations in neurodevelopment during pregnancy.
Dr Duchatel has since transitioned to the Cancer Signalling Research Group (CSRG) of Dr Matthew Dun as a Post-Doctoral Fellow, based at University of Newcastle, Hunter Medical Research Institute. A specialist in DIPG neurosphere in vitro modelling, Dr Duchatel belongs to a team of staff and students investigating the molecular mechanisms underpinning a rare and deadly form of paediatric brain cancer - 'Diffuse Intrinsic Pontine Glioma' or 'DIPG'. The group combines cellular and molecular biology techniques, in vitro and in vivo modelling utilising patient samples, together with high-resolution, quantitative proteomics. He leads the patient derived xenograft, in vivo DIPG modelling of the CSRG, necessary for translation of the group's pre-clinical findings to the clinical trial setting.
Dr Duchatel's current research project, in conjunction with field-leading DIPG research collaborators (Nazarian, Mueller - DIPG Research Centre of Excellence, Switzerland) investigates new and improved treatment strategies to overcome the limitations of current investigative therapies for children with DIPG. Primarily focused on inhibitors of cell growth pathways controlled by 'PI3K' (Phosphoinositide 3-kinase), this has led to the first, high-resolution, quantitative proteomic analysis of DIPG, and identified the compensatory signalling pathways activated in response to PI3K inhibition, which are now under investigation for clinical utility.
Dr Duchatel engages with both the scientific and lay communities to further the reach and relevance of his research. As the Deputy Chair of the Hunter Cancer Research Alliance’s (HCRA), Future Leaders Group, and member of the 2020 HCRA symposium committee and community engagement committee, his position affords him the opportunity to raise awareness and profile of cancer research. He serves on the scientific advisory committee of the Hunter Cancer Biobank, Australia.
Qualifications
- Doctor of Philosophy, University of Newcastle
- Bachelor of Biomedical Sciences, University of Newcastle
- Bachelor of Biomedical Sciences (Hons), University of Newcastle
Keywords
- Acute Myeloid Leukaemia
- Brain Cancer
- Cancer Biology
- Diffuse Intrinsic Pontine Glioma
- Molecular Oncology
- Neurobiology
- Neuroscience
- Schizophrenia
Languages
- English (Mother)
Fields of Research
Code | Description | Percentage |
---|---|---|
320905 | Neurology and neuromuscular diseases | 40 |
321101 | Cancer cell biology | 60 |
Professional Experience
UON Appointment
Title | Organisation / Department |
---|---|
Chadtough Defeat DIPG Fellow | University of Newcastle School of Biomedical Sciences and Pharmacy Australia |
Publications
For publications that are currently unpublished or in-press, details are shown in italics.
Highlighted Publications
Year | Citation | Altmetrics | Link | |||||
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2024 |
Duchatel RJ, Jackson ER, Parackal SG, Kiltschewskij D, Findlay IJ, Mannan A, et al., 'PI3K/mTOR is a therapeutically targetable genetic dependency in diffuse intrinsic pontine glioma.', J Clin Invest, (2024) [C1]
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Journal article (23 outputs)
Year | Citation | Altmetrics | Link | ||||||||
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2024 |
Duchatel RJ, Jackson ER, Parackal SG, Kiltschewskij D, Findlay IJ, Mannan A, et al., 'PI3K/mTOR is a therapeutically targetable genetic dependency in diffuse intrinsic pontine glioma.', J Clin Invest, (2024) [C1]
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2024 |
Koschmann C, Al-Holou WN, Alonso MM, Anastas J, Bandopadhayay P, Barron T, et al., 'A road map for the treatment of pediatric diffuse midline glioma.', Cancer Cell, 42 1-5 (2024) [C1]
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2023 |
Jackson ER, Persson ML, Fish CJ, Findlay IJ, Mueller S, Nazarian J, et al., 'A review of the anti-tumor potential of current therapeutics targeting the mitochondrial protease ClpP in H3K27-altered, diffuse midline glioma.', Neuro Oncol, (2023) [C1]
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2023 |
Jackson ER, Duchatel RJ, Staudt DE, Persson ML, Mannan A, Yadavilli S, et al., 'ONC201 in combination with paxalisib for the treatment of H3K27-altered diffuse midline glioma.', Cancer research, CAN-23-0186 (2023) [C1]
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2023 |
Germon ZP, Sillar JR, Mannan A, Duchatel RJ, Staudt D, Murray HC, et al., 'Blockade of ROS production inhibits oncogenic signaling in acute myeloid leukemia and amplifies response to precision therapies.', Sci Signal, 16 eabp9586 (2023) [C1]
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2022 |
Findlay IJ, De Iuliis GN, Duchatel RJ, Jackson ER, Vitanza NA, Cain JE, et al., 'Pharmaco-proteogenomic profiling of pediatric diffuse midline glioma to inform future treatment strategies', Oncogene, 41 461-475 (2022) [C1] Diffuse midline glioma (DMG) is a deadly pediatric and adolescent central nervous system (CNS) tumor localized along the midline structures of the brain atop the spinal cord. With... [more] Diffuse midline glioma (DMG) is a deadly pediatric and adolescent central nervous system (CNS) tumor localized along the midline structures of the brain atop the spinal cord. With a median overall survival (OS) of just 9¿11-months, DMG is characterized by global hypomethylation of histone H3 at lysine 27 (H3K27me3), driven by recurring somatic mutations in H3 genes including, HIST1H3B/C (H3.1K27M) or H3F3A (H3.3K27M), or through overexpression of EZHIP in patients harboring wildtype H3. The recent World Health Organization¿s 5th Classification of CNS Tumors now designates DMG as, ¿H3 K27-altered¿, suggesting that global H3K27me3 hypomethylation is a ubiquitous feature of DMG and drives devastating transcriptional programs for which there are no treatments. H3-alterations co-segregate with various other somatic driver mutations, highlighting the high-level of intertumoral heterogeneity of DMG. Furthermore, DMG is also characterized by very high-level intratumoral diversity with tumors harboring multiple subclones within each primary tumor. Each subclone contains their own combinations of driver and passenger lesions that continually evolve, making precision-based medicine challenging to successful execute. Whilst the intertumoral heterogeneity of DMG has been extensively investigated, this is yet to translate to an increase in patient survival. Conversely, our understanding of the non-genomic factors that drive the rapid growth and fatal nature of DMG, including endogenous and exogenous microenvironmental influences, neurological cues, and the posttranscriptional and posttranslational architecture of DMG remains enigmatic or at best, immature. However, these factors are likely to play a significant role in the complex biological sequelae that drives the disease. Here we summarize the heterogeneity of DMG and emphasize how analysis of the posttranslational architecture may improve treatment paradigms. We describe factors that contribute to treatment response and disease progression, as well as highlight the potential for pharmaco-proteogenomics (i.e., the integration of genomics, proteomics and pharmacology) in the management of this uniformly fatal cancer.
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2022 |
Staudt DE, Murray HC, Skerrett-Byrne DA, Smith ND, Jamaluddin MFB, Kahl RGS, et al., 'Phospho-heavy-labeled-spiketide FAIMS stepped-CV DDA (pHASED) provides real-time phosphoproteomics data to aid in cancer drug selection', CLINICAL PROTEOMICS, 19 (2022) [C1]
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2022 |
McLachlan T, Matthews WC, Jackson ER, Staudt DE, Douglas AM, Findlay IJ, et al., 'B-cell Lymphoma 6 (BCL6): From Master Regulator of Humoral Immunity to Oncogenic Driver in Pediatric Cancers', Molecular cancer research : MCR, 20 1711-1723 (2022) [C1] B-cell lymphoma 6 (BCL6) is a protooncogene in adult and pediatric cancers, first identified in diffuse large B-cell lymphoma (DLBCL) where it acts as a repressor of the tumor sup... [more] B-cell lymphoma 6 (BCL6) is a protooncogene in adult and pediatric cancers, first identified in diffuse large B-cell lymphoma (DLBCL) where it acts as a repressor of the tumor suppressor TP53, conferring survival, protection, and maintenance of lymphoma cells. BCL6 expression in normal B cells is fundamental in the regulation of humoral immunity, via initiation and maintenance of the germinal centers (GC). Its role in B cells during the production of high affinity immunoglobins (that recognize and bind specific antigens) is believed to underpin its function as an oncogene. BCL6 is known to drive the self-renewal capacity of leukemia-initiating cells (LIC), with high BCL6 expression in acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), and glioblastoma (GBM) associated with disease progression and treatment resistance. The mechanisms underpinning BCL6-driven therapy resistance are yet to be uncovered; however, high activity is considered to confer poor prognosis in the clinical setting. BCL6's key binding partner, BCL6 corepressor (BCOR), is frequently mutated in pediatric cancers and appears to act in concert with BCL6. Using publicly available data, here we show that BCL6 is ubiquitously overexpressed in pediatric brain tumors, inversely to BCOR, highlighting the potential for targeting BCL6 in these often lethal and untreatable cancers. In this review, we summarize what is known of BCL6 (role, effect, mechanisms) in pediatric cancers, highlighting the two sides of BCL6 function, humoral immunity, and tumorigenesis, as well as to review BCL6 inhibitors and highlight areas of opportunity to improve the outcomes of patients with pediatric cancer.
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2021 |
Duchatel RJ, Mannan A, Woldu AS, Hawtrey T, Hindley PA, Douglas AM, et al., 'Preclinical and clinical evaluation of German-sourced ONC201 for the treatment of H3K27M-mutant diffuse intrinsic pontine glioma.', Neuro-oncology advances, 3 vdab169 (2021) [C1]
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2020 |
Afrin F, Chi M, Eamens AL, Duchatel RJ, Douglas AM, Schneider J, et al., 'Can hemp help? Low-THC cannabis and non-THC cannabinoids for the treatment of cancer', Cancers, 12 (2020) [C1]
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2020 |
Dun MD, Mannan A, Rigby CJ, Butler S, Toop HD, Beck D, et al., 'Shwachman Bodian Diamond syndrome (SBDS) protein is a direct inhibitor of protein phosphatase 2A (PP2A) activity and overexpressed in acute myeloid leukaemia', Leukemia, 34 3393-3397 (2020) [C1]
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2019 |
Duchatel RJ, Harms LR, Meehan CL, Michie PT, Bigland MJ, Smith DW, et al., 'Reduced cortical somatostatin gene expression in a rat model of maternal immune activation', PSYCHIATRY RESEARCH, 282 (2019) [C1]
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2019 |
Duchatel RJ, Shannon Weickert C, Tooney PA, 'White matter neuron biology and neuropathology in schizophrenia', npj Schizophrenia, 5 1-9 (2019) [C1]
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2019 |
Duchatel RJ, Jackson ER, Alvaro F, Nixon B, Hondermarck H, Dun MD, 'Signal Transduction in Diffuse Intrinsic Pontine Glioma', PROTEOMICS, 19 (2019) [C1]
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2018 |
Duchatel RJ, Meehan CL, Harms LR, Michie PT, Bigland MJ, Smith DW, et al., 'Late gestation immune activation increases IBA1-positive immunoreactivity levels in the corpus callosum of adult rat offspring', Psychiatry Research, 266 175-185 (2018) [C1] Animal models of maternal immune activation study the effects of infection, an environmental risk factor for schizophrenia, on brain development. Microglia activation and cytokine... [more] Animal models of maternal immune activation study the effects of infection, an environmental risk factor for schizophrenia, on brain development. Microglia activation and cytokine upregulation may have key roles in schizophrenia neuropathology. We hypothesised that maternal immune activation induces changes in microglia and cytokines in the brains of the adult offspring. Maternal immune activation was induced by injecting polyriboinosinic:polyribocytidylic acid into pregnant rats on gestational day (GD) 10 or GD19, with brain tissue collected from the offspring at adulthood. We observed no change in Iba1, Gfap, IL1-ß and TNF-a mRNA levels in the cingulate cortex (CC) in adult offspring exposed to maternal immune activation. Prenatal exposure to immune activation had a significant main effect on microglial IBA1-positive immunoreactive material (IBA1+IRM) in the corpus callosum; post-hoc analyses identified a significant increase in GD19 offspring, but not GD10. No change in was observed in the CC. In contrast, maternal immune activation had a significant main effect on GFAP+IRM in the CC at GD19 (not GD10); post-hoc analyses only identified a strong trend towards increased GFAP+IRM in the GD19 offspring, with no white matter changes. This suggests late gestation maternal immune activation causes subtle alterations to microglia and astrocytes in the adult offspring.
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2016 |
Duchatel RJ, Jobling P, Graham BA, Harms LR, Michie PT, Hodgson DM, Tooney PA, 'Increased white matter neuron density in a rat model of maternal immune activation - Implications for schizophrenia', Progress in Neuro-Psychopharmacology and Biological Psychiatry, 65 118-126 (2016) [C1] Interstitial neurons are located among white matter tracts of the human and rodent brain. Post-mortem studies have identified increased interstitial white matter neuron (IWMN) den... [more] Interstitial neurons are located among white matter tracts of the human and rodent brain. Post-mortem studies have identified increased interstitial white matter neuron (IWMN) density in the fibre tracts below the cortex in people with schizophrenia. The current study assesses IWMN pathology in a model of maternal immune activation (MIA); a risk factor for schizophrenia. Experimental MIA was produced by an injection of polyinosinic:polycytidylic acid (PolyI:C) into pregnant rats on gestational day (GD) 10 or GD19. A separate control group received saline injections. The density of neuronal nuclear antigen (NeuN<sup>+</sup>) and somatostatin (SST<sup>+</sup>) IWMNs was determined in the white matter of the corpus callosum in two rostrocaudally adjacent areas in the 12week old offspring of GD10 (n=10) or GD19 polyI:C dams (n=18) compared to controls (n=20). NeuN<sup>+</sup> IWMN density trended to be higher in offspring from dams exposed to polyI:C at GD19, but not GD10. A subpopulation of these NeuN<sup>+</sup> IWMNs was shown to express SST. PolyI:C treatment of dams induced a significant increase in the density of SST<sup>+</sup> IWMNs in the offspring when delivered at both gestational stages with more regionally widespread effects observed at GD19. A positive correlation was observed between NeuN<sup>+</sup> and SST<sup>+</sup> IWMN density in animals exposed to polyI:C at GD19, but not controls. This is the first study to show that MIA increases IWMN density in adult offspring in a similar manner to that seen in the brain in schizophrenia. This suggests the MIA model will be useful in future studies aimed at probing the relationship between IWMNs and schizophrenia.
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Show 20 more journal articles |
Conference (24 outputs)
Year | Citation | Altmetrics | Link | ||
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2023 |
Duchatel R, Jackson E, Parackal S, Sun C, Daniel P, Mannan A, et al., 'EXPLOITING THE GENETIC DEPENDENCY ON PI3K/ MTOR SIGNALING FOR THE TREATMENT OF H3-ALTERED DIFFUSE MIDLINE GLIOMA', NEURO-ONCOLOGY, CANADA, Vancouver (2023)
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2023 |
Jackson E, Duchatel R, Staudt D, Persson M, Mannan A, Yadavilli S, et al., 'COMBINING ONC201 AND PAXALISIB FOR THE TREATMENT OF DIFFUSE MIDLINE GLIOMA (DMG); THE PRECLINICAL RESULTS UNDERPINNING THE INTERNATIONAL PHASE II CLINICAL TRIAL (NCT05009992).', NEURO-ONCOLOGY, CANADA, Vancouver (2023)
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2022 |
Findlay I, Staudt D, Kearney P, McEwen H, Duchatel R, Jackson E, et al., 'PHARMACO-PHOSPHO-PROTEO-GENOMICS OF PEDIATRIC HIGH-GRADE GLIOMAS - A PILOT STUDY', NEURO-ONCOLOGY, Tampa, FL (2022)
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2015 |
Duchatel R, Jobling P, Graham B, Harms L, Michie P, Hodgson D, Tooney P, 'Modelling white matter neuron pathology in schizophrenia using maternal immune activation', JOURNAL OF NEUROCHEMISTRY, Cairns, AUSTRALIA (2015) [E3]
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Show 21 more conferences |
Other (11 outputs)
Year | Citation | Altmetrics | Link | |||||
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2023 |
Jackson ER, Duchatel RJ, Staudt DE, Persson ML, Mannan A, Yadavilli S, et al., 'Supplementary Data from ONC201 in Combination with Paxalisib for the Treatment of H3K27-Altered Diffuse Midline Glioma', American Association for Cancer Research (AACR) (2023)
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2023 |
Jackson ER, Duchatel RJ, Staudt DE, Persson ML, Mannan A, Yadavilli S, et al., 'Supplementary Data from ONC201 in Combination with Paxalisib for the Treatment of H3K27-Altered Diffuse Midline Glioma', American Association for Cancer Research (AACR) (2023)
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2023 |
Jackson ER, Duchatel RJ, Staudt DE, Persson ML, Mannan A, Yadavilli S, et al., 'Supplementary Data from ONC201 in Combination with Paxalisib for the Treatment of H3K27-Altered Diffuse Midline Glioma', American Association for Cancer Research (AACR) (2023)
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Show 8 more others |
Preprint (2 outputs)
Year | Citation | Altmetrics | Link | |||||
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2023 |
Duchatel R, Jackson E, Parackal S, Sun C, Daniel P, Mannan A, et al., 'PI3K/mTOR is a therapeutically targetable genetic dependency in diffuse intrinsic pontine glioma (2023)
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2022 |
Germon Z, Sillar J, Mannan A, Duchatel R, Staudt D, Murray H, et al., 'Blockade of redox second messengers inhibits JAK/STAT and MEK/ERK signaling sensitizing FLT3-mutant acute myeloid leukemia to targeted therapies (2022)
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Grants and Funding
Summary
Number of grants | 20 |
---|---|
Total funding | $4,277,235 |
Click on a grant title below to expand the full details for that specific grant.
Highlighted grants and funding
ChadTough Defeat DIPG Fellowship Grant$423,060
Funding body: ChadTough Defeat DIPG Foundation
Funding body | ChadTough Defeat DIPG Foundation |
---|---|
Project Team | Doctor Ryan Duchatel |
Scheme | Fellowship Grant |
Role | Lead |
Funding Start | 2023 |
Funding Finish | 2025 |
GNo | G2201034 |
Type Of Funding | C3500 – International Not-for profit |
Category | 3500 |
UON | Y |
20241 grants / $113,000
Utilising a translational nanopharmaceutics approach to improving drug delivery in diffuse intrinsic pontine glioma$113,000
Funding body: Mark Hughes Foundation
Funding body | Mark Hughes Foundation |
---|---|
Project Team | Associate Professor Susan Hua, Miss Lauren Arms, Doctor Ryan Duchatel, Professor Matt Dun, Miss Evie Jackson |
Scheme | Innovation Grant |
Role | Investigator |
Funding Start | 2024 |
Funding Finish | 2025 |
GNo | G2301481 |
Type Of Funding | Scheme excluded from IGS |
Category | EXCL |
UON | Y |
20239 grants / $2,854,340
A chink in the armour of DMG tumours: Exploiting DMG-specific defence systems to improve response to treatment$1,200,000
Funding body: RUN DIPG
Funding body | RUN DIPG |
---|---|
Project Team | Professor Matt Dun, Miss Evie Jackson, Doctor Ryan Duchatel, Miss Evangeline Jackson |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2023 |
Funding Finish | 2026 |
GNo | G2300913 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Precision immunotherapeutic strategy for paediatric brain tumours$635,000
Funding body: Australian Lions Childhood Cancer Research Foundation
Funding body | Australian Lions Childhood Cancer Research Foundation |
---|---|
Project Team | Professor Matt Dun, Doctor Ryan Duchatel, Doctor Pouya Faridi, Doctor Dilana Staudt Barreto |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2023 |
Funding Finish | 2025 |
GNo | G2300290 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
ChadTough Defeat DIPG Fellowship Grant$423,060
Funding body: ChadTough Defeat DIPG Foundation
Funding body | ChadTough Defeat DIPG Foundation |
---|---|
Project Team | Doctor Ryan Duchatel |
Scheme | Fellowship Grant |
Role | Lead |
Funding Start | 2023 |
Funding Finish | 2025 |
GNo | G2201034 |
Type Of Funding | C3500 – International Not-for profit |
Category | 3500 |
UON | Y |
DMG COMBATT 2.0: Diffuse Midline Glioma Combined Anti-Tumor Targeting 2.0$304,092
Funding body: The Cure Starts Now Foundation
Funding body | The Cure Starts Now Foundation |
---|---|
Project Team | Doctor Ryan Duchatel, Professor Matt Dun, Professor Hubert Hondermarck, Professor Jonathan Morris, Professor Jonathan Morris |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2023 |
Funding Finish | 2024 |
GNo | G2200705 |
Type Of Funding | C3500 – International Not-for profit |
Category | 3500 |
UON | Y |
Doubling Down: Enhancing the therapeutic benefit of investigational drugs for diffuse midline glioma$150,000
Funding body: The Blackjack Foundation
Funding body | The Blackjack Foundation |
---|---|
Project Team | Professor Matt Dun, Doctor Ryan Duchatel, Miss Evangeline Jackson |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2023 |
Funding Finish | 2025 |
GNo | G2300289 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Evaluating promising anti-DMG therapies through enhanced collaboration$56,000
Funding body: RUN DIPG
Funding body | RUN DIPG |
---|---|
Project Team | Doctor Ryan Duchatel, Doctor Dilana Staudt Barreto, Doctor Zacary Germon, Miss Evangeline Jackson, Ms Mika Persson, Mr Izac Findlay, Ms Mika Persson, Mr Izac Findlay, Mr Bryce Thomas, Professor Matt Dun, Mr Bryce Thomas |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2023 |
Funding Finish | 2024 |
GNo | G2300438 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Establishment of a developmentally, genomically and immunologically relevant animal avatar of diffuse midline glioma$53,588
Funding body: Isabella and Marcus Foundation Limited
Funding body | Isabella and Marcus Foundation Limited |
---|---|
Project Team | Doctor Ryan Duchatel, Professor Matt Dun |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2023 |
Funding Finish | 2023 |
GNo | G2301063 |
Type Of Funding | C3200 – Aust Not-for Profit |
Category | 3200 |
UON | Y |
Establishment of a developmentally, genomically and immunologically relevant animal avatar of diffuse midline glioma$26,794
Funding body: Little Legs Foundation
Funding body | Little Legs Foundation |
---|---|
Project Team | Doctor Ryan Duchatel, Professor Matt Dun |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2023 |
Funding Finish | 2024 |
GNo | G2301067 |
Type Of Funding | C3200 – Aust Not-for Profit |
Category | 3200 |
UON | Y |
Multimodal advancement of PI3K inhibitor ‘paxalisib’ for the treatment of diffuse midline glioma$5,806
Funding body: Cancer Institute NSW
Funding body | Cancer Institute NSW |
---|---|
Project Team | Doctor Ryan Duchatel, Professor Matt Dun |
Scheme | Travel Grants |
Role | Lead |
Funding Start | 2023 |
Funding Finish | 2023 |
GNo | G2300318 |
Type Of Funding | C2400 – Aust StateTerritoryLocal – Other |
Category | 2400 |
UON | Y |
20221 grants / $814,123
The Wish Lab$814,123
Funding body: RUN DIPG
Funding body | RUN DIPG |
---|---|
Project Team | Professor Matt Dun, Doctor Ryan Duchatel |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2022 |
Funding Finish | 2022 |
GNo | G2200206 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
20212 grants / $255,772
COMBATT DMG: Combined anti-tumour targeting of diffuse midline glioma$203,522
Funding body: The Cure Starts Now Foundation
Funding body | The Cure Starts Now Foundation |
---|---|
Project Team | Professor Matt Dun, Dr Jason Cain, Doctor Ryan Duchatel, Jason Cain |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2021 |
Funding Finish | 2022 |
GNo | G2000780 |
Type Of Funding | C3500 – International Not-for profit |
Category | 3500 |
UON | Y |
Unravelling genomic heterogeneity of diffuse intrinsic pontine glioma$52,250
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Professor Matt Dun, Doctor Ryan Duchatel |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2021 |
Funding Finish | 2023 |
GNo | G2100434 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
20192 grants / $36,000
Moving safe and well-tolerated therapies from the bench to the clinic for the treatment of childhood brain cancer$26,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Professor Matt Dun, Doctor Ryan Duchatel, Doctor Frank Alvaro, Dr Javad Nazarian, Dr Michelle Monje |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2019 |
Funding Finish | 2020 |
GNo | G1901488 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Preclinical research into the potential applications of GDC-0084 in diffuse intrinsic pontine glioma (DIPG)$10,000
Funding body: Kazia Therapeutics Limited
Funding body | Kazia Therapeutics Limited |
---|---|
Project Team | Professor Matt Dun, Associate Professor David Ziegler, Doctor Heather Murray, Doctor Ryan Duchatel, Doctor Frank Alvaro |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2019 |
Funding Finish | 2019 |
GNo | G1801161 |
Type Of Funding | C3100 – Aust For Profit |
Category | 3100 |
UON | Y |
20185 grants / $204,000
Proteomic architecture of diffuse pontine intrinsic glioma$100,000
Funding body: McDonald Jones Charitable Foundation
Funding body | McDonald Jones Charitable Foundation |
---|---|
Project Team | Professor Matt Dun, Doctor Frank Alvaro, Doctor Ryan Duchatel, Doctor Heather Murray, Associate Professor David Ziegler |
Scheme | Postdoctoral fellowship |
Role | Investigator |
Funding Start | 2018 |
Funding Finish | 2020 |
GNo | G1801130 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Non-invasive detection of DIPG specific DNA and protein using sequential blood collections$57,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Professor Matt Dun, Doctor Muhammad Fairuz Jamaluddin, Doctor Ryan Duchatel, Doctor Frank Alvaro |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2018 |
Funding Finish | 2020 |
GNo | G1801235 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Enhancing the efficacy of new inhibitors targeting the PI3K–AKT–mTOR signalling axis for the treatment of high-grade diffuse intrinsic pontine gliomas (DIPG)$30,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Professor Matt Dun, Doctor Ryan Duchatel, Doctor Adjanie Patabendige |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2018 |
Funding Finish | 2018 |
GNo | G1801386 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Building international collaborations for DIPG research$10,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Doctor Ryan Duchatel, Professor Matt Dun |
Scheme | Jennie Thomas Medical Research Travel Grant |
Role | Lead |
Funding Start | 2018 |
Funding Finish | 2018 |
GNo | G1801371 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Targeting oncogenic signalling in DIPG using drugs that cross the blood brain barrier.$7,000
Funding body: Australian Communities Foundation
Funding body | Australian Communities Foundation |
---|---|
Project Team | Professor Matt Dun, Doctor Ryan Duchatel |
Scheme | Isabella and Marcus Paediatric Brainstem Tumour Fund |
Role | Investigator |
Funding Start | 2018 |
Funding Finish | 2018 |
GNo | G1800977 |
Type Of Funding | C3200 – Aust Not-for Profit |
Category | 3200 |
UON | Y |
Research Supervision
Number of supervisions
Past Supervision
Year | Level of Study | Research Title | Program | Supervisor Type |
---|---|---|---|---|
2023 | PhD | Molecular Characterisation of Oncogenic Signalling Networks to Develop Treatment Strategies for Diffuse Intrinsic Pontine Glioma | PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2023 | Honours | Selective hyperactivation of the Mitochondrial Protease ClpP as a potential therapeutic strategy for Diffuse Midline Glioma | Biochemistry & Cell Biology, The University of Newcastle, Australia | Co-Supervisor |
2019 | Honours | In vitro efficacy of ONC201 in diffuse intrinsic pontine glioma (DIPG) | Biochemistry & Cell Biology, Faculty of Health and Medicine, University of Newcastle | Co-Supervisor |
Dr Ryan Duchatel
Position
Chadtough Defeat DIPG Fellow
Cancer Signalling Group
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing
Focus area
Medical Biochemistry
Contact Details
ryan.duchatel@newcastle.edu.au | |
Phone | (02) 49854489 |
Mobile | (+61) 419268714 |
Office
Room | LS338 |
---|---|
Building | Life Science |
Location | Callaghan University Drive Callaghan, NSW 2308 Australia |