Dr Heather Murray
Cancer Institute NSW EC Fellow
School of Biomedical Sciences and Pharmacy
- Email:heather.murray@newcastle.edu.au
- Phone:(02) 4921 6934
Signalling a new future for leukaemia treatment
Despite only recently beginning her research career, Dr Heather Murray has already identified a puzzle piece that could revolutionise the quest for more effective treatment of acute myeloid leukaemia (AML).
Only one in four patients treated for acute myeloid leukaemia (AML), the most aggressive subtype of blood cancer, will survive five years past their diagnosis.
Recent advances in cancer research have improved outcomes, with a focus on genomic-based cell analyses informing customised treatment for each individual patient.
In partnership with key international collaborators, cancer researchers at UON, HMRI and the Hunter Cancer Research Alliance, are taking this research a step further by using proteomics to study proteins, and erroneous signaling, with the hope of identifying potential therapies.
The newest addition to this group of ground breaking collaborators is postdoctoral researcher Dr Heather Murray.
Setting the course
Initially planning a career in pharmacy, Heather found her undergrad degree in biomedical science provided the inspiration to follow a research path.
“In biomed I was exposed to the work of several talented local researchers, and I became interested in the ways that science could be applied to solve biological mysteries and improve treatment outcomes for people suffering with cancer,” Heather explains.
Continuing a study trajectory encompassing undergrad Summer scholarships and an early focus on melanoma, Heather sought out Associate Professor Verrills in a bid to take on a PhD project with maximum translational potential.
“I chose to work on a project researching leukaemia biology because it was different to anything I had done before, and could have massive impact,” Heather says.
Heather was awarded her doctorate by the University of Newcastle in 2020. A postdoctoral research position in the team of Associate Professor Verrills followed.
Heather’s PhD study into a novel therapeutic strategy for AML with mutations in the tyrosine kinase 3 (FLT3) gene, which is mutated in approximately one third of AML cases, has garnered international attention.
A research collaboration between researchers from the University of Newcastle, Hunter Medical Research Institute and Hunter Cancer Research Alliance, and the University of Southern Denmark, Heather is lead author on these findings, recently published in the prestigious international blood cancer journal Leukemia.
Inhibiting AML
In AML, overactive signaling prevents white blood cells from maturing and developing the power to fight infection. Simultaneously, the AML cells divide and grow at accelerated rates, taking over the blood and bone marrow and impeding healthy immune system processes.
Heather hypothesized that identifying unusually active cell proteins could provide invaluable clues to possible targets for therapeutic inhibition.
“I utilised phosphoproteomics to investigate not just whether the protein was there, but I was looking for a phosphorylation state which is a modification on the protein which generally indicates that the protein is active,” Heather says.
“We found that a protein called DNA-PK was highly phosphorylated in mutant FLT3 AML. So that suggested to us that DNA-PK may be highly active in the leukaemia, and therefore targeting DNA-PK would be an effective therapeutic strategy.”
Startling preclinical results suggest that using chemical compounds to simultaneously block the activity of FLT3 and DNA-PK causes the leukaemia cells to die whilst having no effect on normal, healthy cells.
Where to from here
Whilst working toward clinical trials with this new knowledge, Heather and her cancer research collaborators will be looking at whether this combination of inhibitors is relevant in the treatment of other forms of blood cancer, as well as investigating the efficacy of this novel strategy in regard to drug resistance.
“Our working hypothesis is that adding the DNA-PK inhibitor may actually reduce development of resistance,” Heather says.
“We do have funding from the NHMRC to do further work, to look at resistance to the targeted therapies that we’re using and whether we can possibly target pathways to prevent resistance from happening.”
To maximise and streamline experiments using donor cells, the Hunter Leukaemia Program has been established.
“We work closely with clinician researcher Associate Professor Anoop Enjeti, who brings unique insight to our work, making sure we are always working towards taking our work into the clinic,” Heather says.
The collaboration with Dr Enjeti is also crucial to the process of testing potential therapies by facilitating the collection of patient cell donations.
“If a patient arrives to clinic and they consent for some of their sample being used for our research, we can then analyse these cells in the lab and test their response to potential new therapies.”
Heather is dedicated to her research and finds purpose in the possibility of helping those who need effective treatment solutions for leukaemia.
“I find medical research rewarding with the potential to make a difference to peoples’ lives. I am drawn to the problem-solving aspect of research work, whilst the prospect of contributing to improved health and medical treatment in the community also drives my enthusiasm and commitment.”
Signalling a new future for leukaemia treatment
Despite only recently beginning her research career, Dr Heather Murray has already identified a puzzle piece that could revolutionise the quest for more effective treatment of acute myeloid leukaemia (AML).
Career Summary
Biography
Following early work researching DNA repair in melanoma, her research interests are now centred on the use of proteomics for functional characterisation and therapy guidance in cancer, particularly acute leukaemia subtypes.
Dr Murray’s doctoral work was focused on the phosphoproteomic characterisation of FLT3-mutant acute myeloid leukaemia (AML) and the therapeutic targeting of DNA repair in AML. With these findings published in the leading blood cancer journal Leukemia, Dr Murray has transitioned to a postdoctoral research position at the University of Newcastle and Hunter Medical Research Institute in the Molecular Oncology group led by Associate Professor Nikki Verrills. Dr Murray’s current research, in collaboration with field-leading researchers, is focused on combining genomic, proteomic, and phosphoproteomic approaches to characterise acute leukaemia subtypes and identify novel targets for precision therapy. In parallel Dr Murray is involved in pre-clinical testing of novel anti-leukaemic therapies, with the aim of translating the Molecular Oncology group laboratory findings into the clinical trial setting.
In addition to research, Dr Murray has also contributed to the medical research community through her involvement in local scientific committees. She has been involved in organising local scientific meetings, as Chair of the Hunter Cancer Research Alliance Scientific committee 2020, a member of the Hunter Cancer Research Alliance Scientific committee 2018, and Treasurer of the Australian Society for Medical Research Hunter Region Scientific committee 2016-2017. She also co-founded the University of Newcastle Postgraduate Students Association Proteomics Journal Club for which she was Secretary from 2017-2019. Dr Murray is currently a member of the Hunter Cancer Research Alliance Future Leaders Group.
Qualifications
- Doctor of Philosophy in Medical Biochemistry, University of Newcastle
- Bachelor of Biological Science, University of Newcastle
- Bachelor of Biomedical Sciences (Hons), University of Newcastle
- Master of Philosophy, University of Newcastle
Keywords
- Cancer
- DNA repair
- Leukaemia
- Proteomics
Fields of Research
Code | Description | Percentage |
---|---|---|
320506 | Medical biochemistry - proteins and peptides (incl. medical proteomics) | 60 |
321101 | Cancer cell biology | 40 |
Professional Experience
UON Appointment
Title | Organisation / Department |
---|---|
Cancer Institute NSW EC 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.
Journal article (20 outputs)
Year | Citation | Altmetrics | Link | ||||||||
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2024 |
Chen Y, Roselli S, Panicker N, Brzozowski JS, Skerrett-Byrne DA, Murray HC, Verrills NM, 'Proteomic and phosphoproteomic characterisation of primary mouse embryonic fibroblasts.', Proteomics, 24 e2300267 (2024) [C1]
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Nova | |||||||||
2024 |
Mulhall JE, Trigg NA, Bernstein IR, Anderson AL, Murray HC, Sipilä P, et al., 'Immortalized mouse caput epididymal epithelial (mECap18) cell line recapitulates the in-vivo environment.', Proteomics, 24 e2300253 (2024) [C1]
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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, 134 (2024) [C1]
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Nova | |||||||||
2024 |
Murray HC, Miller K, Dun MD, Verrills NM, 'Pharmaco-phosphoproteomic analysis of cancer-associated KIT mutations D816V and V560G.', Proteomics, 24 e2300309 (2024) [C1]
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2024 |
Skerrett-Byrne DA, Stanger SJ, Trigg NA, Anderson AL, Sipila P, Bernstein IR, et al., 'Phosphoproteomic analysis of the adaption of epididymal epithelial cells to corticosterone challenge', ANDROLOGY, [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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Nova | |||||||||
2023 |
Murray HC, Miller K, Brzozowski JS, Kahl RGS, Smith ND, Humphrey SJ, et al., 'Synergistic Targeting of DNA-PK and KIT Signaling Pathways in KIT Mutant Acute Myeloid Leukemia.', Mol Cell Proteomics, 22 100503 (2023) [C1]
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Nova | |||||||||
2022 |
Smyth SP, Nixon B, Anderson AL, Murray HC, Martin JH, MacDougall LA, et al., 'Elucidation of the protein composition of mouse seminal vesicle fluid.', Proteomics, 22 e2100227 (2022) [C1]
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Nova | |||||||||
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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Nova | |||||||||
2021 |
Skerrett-Byrne DA, Bromfield EG, Murray HC, Jamaluddin MFB, Jarnicki AG, Fricker M, et al., 'Time-resolved proteomic profiling of cigarette smoke-induced experimental chronic obstructive pulmonary disease', Respirology, 26 960-973 (2021) [C1] Background and objective: Chronic obstructive pulmonary disease (COPD) is the third leading cause of illness and death worldwide. Current treatments aim to control symptoms with n... [more] Background and objective: Chronic obstructive pulmonary disease (COPD) is the third leading cause of illness and death worldwide. Current treatments aim to control symptoms with none able to reverse disease or stop its progression. We explored the major molecular changes in COPD pathogenesis. Methods: We employed quantitative label-based proteomics to map the changes in the lung tissue proteome of cigarette smoke-induced experimental COPD that is induced over 8 weeks and progresses over 12 weeks. Results: Quantification of 7324 proteins enabled the tracking of changes to the proteome. Alterations in protein expression profiles occurred in the induction phase, with 18 and 16 protein changes at 4- and 6-week time points, compared to age-matched controls, respectively. Strikingly, 269 proteins had altered expression after 8 weeks when the hallmark pathological features of human COPD emerge, but this dropped to 27 changes at 12 weeks with disease progression. Differentially expressed proteins were validated using other mouse and human COPD bronchial biopsy samples. Major changes in RNA biosynthesis (heterogeneous nuclear ribonucleoproteins C1/C2 [HNRNPC] and RNA-binding protein Musashi homologue 2 [MSI2]) and modulators of inflammatory responses (S100A1) were notable. Mitochondrial dysfunction and changes in oxidative stress proteins also occurred. Conclusion: We provide a detailed proteomic profile, identifying proteins associated with the pathogenesis and disease progression of COPD establishing a platform to develop effective new treatment strategies.
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Nova | |||||||||
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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Nova | |||||||||
2018 |
Staudt D, Murray HC, McLachlan T, Alvaro F, Enjeti AK, Verrills NM, Dun MD, 'Targeting Oncogenic Signaling in Mutant FLT3 Acute Myeloid Leukemia: The Path to Least Resistance', INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 19 (2018) [C1]
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Nova | |||||||||
2018 |
Degryse S, De Bock CE, Demeyer S, Govaerts I, Bornschein S, Verbeke D, et al., 'Mutant JAK3 phosphoproteomic profiling predicts synergism between JAK3 inhibitors and MEK/BCL2 inhibitors for the treatment of T-cell acute lymphoblastic leukemia', Leukemia, 32 788-800 (2018) [C1] Mutations in the interleukin-7 receptor (IL7R) or the Janus kinase 3 (JAK3) kinase occur frequently in T-cell acute lymphoblastic leukemia (T-ALL) and both are able to drive cellu... [more] Mutations in the interleukin-7 receptor (IL7R) or the Janus kinase 3 (JAK3) kinase occur frequently in T-cell acute lymphoblastic leukemia (T-ALL) and both are able to drive cellular transformation and the development of T-ALL in mouse models. However, the signal transduction pathways downstream of JAK3 mutations remain poorly characterized. Here we describe the phosphoproteome downstream of the JAK3(L857Q)/(M511I) activating mutations in transformed Ba/F3 lymphocyte cells. Signaling pathways regulated by JAK3 mutants were assessed following acute inhibition of JAK1/JAK3 using the JAK kinase inhibitors ruxolitinib or tofacitinib. Comprehensive network interrogation using the phosphoproteomic signatures identified significant changes in pathways regulating cell cycle, translation initiation, mitogen-activated protein kinase and phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/AKT signaling, RNA metabolism, as well as epigenetic and apoptotic processes. Key regulatory proteins within pathways that showed altered phosphorylation following JAK inhibition were targeted using selumetinib and trametinib (MEK), buparlisib (PI3K) and ABT-199 (BCL2), and found to be synergistic in combination with JAK kinase inhibitors in primary T-ALL samples harboring JAK3 mutations. These data provide the first detailed molecular characterization of the downstream signaling pathways regulated by JAK3 mutations and provide further understanding into the oncogenic processes regulated by constitutive kinase activation aiding in the development of improved combinatorial treatment regimens.
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Nova | |||||||||
2017 |
Murray HC, Dun MD, Verrills NM, 'Harnessing the power of proteomics for identification of oncogenic, druggable signalling pathways in cancer', Expert Opinion on Drug Discovery, 12 431-447 (2017) [C1] Introduction: Genomic and transcriptomic profiling of tumours has revolutionised our understanding of cancer. However, the majority of tumours possess multiple mutations, and dete... [more] Introduction: Genomic and transcriptomic profiling of tumours has revolutionised our understanding of cancer. However, the majority of tumours possess multiple mutations, and determining which oncogene, or even which pathway, to target is difficult. Proteomics is emerging as a powerful approach to identify the functionally important pathways driving these cancers, and how they can be targeted therapeutically. Areas covered: The authors provide a technical overview of mass spectrometry based approaches for proteomic profiling, and review the current and emerging strategies available for the identification of dysregulated networks, pathways, and drug targets in cancer cells, with a key focus on the ability to profile cancer kinomes. The potential applications of mass spectrometry in the clinic are also highlighted. Expert opinion: The addition of proteomic information to genomic platforms¿¿proteogenomics¿¿is providing unparalleled insight in cancer cell biology. Application of improved mass spectrometry technology and methodology, in particular the ability to analyse post-translational modifications (the PTMome), is providing a more complete picture of the dysregulated networks in cancer, and uncovering novel therapeutic targets. While the application of proteomics to discovery research will continue to rise, improved workflow standardisation and reproducibility is required before mass spectrometry can enter routine clinical use.
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Nova | |||||||||
2016 |
Murray HC, Maltby VE, Smith DW, Bowden NA, 'Nucleotide excision repair deficiency in melanoma in response to UVA', Experimental Hematology and Oncology, 5 (2016) [C1] Background: The causative link between UV exposure and melanoma development is well known, however the mechanistic relationship remains incompletely characterised. UVA and UVB com... [more] Background: The causative link between UV exposure and melanoma development is well known, however the mechanistic relationship remains incompletely characterised. UVA and UVB components of sunlight are implicated in melanomagenesis; however the majority of studies have focused on the effects of UVB and UVC light. Interestingly, melanoma tumour sequencing has revealed an overrepresentation of mutations signature of unrepaired UV-induced DNA damage. Repair of UVA-induced DNA damage is thought to occur primarily through the Nucleotide Excision Repair (NER) pathway, which recognises and repairs damage either coupled to transcription (Transcription Coupled Repair; TCR), or through global genome scanning (Global Genome Repair; GGR). Current literature suggests NER is deficient in melanoma, however the cause of this remains unknown; and whether reduced NER activity in response to UVA may be involved in melanoma development remains uncharacterised. In this study we aimed to determine if melanoma cells exhibit reduced levels of NER activity in response to UVA. Methods: Melanocyte and melanoma cell lines were UVA-irradiated, and DNA damage levels assessed by immunodetection of Cyclobutane Pyrimidine Dimer (CPD) and (6-4) Photoproduct [(6-4)PP] lesions. Expression of NER pathway components and p53 following UVA treatment was quantified by qPCR and western blot. Results: UVA did not induce detectable induction of (6-4)PP lesions, consistent with previous studies. Repair of CPDs induced by UVA was initiated at 4 h and complete within 48 h in normal melanocytes, whereas repair initiation was delayed to 24 h and >40 % of lesions remained in melanoma cell lines at 48 h. This was coupled with a delayed and reduced induction of GGR component XPC in melanoma cells, independent of p53. Conclusion: These findings support that NER activity is reduced in melanoma cells due to deficient GGR. Further investigation into the role of NER in UVA-induced melanomagenesis is warranted and may have implications for melanoma treatment.
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Nova | |||||||||
2013 |
Bowden NA, Ashton KA, Vilain RE, Avery-Kiejda KA, Davey RJ, Murray HC, et al., 'Regulators of Global Genome Repair Do Not Respond to DNA Damaging Therapy but Correlate with Survival in Melanoma', PLOS ONE, 8 (2013) [C1]
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Show 17 more journal articles |
Conference (22 outputs)
Year | Citation | Altmetrics | Link | ||
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2023 |
Murray HC, Enjeti AK, Samaraweera S, Brzozowski JS, Miller K, D'Andrea RJ, Verrills NM, 'Proteogenomics Coupled with Ex Vivo Profiling for Therapeutic Targeting in AML', BLOOD, CA, San Diego (2023)
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2023 |
Verrills NM, Murray HC, Brzozowski JS, Panicker N, Miller K, Messina M, et al., 'Preclinical Evaluation of Bisantrene As Single Agent and in Combination with Decitabine for Acute Myeloid Leukemia', BLOOD, CA, San Diego (2023)
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2021 |
Chen Y, Murray H, AlMazi J, Brozozwski J, Mannan A, Panicker N, et al., 'Proteogenomics identifies oncogenic signalling pathways regulated by the tumour suppressor, PP2A-B55 alpha', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2021)
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2015 |
Dun M, Murray H, Al-mazi J, Kahl R, Flanagan H, Smith N, et al., 'IDENTIFICATION AND SYNERGISTIC TARGETING OF FLT3-ACTIVATED PATHWAYS IN ACUTE MYELOID LEUKAEMIA', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2015) [E3]
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Show 19 more conferences |
Preprint (2 outputs)
Year | Citation | Altmetrics | Link | |||||
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2024 |
Bond DR, Burnard SM, Uddipto K, Hunt KV, Harvey BM, Reinhardt LS, et al., 'Upregulated cholesterol biosynthesis facilitates the survival of methylation-retaining AML cells following decitabine treatment (2024)
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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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Grants and Funding
Summary
Number of grants | 13 |
---|---|
Total funding | $1,872,476 |
Click on a grant title below to expand the full details for that specific grant.
20243 grants / $924,155
Mesenchymal Signal Targeting in Myelodysplasia as a pathway to transfusion independence and blood count improvement – the MESSAGE study$827,655
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Doctor Anoop Enjeti, Doctor Danielle Bond, Dr Belinda Butcher, Dr Robin Gasiorowsko, Dr Devendra Hiwase, Associate Professor Zoe McQuilten, Doctor Heather Murray, Prof Andrew Wei, Dr Chun Yew Fong |
Scheme | MRFF - Early to Mid-Career Researchers Grant |
Role | Investigator |
Funding Start | 2024 |
Funding Finish | 2027 |
GNo | G2300838 |
Type Of Funding | C1300 - Aust Competitive - Medical Research Future Fund |
Category | 1300 |
UON | Y |
Targeting DNA-PK to overcome resistance to venetoclax in acute myeloid leukaemia (AML)$90,000
Funding body: Cure Cancer Australia Foundation
Funding body | Cure Cancer Australia Foundation |
---|---|
Project Team | Doctor Heather Murray |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2024 |
Funding Finish | 2024 |
GNo | G2301048 |
Type Of Funding | C3200 – Aust Not-for Profit |
Category | 3200 |
UON | Y |
The Mike and Karin Calford Travel Fellowship$6,500
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Doctor Heather Murray |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2024 |
Funding Finish | 2024 |
GNo | G2301275 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
20232 grants / $104,995
Targeting insulin signalling to overcome resistance to venetoclax in acute myeloid leukaemia (AML)$100,000
Funding body: Cure Cancer Australia Foundation
Funding body | Cure Cancer Australia Foundation |
---|---|
Project Team | Doctor Heather Murray, Dr Natasha Anstee, Doctor Natasha Anstee, Professor Matt Dun, Doctor Anoop Enjeti, Associate Professor Nikki Verrills, Prof Andrew Wei |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2023 |
Funding Finish | 2023 |
GNo | G2200755 |
Type Of Funding | C1700 - Aust Competitive - Other |
Category | 1700 |
UON | Y |
Elucidating markers of response to hypomethylating agents in blood cancers$4,995
Funding body: University of Newcastle
Funding body | University of Newcastle |
---|---|
Project Team | Doctor Heather Murray, Doctor Jonathan Sillar, Dr Ashwin Unnikrishnan, Associate Professor Nikki Verrills |
Scheme | Pilot Funding Scheme |
Role | Lead |
Funding Start | 2023 |
Funding Finish | 2023 |
GNo | G2300457 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
20221 grants / $600,000
Targeting the spliceosome as a novel approach for acute myeloid leukaemia (AML) therapy$600,000
Funding body: Cancer Institute NSW
Funding body | Cancer Institute NSW |
---|---|
Project Team | Doctor Heather Murray |
Scheme | Early Career Fellowship |
Role | Lead |
Funding Start | 2022 |
Funding Finish | 2024 |
GNo | G2100789 |
Type Of Funding | C2300 – Aust StateTerritoryLocal – Own Purpose |
Category | 2300 |
UON | Y |
20212 grants / $126,996
Cracking the Code: The launch of a genomic, epigenetic and proteomic pre-clinical platform to improve the treatment of paediatric leukemias$122,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Professor Matt Dun, Associate Professor Nikki Verrills, Doctor Heather Lee, Doctor Janis Chamberlain, Doctor Frank Alvaro, Doctor Anoop Enjeti, Associate Professor Kathryn Skelding, Doctor Lisa Lincz, Doctor Abdul Mannan, Doctor Heather Murray, Kristy McCarthy, Elizabeth Heskett, Paola Baeza, Kathleen Irish |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2021 |
Funding Finish | 2021 |
GNo | G2001337 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
Pilot data for study: Novel therapies for molecular subtypes of acute myeloid leukaemia (AML)$4,996
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Doctor Heather Murray |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2021 |
Funding Finish | 2021 |
GNo | G2100163 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
20192 grants / $10,300
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 |
Australasian Proteomics Society ECR Travel Award$300
Funding body: Australasian Proteomics Society
Funding body | Australasian Proteomics Society |
---|---|
Scheme | The Human Proteome Organisation Conference 2019 Awards |
Role | Lead |
Funding Start | 2019 |
Funding Finish | 2019 |
GNo | |
Type Of Funding | External |
Category | EXTE |
UON | N |
20181 grants / $100,000
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 |
20172 grants / $6,030
HCRA Biomarkers and Targeted Therapies flagship RHD student grant$5,000
Funding body: HCRA Hunter Cancer Research Alliance
Funding body | HCRA Hunter Cancer Research Alliance |
---|---|
Scheme | Research Project |
Role | Lead |
Funding Start | 2017 |
Funding Finish | 2017 |
GNo | |
Type Of Funding | Not Known |
Category | UNKN |
UON | N |
European Society of Molecular Oncology travel award$1,030
Funding body: ESMO
Funding body | ESMO |
---|---|
Scheme | ESMO Signaling Pathways Symposium 2017 |
Role | Lead |
Funding Start | 2017 |
Funding Finish | 2017 |
GNo | |
Type Of Funding | Not Known |
Category | UNKN |
UON | N |
Research Supervision
Number of supervisions
Current Supervision
Commenced | Level of Study | Research Title | Program | Supervisor Type |
---|---|---|---|---|
2022 | PhD | Activation Of A Tumour Suppressor In Triple Negative Breast Cancer | PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
Past Supervision
Year | Level of Study | Research Title | Program | Supervisor Type |
---|---|---|---|---|
2024 | PhD | Multiomic Characterisation of Cellular Signalling Regulated by PP2A-B55a in Breast Cancer and Development | PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
2020 | Honours |
Pre-clinical testing of a novel anti-cancer therapy <p>Bachelor of Biomedical Science (Hons)</p> |
Biochemistry & Cell Biology, University of Newcastle | Co-Supervisor |
2020 | Honours |
Precision medicine for acute myeloid leukaemia Bachelor of Pharmacy (Hons) |
Biochemistry & Cell Biology, The University of Newcastle | Co-Supervisor |
Research Projects
Verrills Laboratory 2012 -
Grants
A dual approach to activate a tumour suppressor for breast cancer therapy
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Doctor Severine Roselli Dayas, Associate Professor Jonathan Morris, Associate Professor Nikki Verrills |
Scheme | Ideas Grants |
Targeting DNA-PK in acute myeloid leukaemia
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Associate Professor Nikki Verrills, Associate Professor Anoop Enjeti |
Scheme | Ideas Grants |
Publications
Roberts KG, Smith AM, McDougall FK, Carpenter HC, Horan MP, Neviani P, et al., 'Essential requirement for PP2A inhibition by the oncogenic receptor c-KIT suggests PP2A reactivation as a strategy to treat c-KIT+ cancers', Cancer Research, 70 5438-5447 (2010) [C1]
Smith AM, Dun MD, Lee EM, Harrison C, Kahl R, Flanagan H, et al., 'Activation of protein phosphatase 2A in FLT3+ acute myeloid leukemia cells enhances the cytotoxicity of FLT3 tyrosine kinase inhibitors', Oncotarget, 7 47465-47478 (2016) [C1]
Murray HC, Dun MD, Verrills NM, 'Harnessing the power of proteomics for identification of oncogenic, druggable signalling pathways in cancer', Expert Opinion on Drug Discovery, 12 431-447 (2017) [C1]
Watt LF, Panicker N, Mannan A, Copeland B, Kahl RGS, Dun MD, et al., 'Functional importance of PP2A regulatory subunit loss in breast cancer', Breast Cancer Research and Treatment, 166 117-131 (2017) [C1]
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]
Panicker N, Coutman M, Lawlor-O'Neill C, Kahl RGS, Roselli S, Verrills NM, 'Ppp2r2aKnockout Mice Reveal That Protein Phosphatase 2A Regulatory Subunit, PP2A-B55 alpha, Is an Essential Regulator of Neuronal and Epidermal Embryonic Development', FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY, 8 (2020) [C1]
Murray HC, Enjeti AK, Kahl RGS, Flanagan HM, Sillar J, Skerrett-Byrne DA, et al., 'Quantitative phosphoproteomics uncovers synergy between DNA-PK and FLT3 inhibitors in acute myeloid leukaemia', LEUKEMIA, 35 1782-1787 (2021)
Students
Program | Research Title |
---|---|
PhD College of Health, Medicine and Wellbeing |
Multiomic Characterisation of Cellular Signalling Regulated by PP2A-B55a in Breast Cancer and Development |
Collaborators
Name | Organisation |
---|---|
Doctor Heather Constance Murray | University of Newcastle |
Doctor Nikita Panicker | University of Newcastle |
Miss Charley Louise Lawlor-O'Neill | University of Newcastle |
Doctor Lauren Frances Watt | University of Newcastle |
Miss Kasey Erin Miller | University of Newcastle |
Mr Joshua Stephen Sidney Brzozowski | University of Newcastle |
Doctor Yanfang Chen | University of Newcastle |
Doctor Severine Roselli Melanie Dayas | University of Newcastle |
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News
News • 3 Feb 2023
Early-career researchers boosted in mission to beat cancer
On the eve of World Cancer Day on 4 February, four University of Newcastle early career cancer researchers have been awarded $360,000 in grants to support their work investigating blood, gynaecological and colorectal cancers.
News • 15 Dec 2021
Researchers on mission to improve cancer outcomes
Three University of Newcastle researchers have been awarded 2022 Early Career Fellowships by the Cancer Institute NSW. Dr Rebecca Wyse, Dr Yuchen Feng and Dr Heather Murray will each receive a $600,000 scholarship to advance projects designed to improve treatment and outcomes for cancer patients.
News • 2 Nov 2020
New treatment idea discovered for leukaemia
Newcastle researchers have discovered a new way to kill leukaemia cells.
Dr Heather Murray
Position
Cancer Institute NSW EC Fellow
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing
Contact Details
heather.murray@newcastle.edu.au | |
Phone | (02) 4921 6934 |
Link | Research Networks |
Office
Room | LS3-37 |
---|---|
Building | Life Sciences |
Location | Callaghan University Drive Callaghan, NSW 2308 Australia |