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Dr Matt Dun

Cancer Institute NSW EC Fellow

School of Biomedical Sciences and Pharmacy

Career Summary

Biography

Research Philosophy 

Dedication, collaboration and hard work are the hallmarks of my medical research career focused on providing novel insights into some of the most common and devastating types of cancer; acute myeloid leukaemia (AML), paediatric T cell acute lymphoblastic leukaemia, breast and prostate cancers. 

My PhD program of research was achieved by publication, with distinction, in less than three years and decorated by eleven national and international research awards. During which I was fortunate to be mentored by two of the Universities most respected scientists in Prof. John Aitken and Prof. Brett Nixon. The significant contributions made to my field by PhD resulted in my dissertation being awarded the Annual Vice Chancellors Award for Research High Degree Excellence (2012), and has subsequently laid the foundations for me to achieve my ambitions of developing a successful and internationally competitive research program here at the University of Newcastle and the Hunter Medical Research Institute (HMRI).

My research program in collaboration with Dr Nicole Verrills and Dr Anoop Enjeti is focused on developing new anti-leukaemia drugs synthesised in collaboration with the UNSW Chemistry Department (Prof Morris). This targeted anti-cancer approach is complemented by a program of discovery research focused on furthering our understandings into how common gene mutations regulate growth, survival and proliferation in cancer cells.This work is funding by the Cancer Institute of NSW whom awarded me an esteemed Early Career Research Fellowship 2014-2016 ('Identifying novel therapeutic targets for the treatment of acute myeloid leukaemia (AML)'). I am also interested in cellular signalling regulated by growth factors in stem cells and have a program of research studying the molecular switch from quiescences to activation regulated by protein phosphatases.

I have been very fortunate to receive the support of the HMRI whose public advocacy has helped to develop my research program. Specifically, generous support from the Life Governor of the HMRI Jennie Thomas and Mrs Alyson Gearing has enabled me to study and work in the laboratories of field leading scientists in Belgium and Denmark. Further, the Estate of the Late Mr James Scott Lawrie and the Hunter Ski Club Project Grants has enabled me to continue my work into developing new treatments for AML and other paediatric blood diseases.

I am very fortunate to have extensive national and international collaborators with field leading scientists and haematologists. These opportunities provide my group with access to the world's most sophisticated technologies and relevant patient samples. These technologies are bridging the very large gap that currently exists between cancer genomics and proteomics. Our sophisticated studies are helping to identify new bona fide biomarkers for the development of new-targeted therapies to treat AML, ALL, breast cancers and prostate cancer.

Aside from research, I am committed to scientific advocacy and the promoting of the research achievements of our young local researchers. I am a Director of the Australian Society for Medical Research (ASMR) and locally I have formed the ASMR Newcastle committee, which now hosts 'The ASMR Satellite Scientific Meeting' annually at the HMRI. This meeting showcases the recent research achievements of young Hunter based scientists and clinicians. The meeting also helps to encourage postgraduate and student interactions and fosters collaborations between researchers affiliated within the Faculty of Health and Medicine, the Faculty of Science and Information Technology and the HMRI. If you would like information on this conference please contact Dr Nicole Ryan Nicole.Ryan@newcastle.edu.au

My goal is to continue to attract talented students to join my research program while continuing to generate the required research funding to enable us to translate our important medical discoveries into new treatments options for cancer patients.

If you are interesting in joining my team or supporting my research please contact me at: Matt.Dun@newcastle.edu.au.

Research Expertise

Since the completion of my PhD I have commenced my postdoctoral training within the Faculty of Health and Medicine Priority Research Centre for Cancer Research at the Hunter Medical Research Institute (HMRI), associated with the Hunter Cancer Research Alliance (HCRA) and in collaboration with the Calvary Mater Hospital Medical Oncology Department. My Research Program is focused on elucidating the biochemical mechanisms that underpin novel anti-cancer therapies for improved treatment of acute myeloid leukaemia (AML), paediatric T cell acute lymphoblastic leukaemia (T ALL), breast and prostate cancers. In this context, my technical strengths in many aspects of cell analysis, including: characterisation of protein expression, proteomic profiling including iTRAQ and SILAC, phosphoproteomics, DNA mutational analysis, cellular imagery, identification of protein-protein interactions via Co-immunoprecipitation, Far-Western blotting and Blue Native PAGE, cell culture, functional assays and the generation of recombinant proteins and polyclonal antibodies has been recognised. My ever growing knowledge and skill base has benefited from close association with national and international colleagues. Funding in 2015 enabled me to conduct leukaemia genomics and animal training at the VIB KU Leuven in Belgium, and funding from  2013 and 2014 has enabled me to spend three months working at Institut for Biokemi og Molekylær Biologi at the Syddansk Universitet where I worked with experts in proteomic assays, including phosphoproteomics, membrane proteomics, glycoproteomics, iTRAQ and SILIC. These phosphoproteomics studies utilised Hunter AML patients samples and is allowing us to determine the role oncogenic signalling has on growth and survival of the cancer which will help us identify novel treatment targets and identify the disease causing mutations that are associated with recurrent DNA mutations These complex investigations are aimed at unravelling the pathogenesis of disease, with the resulting data providing us with a better understanding of each condition. Following this sabbatical I was fortunate to present my work on AML at the American Association of Cancer Research in Washington DC.

In 2013 I received the Australian Society for Medical Research Recipient of the NSW Office for Health and Medical Research Postdoctoral Award for Excellence in Medical Research. This award was presented at the ASMR NSW Scientific Meeting. Commencing 2014 my research program is strongly supported thanks to the Cancer Institute of NSW Early Career Research Fellowship. This funding is for three years and aims to 'Identify novel therapeutic targets for the treatment of Acute Myeloid Leukaemia'. These experiences are helping me to establishing a firm foundation for a productive career in cancer cell biology. My ambitions are to attract talented students and integrate my many technical skills on Australian patients samples and to use model systems to further elucidate the mechanisms of disease. Please contact me if you are interesting in joining my team. Matt.Dun@newcastle.edu.au

Teaching Expertise

• 2012 - 2014: Lecturer, HUBS1202 Human Genomics and Biomolecular Analysis. • 2012 - : Head Tutor, HUBS3302 Bioinformatics and Functional Genomics. • • 2011: Lecturer and Head Demonstrator, BIOL2020 Animal Physiology & Development. • 2011: Head Demonstrator, BIOL3020 Reproductive Physiology & Development head demonstrator. • 2011: Demonstrator, BIOL3001 Advanced Laboratory Skills. • 2010: Lecturer and Head Demonstrator, BIOL2020 Animal Physiology & Development. • 2010: Head Demonstrator, BIOL3020 Reproductive Physiology & Development head demonstrator. • 2010: Demonstrator, BIOL3001 Advanced Laboratory Skills. • 2009: Head Demonstrator, BIOL2020 Animal Physiology & Development. • 2009: Head Demonstrator, BIOL3020 Reproductive Physiology & Development head demonstrator. • 2009: Demonstrator, BIOL3001 Advanced Laboratory Skills. I am a lecturer for the Bachelor of Biomedical Science degree specifically, HUBS1202 Human Genomics and Biomolecular Analysis and HUBS3302 Bioinformatics and Functional Genomics. During my PhD I carried a significant teaching load, lecturing 2nd year Physiology for Biotech/Science students and spending almost 500 hours as Laboratory Head Demonstrator. Also during my studies I played Rugby Union for the University of Newcastle and was awarded runner up for Sports Person of the Year, awarded a University Blue and represented NSW in rugby union for five consecutive years. I was also awarded the Representative Player of the Year for the Newcastle and Hunter Rugby Union and in the same year was awarded the NSW Country Rugby Union Championships Player of the Tournament.

Administrative Expertise

Professional memberships:  • 2015 – Director the Australian Society for Medical Research. • 2014 –, Hunter Cancer Research Alliance Flagship Program in Implementation Scientific Committee Member • 2014, Convenor of the Australian Society for Medical Research (ASMR) Satellite Scientific Meeting • 2013 –, Committee Member of the Australian Society for Medical Research (ASMR) • 2012 –, Member of the American Association of Cancer Research (AACR) • 2012 –, Member of the Australian Leukaemia and Lymphoma Group (ALLG) • 2012 –, Member of the Australian Society of Medical Research (ASMR) • 2011 – 2012. Society of Reproductive Biology (SRB) Australian Student Representative to council • 2010 – 2012. Young Investigators of Reproductive Biology Epididymis Council Co-Chair (International Society) • 2010 – 2012. Priority Research Centre Reproductive Biology Meetings Co-Organiser (Reproductive Sciences, Eggs to Embryos and Mothers and Babies Groups) • 2010. University of Newcastle Research Higher Degree Committee, Conference Organising Chair

Collaborations

• Dr Nicole Verrills Medical Biochemistry, The University of Newcastle and HMRI.

• Dr Anoop Enjeti, Clinical Haematologist, The Calvary Mater Hospital.

• Dr Andrew Wei, Clinical Haematologist, The Alfred Hospital and Monash University.

• Prof Jan Cools and Dr Charley De Bock at the Department of Human Genetic VIB KU Leuven Belgium.

• Prof Martin Larsen, Institute of Biochemistry and Molecular Biology, The University of Southern Denmark.

  • • Prof Steve Ackland, Dr Jenntte Sakoff and Dr Jayne Gilbert, Medical Oncology, The Calvary Mater Hospital and HMRI.

• Prof Hubert Hondermarck, Professor of Medical Biochemistry, The University of Newcastle.

• Prof Martin Larsen, Institute of Biochemistry and Molecular Biology, The University of Southern Denmark.

• Prof Jonathan Morris and Hamish Toop, Chemistry Department, University of New South Wales.

• Prof Richard Locke, Dr Anthony Don and Dr Anchit Khanna Lowy Cancer Research Centre, Prince of Wales Clinical School, Faculty of Medicine, The University of New South Wales.

• Prof Jenny Martin, Clinical Pharmacologist, The Calvary Mater Hospital, The University of Newcastle and HMRI.

• Prof Brett Nixon, Reproductive Science Group, The University of Newcastle and HMRI.

• A/Prof Brett Nixon, Reproductive Science Group, The University of Newcastle and HMRI.


Qualifications

  • PhD (Biological Science), University of Newcastle
  • Bachelor of Biotechnology, University of Newcastle
  • Bachelor of Biotechnology (Honours), University of Newcastle

Keywords

  • Anti-Cancer Drug Targeting
  • Biochemical Assays
  • Biochemistry
  • Cancer
  • Chemical Proteomics
  • Leukaemia
  • Nucleic Acids
  • Phosphoproteomics
  • Protein Chemistry
  • Proteomics

Fields of Research

Code Description Percentage
060109 Proteomics and Intermolecular Interactions (excl. Medical Proteomics) 30
110106 Medical Biochemistry: Proteins and Peptides (incl. Medical Proteomics) 30
111201 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

Academic appointment

Dates Title Organisation / Department
1/12/2013 -  Cancer Instititue NSW Early Career Fellowship Cancer Instititue NSW
School of Biomedical Sciences and Pharmacy, Medical Biochemistry
Australia
1/01/2013 -  Conference Chair - The Australian Society for Medical Research, Satellite Scientific Meeting Convenor The Australian Society for Medical Research
1/10/2011 - 1/12/2013 HMRI Cancer Research Program Chemical Proteomics Postdoctoral Fellow University of Newcastle
HMRI Cancer Research Program
Australia

Membership

Dates Title Organisation / Department
1/01/2013 -  Membership - The Australian Society for Medical Research The Australian Society for Medical Research
Edit

Publications

For publications that are currently unpublished or in-press, details are shown in italics.


(47 outputs)

Year Citation Altmetrics Link
2017 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, (2017)
DOI 10.1038/leu.2017.276
2017 Murray HC, Dun MD, Verrills NM, 'Harnessing the power of proteomics for identification of oncogenic, druggable signalling pathways in cancer.', Expert Opin Drug Discov, 12 431-447 (2017)
DOI 10.1080/17460441.2017.1304377
Citations Scopus - 1
Co-authors Nikki Verrills
2017 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, 1-15 (2017)

© 2017 Springer Science+Business Media, LLC Purpose: Protein phosphatase 2A (PP2A) is a family of serine/threonine phosphatases that regulate multiple cellular signalling pathway... [more]

© 2017 Springer Science+Business Media, LLC Purpose: Protein phosphatase 2A (PP2A) is a family of serine/threonine phosphatases that regulate multiple cellular signalling pathways involved in proliferation, survival and apoptosis. PP2A inhibition occurs in many cancers and is considered a tumour suppressor. Deletion/downregulation of PP2A genes has been observed in breast tumours, but the functional role of PP2A subunit loss in breast cancer has not been investigated. Methods: PP2A subunit expression was examined by immunohistochemistry in human breast tumours, and by qPCR and immunoblotting in breast cancer cell lines. PP2A subunits were inhibited by shRNA, and mutant PP2A genes overexpressed, in MCF10A and MCF7 cells, and growth and signalling in standard and three-dimensional cultures were assessed. Results: Expression of PP2A-Aa, PP2A-Ba and PP2A-B'a subunits was significantly lower in primary human breast tumours and lymph node metastases, compared to normal mammary tissue. PP2A-Aa and the regulatory subunits PP2A-Ba, -Bd and -B'¿ were also reduced in breast cancer cell lines compared to normal mammary epithelial cells. Functionally, shRNA-mediated knockdown of PP2A-Ba, -B'a and -B'¿, but not PP2A-Aa, induced hyper-proliferation and large multilobular acini in MCF10A 3D cultures, characterised by activation of ERK. Expression of a breast cancer-associated PP2A-A mutant, PP2A-Aa-E64G, which inhibits binding of regulatory subunits to the PP2A core, induced a similar hyper-proliferative phenotype. Knockdown of PP2A-Ba also induced hyper-proliferation in MCF7 breast cancer cells. Conclusion: These results suggest that loss of specific PP2A regulatory subunits is functionally important in breast tumourigenesis, and support strategies to enhance PP2A activity as a therapeutic approach in breast cancer.

DOI 10.1007/s10549-017-4403-5
Co-authors Nikki Verrills
2017 Hutcheon K, McLaughlin EA, Stanger SJ, Bernstein IR, Dun MD, Eamens AL, Nixon B, 'Analysis of the small non-protein-coding RNA profile of mouse spermatozoa reveals specific enrichment of piRNAs within mature spermatozoa.', RNA Biol, 0 (2017)
DOI 10.1080/15476286.2017.1356569
Co-authors Brett Nixon, Eileen Mclaughlin
2017 Ong LK, Page S, Briggs GD, Guan L, Dun MD, Verrills NM, et al., 'Peripheral Lipopolysaccharide Challenge Induces Long-Term Changes in Tyrosine Hydroxylase Regulation in the Adrenal Medulla.', J Cell Biochem, 118 2096-2107 (2017)
DOI 10.1002/jcb.25839
Co-authors Linkooi Ong, Nikki Verrills, Phil Dickson, Peter Dunkley
2017 de Bock CE, Hughes MR, Snyder K, Alley S, Sadeqzadeh E, Dun MD, et al., 'Protein interaction screening identifies SH3RF1 as a new regulator of FAT1 protein levels', FEBS LETTERS, 591 667-678 (2017) [C1]
DOI 10.1002/1873-3468.12569
Co-authors Rick Thorne, Hubert Hondermarck
2016 Nixon B, Dun MD, Aitken RJ, 'Proteomic analysis of human spermatozoa', Immune Infertility: Impact of Immune Reactions on Human Fertility, Second Edition 3-22 (2016)

© Springer International Publishing Switzerland 2017. Novel technological innovations in high-resolution mass spectrometry have ushered in a new era in proteomic analyses. Couple... [more]

© Springer International Publishing Switzerland 2017. Novel technological innovations in high-resolution mass spectrometry have ushered in a new era in proteomic analyses. Coupled with enhanced methods for cellular and protein pre-fractionation, such developments have enabled the detailed characterization of proteomes from various cell types, including the spermatozoa of a number of species. Collectively, these studies have generated complex inventories consisting of thousands of sperm proteins and served as an important platform for advancing our understanding of sperm biology. In this context, exciting advances have been made into comparative and quantitative approaches that enable sophisticated analysis of the proteomic signature of spermatozoa in different functional states (immature vs. mature, non-capacitated vs. capacitated, fertile vs. infertile). These techniques have helped to define which specific elements of the proteome are of functional significance and improved our understanding of the cascade of post-translational modifications (e.g. phosphorylation, glycosylation, acetylation, proteolytic cleavage) involved in generating a fertilization competent spermatozoon. Such fundamental information holds considerable promise for identifying key biomarkers of male fertility in addition to elements of sperm maturation that might be targeted for fertility regulation both in the context of contraceptive development and therapeutic intervention. In this review, we have sought to present an overview of the use of contemporary proteomics to address many of the long-standing challenges in the field of human sperm biology as well as to speculate on the future clinical applications of these technologies.

DOI 10.1007/978-3-319-40788-3_1
Co-authors John Aitken, Brett Nixon
2016 Toop HD, Dun MD, Ross BK, Flanagan HM, Verrills NM, Morris JC, 'Development of novel PP2A activators for use in the treatment of acute myeloid leukaemia', Organic and Biomolecular Chemistry, 14 4605-4616 (2016) [C1]

© The Royal Society of Chemistry. AAL(S), the chiral deoxy analog of the FDA approved drug FTY720, has been shown to inhibit proliferation and apoptosis in several cancer cell li... [more]

© The Royal Society of Chemistry. AAL(S), the chiral deoxy analog of the FDA approved drug FTY720, has been shown to inhibit proliferation and apoptosis in several cancer cell lines. It has been suggested that it does this by activating protein phosphatase 2A (PP2A). Here we report the synthesis of new cytotoxic analogs of AAL(S) and the evaluation of their cytotoxicity in two myeloid cell lines, one of which is sensitive to PP2A activation. We show that these analogs activate PP2A in these cells supporting the suggested mechanism for their cytotoxic properties. Our findings identify key structural motifs required for anti-cancer effects.

DOI 10.1039/c6ob00556j
Citations Scopus - 4Web of Science - 4
Co-authors Nikki Verrills
2016 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]

Constitutive activation of the receptor tyrosine kinase Fms-like tyrosine kinase 3 (FLT3), via co-expression of its ligand or by genetic mutation, is common in acute myeloid leuke... [more]

Constitutive activation of the receptor tyrosine kinase Fms-like tyrosine kinase 3 (FLT3), via co-expression of its ligand or by genetic mutation, is common in acute myeloid leukemia (AML). In this study we show that FLT3 activation inhibits the activity of the tumor suppressor, protein phosphatase 2A (PP2A). Using BaF3 cells transduced with wildtype or mutant FLT3, we show that FLT3-induced PP2A inhibition sensitizes cells to the pharmacological PP2A activators, FTY720 and AAL(S). FTY720 and AAL(S) induced cell death and inhibited colony formation of FLT3 activated cells. Furthermore, PP2A activators reduced the phosphorylation of ERK and AKT, downstream targets shared by both FLT3 and PP2A, in FLT3/ITD + BaF3 and MV4-11 cell lines. PP2A activity was lower in primary human bone marrow derived AML blasts compared to normal bone marrow, with blasts from FLT3-ITD patients displaying lower PP2A activity than WT-FLT3 blasts. Reduced PP2A activity was associated with hyperphosphorylation of the PP2A catalytic subunit, and reduced expression of PP2A structural and regulatory subunits. AML patient blasts were also sensitive to cell death induced by FTY720 and AAL(S), but these compounds had minimal effect on normal CD34+ bone marrow derived monocytes. Finally, PP2A activating compounds displayed synergistic effects when used in combination with tyrosine kinase inhibitors in FLT3-ITD + cells. A combination of Sorafenib and FTY720 was also synergistic in the presence of a protective stromal microenvironment. Thus combining a PP2A activating compound and a FLT3 inhibitor may be a novel therapeutic approach for treating AML.

DOI 10.18632/oncotarget.10167
Citations Scopus - 4Web of Science - 3
Co-authors Leonie Ashman, Nikki Verrills, Kathryn Skelding
2016 Sillar J, Murray H, Al Mazi J, Skerrett-Byrne D, Kahl R, Flanagan H, et al., 'QUANTITATIVE, HIGH-RESOLUTION PROTEOMICS FOR A SYSTEMS BIOLOGICAL ANALYSIS OF ACUTE MYELOID LEUKEMIA', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
Co-authors Hubert Hondermarck
2016 Al Mazi JT, Verrills N, Smith N, Pockney P, Hondermarck H, Dun M, 'A COMPARISON BETWEEN DATA-DEPENDENT ANALYSIS AND HIGH-RESOLUTION ACCURATE MASS TARGETED PROTEOMICS APPROACHES FOR THE QUANTIFICATION OF PLASMA BIOMARKERS IN COLORECTAL CANCER', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
Co-authors Hubert Hondermarck
2016 Li X, Al Mazi J, Smith N, Dun M, Hondermarck H, 'DEVELOPMENT OF A HIGHLY SENSITIVE AND SPECIFIC TARGETED MASS SPECTROMETRY ASSAY FOR PSA IN PROSTATE CANCER', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
Co-authors Hubert Hondermarck
2016 Mannan A, Panicker N, Kahl R, Dun M, Skelding K, Verrills N, 'REDUCED EXPRESSION OF THE PROTEIN PHOSPHATASE 2A REGULATORY SUBUNIT B55 alpha: IMPACT ON LUMINAL B BREAST CANCER CELLS PROGRESSION AND DNA DAMAGE REPAIR', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
2016 Murray H, Al Mazi J, Kahl R, Flanagan H, Smith N, Enjeti A, et al., 'DNA-PK INHIBITION SENSITIZES FLT3-ITD AML CELLS TO CYTARABINE AND SORAFENIB', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
2016 Chen Y, Al Mazi J, Panicker N, Mannan A, Dun M, Verrills N, 'DEVELOPMENT OF A SENSITIVE AND QUANTITATIVE MASS SPECTROMETRY-BASED ASSAY FOR THE QUANTITATION OF DNA DAMAGE REPAIR PATHWAYS IN HUMAN CANCERS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
2015 Dun MD, Chalkley RJ, Faulkner S, Keene S, Avery-Kiejda KA, Scott RJ, et al., 'Proteotranscriptomic profiling of 231-BR breast cancer cells: Identification of potential biomarkers and therapeutic targets for brain metastasis', Molecular and Cellular Proteomics, 14 2316-2330 (2015) [C1]

© 2015 by The American Society for Biochemistry and Molecular Biology, Inc. Brain metastases are a devastating consequence of cancer and currently there are no specific biomarker... [more]

© 2015 by The American Society for Biochemistry and Molecular Biology, Inc. Brain metastases are a devastating consequence of cancer and currently there are no specific biomarkers or therapeutic targets for risk prediction, diagnosis, and treatment. Here the proteome of the brain metastatic breast cancer cell line 231-BR has been compared with that of the parental cell line MDA-MB-231, which is also metastatic but has no organ selectivity. Using SILAC and nanoLC-MS/MS, 1957 proteins were identified in reciprocal labeling experiments and 1584 were quantified in the two cell lines. A total of 152 proteins were confidently determined to be up- or down-regulated by more than twofold in 231-BR. Of note, 112/152 proteins were decreased as compared with only 40/152 that were increased, suggesting that down-regulation of specific proteins is an important part of the mechanism underlying the ability of breast cancer cells to metastasize to the brain. When matched against transcriptomic data, 43% of individual protein changes were associated with corresponding changes in mRNA, indicating that the transcript level is a limited predictor of protein level. In addition, differential miRNA analyses showed that most miRNA changes in 231-BR were up- (36/45) as compared with down-regulations (9/45). Pathway analysis revealed that proteome changes were mostly related to cell signaling and cell cycle, metabolism and extracellular matrix remodeling. The major protein changes in 231-BR were confirmed by parallel reaction monitoring mass spectrometry and consisted in increases (by more than fivefold) in the matrix metalloproteinase-1, ephrin-B1, stomatin, myc target-1, and decreases (by more than 10-fold) in transglutaminase-2, the S100 calcium-binding protein A4, and L-plastin. The clinicopathological significance of these major proteomic changes to predict the occurrence of brain metastases, and their potential value as therapeutic targets, warrants further investigation.

DOI 10.1074/mcp.M114.046110
Citations Scopus - 8Web of Science - 9
Co-authors Murray Cairns, Hubert Hondermarck, Kelly Kiejda, Rodney Scott
2015 Faulkner S, Dun MD, Hondermarck H, 'Proteogenomics: Emergence and promise', Cellular and Molecular Life Sciences, 72 953-957 (2015) [C1]

© Springer Basel 2015. Proteogenomics, or the integration of proteomics with genomics and transcriptomics, is emerging as the next step towards a unified understanding of cellula... [more]

© Springer Basel 2015. Proteogenomics, or the integration of proteomics with genomics and transcriptomics, is emerging as the next step towards a unified understanding of cellular functions. Looking globally and simultaneously at gene structure, RNA expression, protein synthesis and posttranslational modifications have become technically feasible and offer a new perspective to molecular processes. Recent publications have highlighted the value of proteogenomics in oncology for defining the molecular signature of human tumors, and translation to other areas of biomedicine and life sciences is anticipated. This minireview will discuss recent developments, challenges and perspectives in proteogenomics.

DOI 10.1007/s00018-015-1837-y
Citations Scopus - 15Web of Science - 15
Co-authors Hubert Hondermarck
2015 Nixon B, Stanger SJ, Mihalas BP, Reilly JN, Anderson AL, Dun MD, et al., 'Next generation sequencing analysis reveals segmental patterns of microRNA expression in mouse epididymal epithelial cells', PLoS ONE, 10 (2015) [C1]

© 2015 Nixon et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and repr... [more]

© 2015 Nixon et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The functional maturation of mammalian spermatozoa is accomplished as the cells descend through the highly specialized microenvironment of the epididymis. This dynamic environment is, in turn, created by the combined secretory and absorptive activity of the surrounding epithelium and displays an extraordinary level of regionalization. Although the regulatory network responsible for spatial coordination of epididymal function remains unclear, recent evidence has highlighted a novel role for the RNA interference pathway. Indeed, as noncanonical regulators of gene expression, small noncoding RNAs have emerged as key elements of the circuitry involved in regulating epididymal function and hence sperm maturation. Herein we have employed next generation sequencing technology to profile the genome-wide miRNA signatures of mouse epididymal cells and characterize segmental patterns of expression. An impressive profile of some 370 miRNAs were detected in the mouse epididymis, with a subset of these specifically identified within the epithelial cells that line the tubule (218). A majority of the latter miRNAs (75%) were detected at equivalent levels along the entire length of the mouse epididymis. We did however identify a small cohort of miRNAs that displayed highly regionalized patterns of expression, including miR-204-5p and miR-196b-5p, which were down- and up-regulated by approximately 39- and 45-fold between the caput/caudal regions, respectively. In addition we identified 79 miRNAs (representing ~ 21% of all miRNAs) as displaying conserved expression within all regions of the mouse, rat and human epididymal tissue. These included 8/14 members of let-7 family of miRNAs that have been widely implicated in the control of androgen signaling and the repression of cell proliferation and oncogenic pathways. Overall these data provide novel insights into the sophistication of the miRNA network that regulates the function of the male reproductive tract.

DOI 10.1371/journal.pone.0135605
Citations Scopus - 9Web of Science - 10
Co-authors Eileen Mclaughlin, Janet Holt, Brett Nixon
2015 Nixon B, Bromfield EG, Dun MD, Redgrove KA, McLaughlin EA, Aitken RJ, 'The role of the molecular chaperone heat shock protein A2 (HSPA2) in regulating human sperm-egg recognition', ASIAN JOURNAL OF ANDROLOGY (2015) [C1]
DOI 10.4103/1008-682X.151395
Citations Scopus - 13Web of Science - 7
Co-authors Brett Nixon, John Aitken, Kate Redgrove, Eileen Mclaughlin, Elizabeth Bromfield
2015 Watt LF, Panicker N, Copeland B, Kahl RGS, Dun MD, Young B, et al., 'PP2A ¿ a novel biomarker and therapeutic target for poor outcome breast cancer', Proceedings of the Lowy Cancer Conference (2015) [E3]
Co-authors Nikki Verrills, Kathryn Skelding
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]
Co-authors Nikki Verrills
2015 Al-mazi J, Dun M, Smith N, Verrills N, 'DEVELOPMENT OF NOVEL MULTIPLE REACTION MONITORING (MRM) ASSAY FOR BIOMARKER QUANTITATION IN CANCER CELLS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2015) [E3]
Co-authors Nikki Verrills
2015 Brzozowski J, Coldie B, Jankowski H, Bond D, Scarlett C, Dun M, et al., 'THE EFFECTS OF ALTERED CD9 AND CD151 EXPRESSION ON PROSTATE EXOSOMES', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2015) [E3]
Co-authors Danielle Bond, Judith Weidenhofer, C Scarlett, Kathryn Skelding
2015 Lehman W, Kahl R, Flanagan H, Verrills N, Dun M, 'DETERMINING THE MECHANISM OF LEUKAEMOGENESIS INDUCED BY SHWACHMAN-DIAMOND SYNDROME (SDS) USING COMPARATIVE AND QUANTITATIVE PROTEOMICS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2015) [E3]
Co-authors Nikki Verrills
2015 Li X, Flanagan H, Kahl R, Rigby C, Verrills N, Dun M, 'CHEMICAL PROTEOMICS TO IDENTIFY THE MECHANISM OF PROTEIN PHOSPHATASE 2A (PP2A) INHIBITION IN ACUTE MYELOID LEUKAEMIA (AML)', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2015) [E3]
Co-authors Nikki Verrills
2015 Mannan A, Panicker N, Watt L, Kahl R, Dun M, Skelding K, Verrills N, 'ROLE OF REDUCED PROTEIN PHOSPHATASE 2A SUBUNIT, B55A, EXPRESSION IN LUMINAL B BREAST CANCER CELL LINE DNA DAMAGE REPAIR PATHWAY', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2015) [E3]
Co-authors Kathryn Skelding, Nikki Verrills
2015 Panicker N, Watt L, Kahl R, Dun M, Greer P, Skelding K, Verrills N, 'REDUCED EXPRESSION OF PROTEIN PHOSPHATASE 2A SUBUNIT, B55A, IN BREAST CANCER DNA DAMAGE REPAIR PATHWAYS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2015) [E3]
Co-authors Nikki Verrills, Kathryn Skelding, Peter Greer
2015 Rigby C, Kahl R, Flanagan H, Li X, Enjeti A, Verrills N, Dun M, 'CHARACTERISATION OF A NOVEL PP2A INHIBITORY ONCOPROTEIN IN ACUTE MYELOID LEUKAEMIA (AML)', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2015) [E3]
Co-authors Nikki Verrills
2015 Udeh R, Kahl R, Flanagan H, Verrills N, Dun M, 'IDENTIFYING THE FUNCTIONAL ROLE OF TSR, A NOVEL DRUG TARGET IN AML', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2015) [E3]
Co-authors Nikki Verrills
2014 Goldie BJ, Dun MD, Lin M, Smith ND, Verrills NM, Dayas CV, Cairns MJ, 'Activity-associated miRNA are packaged in Map1b-enriched exosomes released from depolarized neurons.', Nucleic Acids Research, 42 9195-9208 (2014) [C1]
DOI 10.1093/nar/gku594
Citations Scopus - 33Web of Science - 31
Co-authors Nikki Verrills, Murray Cairns, Christopher Dayas
2014 Sadeqzadeh E, De Bock CE, Wojtalewicz N, Holt JE, Smith ND, Dun MD, et al., 'Furin processing dictates ectodomain shedding of human FAT1 cadherin', Experimental Cell Research, 323 41-55 (2014) [C1]

Fat1 is a single pass transmembrane protein and the largest member of the cadherin superfamily. Mouse knockout models and in vitro studies have suggested that Fat1 influences cell... [more]

Fat1 is a single pass transmembrane protein and the largest member of the cadherin superfamily. Mouse knockout models and in vitro studies have suggested that Fat1 influences cell polarity and motility. Fat1 is also an upstream regulator of the Hippo pathway, at least in lower vertebrates, and hence may play a role in growth control. In previous work we have established that FAT1 cadherin is initially cleaved by proprotein convertases to form a noncovalently linked heterodimer prior to expression on the cell surface. Such processing was not a requirement for cell surface expression, since melanoma cells expressed both unprocessed FAT1 and the heterodimer on the cell surface. Here we further establish that the site 1 (S1) cleavage step to promote FAT1 heterodimerisation is catalysed by furin and we identify the cleavage site utilised. For a number of other transmembrane receptors that undergo heterodimerisation the S1 processing step is thought to occur constitutively but the functional significance of heterodimerisation has been controversial. It has also been generally unclear as to the significance of receptor heterodimerisation with respect to subsequent post-translational proteolysis that often occurs in transmembrane proteins. Exploiting the partial deficiency of FAT1 processing in melanoma cells together with furin-deficient LoVo cells, we manipulated furin expression to demonstrate that only the heterodimer form of FAT1 is subject to cleavage and subsequent release of the extracellular domain. This work establishes S1-processing as a clear functional prerequisite for ectodomain shedding of FAT1 with general implications for the shedding of other transmembrane receptors. © 2014.

DOI 10.1016/j.yexcr.2014.02.012
Citations Scopus - 2Web of Science - 2
Co-authors Janet Holt, Rick Thorne
2014 Hatchwell L, Girkin J, Morten M, Collison A, Mattes J, Foster PS, et al., 'Salmeterol attenuates chemotactic responses in rhinovirus-induced exacerbation of allergic airways disease¿by modulating protein phosphatase 2A', Journal of Allergy and Clinical Immunology, (2014) [C1]

Background: ß-Agonists are used for relief and control of asthma symptoms by reversing bronchoconstriction. They might also have anti-inflammatory properties, but the underpinnin... [more]

Background: ß-Agonists are used for relief and control of asthma symptoms by reversing bronchoconstriction. They might also have anti-inflammatory properties, but the underpinning mechanisms remain poorly understood. Recently, a direct interaction between formoterol and protein phosphatase 2A (PP2A) has been described in¿vitro. Objective: We sought to elucidate the molecular mechanisms by which ß-agonists exert anti-inflammatory effects in allergen-driven and rhinovirus 1B-exacerbated allergic airways disease (AAD). Methods: Mice were sensitized and then challenged with house dust mite to induce AAD while receiving treatment with salmeterol, formoterol, or salbutamol. Mice were also infected with rhinovirus 1B to exacerbate lung inflammation and therapeutically administered salmeterol, dexamethasone, or the PP2A-activating drug (S)-2-amino-4-(4-[heptyloxy]phenyl)-2-methylbutan-1-ol (AAL[S]). Results: Systemic or intranasal administration of salmeterol protected against the development of allergen- and rhinovirus-induced airway hyperreactivity and decreased eosinophil recruitment to the lungs as effectively as dexamethasone. Formoterol and salbutamol also showed anti-inflammatory properties. Salmeterol, but not dexamethasone, increased PP2A activity, which reduced CCL11, CCL20, and CXCL2 expression and reduced levels of phosphorylated extracellular signal-regulated kinase 1 and active nuclear factor ¿B subunits in the lungs. The anti-inflammatory effect of salmeterol was blocked by targeting the catalytic subunit of PP2A with small RNA interference. Conversely, increasing PP2A activity with AAL(S) abolished rhinovirus-induced airway hyperreactivity, eosinophil influx, and CCL11, CCL20, and CXCL2 expression. Salmeterol also directly activated immunoprecipitated PP2A in¿vitro isolated from human airway epithelial cells. Conclusions: Salmeterol exerts anti-inflammatory effects by increasing PP2A activity in AAD and rhinovirus-induced lung inflammation, which might potentially account for some of its clinical benefits. © 2013 American Academy of Allergy, Asthma & Immunology.

DOI 10.1016/j.jaci.2013.11.014
Citations Scopus - 18Web of Science - 16
Co-authors Nikki Verrills, Paul Foster, Joerg Mattes, Adam Collison
2014 Dun MD, Chalkley RJ, Keene S, Bradshaw RA, Hondermarck H, 'Proteomics versus Transcriptomics for the Identification of Cancer Biomarkers: the Case of Brain-derived Metastatic Breast Cancer Cells', MOLECULAR & CELLULAR PROTEOMICS (2014) [E3]
Co-authors Hubert Hondermarck
2014 Dun MD, Kahl RGS, Flanagan H, Cairns MMJ, Smith ND, Enjeti AK, et al., 'IDENTIFICATION OF ONCOGENIC SIGNALLING PATHWAYS IN ACUTE MYELOID LEUKAEMIA (AML) PATIENTS BY PHOSPHOPROTEOMICS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
Co-authors Murray Cairns, Nikki Verrills
2014 De Iuliis GN, Verrills NM, Dun MD, 'IN SILICO ANALYSIS OF THE TARGETS OF SMALL-MOLECULE, ANTI-CANCER COMPOUNDS FOR IMPROVED CANCER THERAPEUTICS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
Co-authors Nikki Verrills, Geoffry DeiuliIs
2014 Gilbert J, Dun MD, De Iuliis GN, McCluskey A, Sakoff JA, 'SELECTIVELY TARGETING BREAST CANCER CELLS VIA CHECKPOINT ACTIVATION', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
Co-authors Adam Mccluskey, Geoffry DeiuliIs, Jennette Sakoff
2013 Smith TB, Dun MD, Smith ND, Curry BJ, Connaughton HS, Aitken RJ, 'The presence of a truncated base excision repair pathway in human spermatozoa that is mediated by OGG1', JOURNAL OF CELL SCIENCE, 126 1488-1497 (2013) [C1]
DOI 10.1242/jcs.121657
Citations Scopus - 38Web of Science - 32
Co-authors Ben Curry, John Aitken
2013 Dun MD, Smith AM, Kahl RGS, Smith ND, Khanna A, Don AS, et al., 'Unraveling the mechanism of action: drugs that activate the tumor suppressor 2A.', CANCER RESEARCH (2013) [E3]
DOI 10.1158/1538-7445.AM2013-2038
Co-authors Nikki Verrills
2012 Dun MD, Anderson AL, Bromfield EG, Asquith KL, Emmett BJ, McLaughlin EA, et al., 'Investigation of the expression and functional significance of the novel mouse sperm protein, a disintegrin and metalloprotease with thrombospondin type 1 motifs number 10 (ADAMTS10)', International Journal of Andrology, 35 572-589 (2012) [C1]
DOI 10.1111/j.1365-2605.2011.01235.x
Citations Scopus - 14Web of Science - 12
Co-authors Brett Nixon, Eileen Mclaughlin, Elizabeth Bromfield, John Aitken
2012 Dun MD, Aitken RJ, Nixon B, 'The role of molecular chaperones in spermatogenesis and the post-testicular maturation of mammalian spermatozoa', Human Reproduction Update, 18 420-435 (2012) [C1]
DOI 10.1093/humupd/dms009
Citations Scopus - 29Web of Science - 25
Co-authors John Aitken, Brett Nixon
2012 Aitken RJ, Nixon B, Redgrove KA, Dun M, Baker MA, 'The molecular origins of defective sperm function', HUMAN REPRODUCTION (2012) [E3]
Co-authors Kate Redgrove, John Aitken, Mark Baker, Brett Nixon
2011 Redgrove KA, Anderson AL, Dun MD, McLaughlin EA, O'Bryan MK, Aitken RJ, Nixon B, 'Involvement of multimeric protein complexes in mediating the capacitation-dependent binding of human spermatozoa to homologous zonae pellucidae', Developmental Biology, 356 460-474 (2011) [C1]
DOI 10.1016/j.ydbio.2011.05.674
Citations Scopus - 36Web of Science - 36
Co-authors Eileen Mclaughlin, Kate Redgrove, John Aitken, Brett Nixon
2011 Dun MD, Smith ND, Baker MA, Lin M, Aitken RJ, Nixon B, 'The chaperonin containing TCP1 complex (CCT/TRiC) is involved in mediating sperm-oocyte interaction', Journal of Biological Chemistry, 286 36875-36887 (2011) [C1]
DOI 10.1074/jbc.m110.188888
Citations Scopus - 45Web of Science - 39
Co-authors Mark Baker, John Aitken, Brett Nixon
2011 Dun MD, Aitken JR, Nixon B, 'The CCT/TRiC Complex Is Involved in Mediating Sperm-Oocyte Interaction', BIOLOGY OF REPRODUCTION (2011) [E3]
Co-authors John Aitken, Brett Nixon
2010 Dun MD, Mitchell LA, Aitken RJ, Nixon B, 'Sperm-zona pellucida interaction: Molecular mechanisms and the potential for contraceptive intervention', Fertility Control, Springer, Berlin 139-178 (2010) [B1]
Citations Scopus - 10
Co-authors Brett Nixon, John Aitken
2010 Dun MD, Aitken RJ, Nixon B, 'The Chaperonin Containing TCP-1 (CCT/TRIC) Multisubunit Complex is Involved in Mediating Sperm-Oocyte Interactions', Reproduction, Fertility and Development (2010) [E3]
Co-authors John Aitken, Brett Nixon
Bromfield EG, Mihalas BP, Dun MD, Aitken RJ, McLaughlin EA, Walters JLH, Nixon B, 'Inhibition of arachidonate 15-lipoxygenase prevents 4-hydroxynonenal-induced protein damage in male germ cells.', Biol Reprod, 96 598-609
DOI 10.1093/biolre/iox005
Co-authors John Aitken, Elizabeth Bromfield, Brett Nixon, Eileen Mclaughlin
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Grants and Funding

Summary

Number of grants 22
Total funding $2,968,139

Click on a grant title below to expand the full details for that specific grant.


20175 grants / $400,381

Anticancer properties of cannabis oil and its individual components$200,000

Funding body: Australian Natural Therapeutics Group Pty Ltd

Funding body Australian Natural Therapeutics Group Pty Ltd
Project Team Doctor Matt Dun
Scheme Research Grant
Role Lead
Funding Start 2017
Funding Finish 2018
GNo G1700581
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Targeting activated signalling and oxidative stress pathways in acute myeloid leukaemia$150,000

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Doctor Matt Dun
Scheme Early Career Fellowship
Role Lead
Funding Start 2017
Funding Finish 2019
GNo G1600806
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

Receptor tyrosine kinase mutations in acute myeloid leukaemia promote PP2A and p53 inhibition through the phosphorylation of SBDS$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Matt Dun, Doctor Nikki Verrills
Scheme Project Grant
Role Lead
Funding Start 2017
Funding Finish 2017
GNo G1700272
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Targeting a tumour suppressor for new cancer therapies $22,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Nikki Verrills, Doctor Matt Dun, Doctor Severine Roselli
Scheme Project Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1700588
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Jennie Thomas Medical Research Travel Grant$3,381

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Mr David Skerrett-Byrne, Professor Phil Hansbro, Doctor Matt Dun
Scheme Jennie Thomas Medical Research Travel Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1701070
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20162 grants / $115,000

Targeting DNA repair for the improved treatment of blood cancers$100,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Matt Dun, Doctor Nikki Verrills
Scheme Project Grant
Role Lead
Funding Start 2016
Funding Finish 2016
GNo G1601127
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Understanding how lung infections in childhood promote the development of chronic lung diseases in later life$15,000

Funding body: Hunter Medical Research Institute (HMRI)

Funding body Hunter Medical Research Institute (HMRI)
Project Team

Doctor Malcolm Starkey, Doctor Matt Dun, Doctor Richard Kim, Professor Phil Hansbro

Scheme Project Grant
Role Investigator
Funding Start 2016
Funding Finish 2016
GNo
Type Of Funding Aust Competitive - Non Commonwealth
Category 1NS
UON N

20155 grants / $1,031,250

High resolution fourier transform mass spectrometry platform for the discovery of novel cancer biomarkers and drug targets using label-free and isobaric-tagged approaches for quantitative proteomics.$500,000

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Professor Xu Dong Zhang, Doctor Matt Dun, Professor Jennifer Martin, Professor Hubert Hondermarck, Laureate Professor John Aitken, Doctor Nikki Verrills, Doctor Pradeep Tanwar, Laureate Professor Rodney Scott, Professor Maria Kavallaris, Dr Darren Saunders
Scheme Research Equipment Grant
Role Investigator
Funding Start 2015
Funding Finish 2016
GNo G1500599
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

Advanced Technical Support for Oncology Single Cell Analysis Technologies$300,000

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Laureate Professor Rodney Scott, Professor Xu Dong Zhang, Professor Hubert Hondermarck, Conjoint Professor Stephen Ackland, Doctor Craig Gedye, Doctor Pradeep Tanwar, Doctor Chen Chen Jiang, Doctor Matt Dun, Professor Paul de Souza, Associate Professor Kevin Spring, Dr Tao Liu
Scheme Research Infrastructure Grants
Role Investigator
Funding Start 2015
Funding Finish 2018
GNo G1500824
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

High resolution fourier transform mass spectrometry platform for the discovery of novel cancer biomarkers and drug targets using label-free and isobaric-tagged approaches for quantitative proteomics.$196,250

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Professor Xu Dong Zhang, Doctor Matt Dun, Professor Jennifer Martin, Professor Hubert Hondermarck, Laureate Professor John Aitken, Doctor Nikki Verrills, Doctor Pradeep Tanwar, Laureate Professor Rodney Scott, Professor Maria Kavallaris, Dr Darren Saunders
Scheme Equipment Grant
Role Investigator
Funding Start 2015
Funding Finish 2015
GNo G1500935
Type Of Funding Internal
Category INTE
UON Y

Identification of better diagnostic tools and new treatment options for children suffering from Shwachman-Diamond Syndrome (SDS)$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Matt Dun, Doctor Nikki Verrills
Scheme Research Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1500757
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Jennie Thomas Medical Research Travel Grant$10,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Matt Dun
Scheme Jennie Thomas Medical Research Travel Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1501429
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20146 grants / $1,289,412

Identifying novel therapeutic targets for the treatment of Acute Myeloid Leukaemia$600,000

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Doctor Matt Dun, Doctor Nikki Verrills, Associate Professor Martin Larsen
Scheme Early Career Fellowship
Role Lead
Funding Start 2014
Funding Finish 2016
GNo G1300952
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

Tetraspanin CD9; more than just an exosome marker - A novel biomarker to target for prostate cancer$400,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Jude Weidenhofer, Doctor Kathryn Skelding, Doctor Matt Dun, Ms Belinda Goldie, Doctor Danielle Bond
Scheme Project Grant
Role Investigator
Funding Start 2014
Funding Finish 2017
GNo G1400921
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Visualisation of microparticles for development of biomarkers and targeted drug delivery mechanisms$125,199

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Associate Professor Christopher Scarlett, Doctor Kathryn Skelding, Doctor Jude Weidenhofer, Doctor Matt Dun, Doctor Kelly Kiejda, Professor Adam McCluskey, Ms Elham Sadeqzadeh, Professor Hubert Hondermarck, Doctor Rick Thorne, Laureate Professor Rodney Scott
Scheme Research Equipment Grant
Role Investigator
Funding Start 2014
Funding Finish 2014
GNo G1400627
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

JuLI Stage $71,674

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Doctor Pradeep Tanwar, Professor Eileen McLaughlin, Professor Robin Callister, Professor Xu Dong Zhang, Professor Murray Cairns, Professor Brett Nixon, Professor Hubert Hondermarck, Associate Professor Phillip Dickson, Doctor Nikki Verrills, Doctor Matt Dun, Doctor Jessie Sutherland, Doctor Janani Kumar, Doctor Jay Horvat, Doctor Susan Hua, Associate Professor Liz Milward, Associate Professor Estelle Sontag, Professor Dirk Van Helden, Doctor Janet Bristow, Doctor Jean-Marie Sontag
Scheme Equipment Grant
Role Investigator
Funding Start 2014
Funding Finish 2014
GNo G1500860
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

Identifying novel therapeutic targets for the treatment of Acute Myeloid Leukaemia$67,539

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Matt Dun, Doctor Nikki Verrills
Scheme Project Grant
Role Lead
Funding Start 2014
Funding Finish 2017
GNo G1301353
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Defining the role of shwachman-bodien diamond syndrome protein (SBDS) in PP2A inhibition in acute myeloid leukaemia (AML).$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Matt Dun, Doctor Nikki Verrills
Scheme Project Grant
Role Lead
Funding Start 2014
Funding Finish 2014
GNo G1301442
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20133 grants / $32,096

Ultra-Low Temperature Cryogenic Freezer$24,596

Funding body: NHMRC (National Health & Medical Research Council)

Proteomics of Cancer$6,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Matt Dun, Doctor Nikki Verrills, Dr Anoop Enjeti
Scheme Project Grant
Role Lead
Funding Start 2013
Funding Finish 2013
GNo G1300054
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

American Association of Cancer Research, Washington Convention Centre Washington DC USA, 6 - 10 April 2012$1,500

Funding body: University of Newcastle - Faculty of Health and Medicine

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Matt Dun
Scheme Travel Grant
Role Lead
Funding Start 2013
Funding Finish 2013
GNo G1201225
Type Of Funding Internal
Category INTE
UON Y

20121 grants / $100,000

Cancer Institute of NSW Hunter Translation Cancer Research Fellowship$100,000

Fellowship to investigate the mechanism of action of novel anti-cancer compounds.

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team

Matthew Dun

Scheme Translational Cancer Research Unit
Role Lead
Funding Start 2012
Funding Finish 2013
GNo
Type Of Funding External
Category EXTE
UON N
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Research Supervision

Number of supervisions

Completed4
Current7

Total current UON EFTSL

PhD2.45

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2017 PhD Application of a Sensitive, Robust and Quantitative Parallel Reaction Monitoring (PRM) Assay for Measurement of Activated Signalling Pathways in Breast Cancers PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2017 PhD Molecular Characterisation of Treatment Resistance in Acute Myeloid Leukaemia. PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2017 PhD A Novel Biomarker and Innovative Therapeutic Strategy for Oesophageal Cancer PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2016 PhD Reduced Expression of Protein Phosphatase 2A Subunit, PPP2R2A and its Role in Breast Cancer PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2015 PhD Identifying novel therapeutic targets for the treatment of Acute Myeloid Leukaemia PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2015 PhD PPP2R2A - A Novel Biomarker and Therapeutic Target for Luminal B Breast Cancer PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2014 PhD Chronic Obstructive Pulmonary Disease (COPD) PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor

Past Supervision

Year Level of Study Research Title Program Supervisor Type
2016 Honours Prostate cancer: Quantification of proNGF by targeted proteomics
Background. Prostate cancer (PCa) is one of the most prevalent cancers in Australia. The PCa serum biomarker prostate specific antigen (PSA) is used for screening, diagnosis and prognosis, but increasing evidence indicates that PSA testing has serious limitations. Not only does it lack specificity (with false positive and negative detections), but it also fails in identifying the most aggressive forms of PCa that require treatment as compared to the indolent forms of the disease. There is therefore an urgent need for new biomarkers to improve the diagnosis and prognosis of PCa. &nbsp;<br />Preliminary data from our lab have identified the precursor of nerve growth factor (proNGF) as a new potential serum biomarker for PCa. ProNGF expression is increased in cancer cells and positively correlates with PCa aggressiveness. In addition, PCa cells secrete proNGF, and by ELISA increased concentration of proNGF were found in the serum of PCa patients, in particular in case of aggressive tumours. These data suggest that proNGF could be a novel serum biomarker for diagnosis and prognosis of PCa. &nbsp;<br />Aims. This project is focused on developing a targeted proteomic assay (in parallel reaction monitoring - PRM) to reliably quantify proNGF in serum samples. The assay will subsequently be applied for the analysis of PCa serum samples. &nbsp;<br />Methods. After in silico trypsin digestion, two tryptic peptides unique to proNGF were selected with molecular mass and charge appropriate for detection in mass spectrometry. We have obtained the corresponding stable isotope labelled (SIL) peptides and we have established all experimental conditions for their detection in the serum and quantification in PRM mass spectrometry. In particular, we have analysed a series of PCa samples (n=40) of different grade and a series of benign prostatic hyperplasia (BPH, n=20). The results were compared with data obtained by ELISA for proNGF in the same samples. &nbsp;<br />Results. 1. An optimised PRM quantification approach was achieved by analysing twoproNGF SIL peptides LQHSLDTALR and SAPAAAIAAR (by direct injection and in complex serum background). 2. Standard curves for both proNGF SIL peptides in complex serum background were generated and performed to normalise inter-run variability of the mass spectrometer. 3. The average quantity of proNGF endogenous peptide LQHSLDTALR in serum samples was 0.021 &plusmn; 0.050 ng/mL, whereas proNGF endogenous peptide SAPAAAIAAR was undetectable. 4. No significant difference of proNGF peptide LQHSLDTALR quantity was found either between BPH and PCa cancer or across BPH group, low-risk PCa (Gleason 6) and high-risk PCa (Gleason 8 &amp; 9). 5. The correlation factor (r) between PRM data for peptide LQHSLDTALR and the ELISA for proNGF was 0.21, indicating a limited correspondence between data obtained by the two methods. <br />Conclusion. We have developed a PRM based assay for quantifying proNGF in biological samples with a very good specificity/sensitivity (picogram/mL level). However, its use to quantify proNGF in the serum of PCa patients needs further improvements and in particular further optimisation in sample preparation, such as albumin depletion and deglycosylation. Such a PRM assay for proNGF could find biomedical applications beyond PCa, as proNGF has recently been reported to be increased in the cerebrospinal fluid of patients with neurodegenerative disease.&nbsp; <br />6
Medical Science, Faculty of Health and Medicine, University of Newcastle Co-Supervisor
2016 Honours Development of a sensitive, robust and quantitative mass spectrometry assay for the measurement of activated signalling pathways in human breast cancers
<p style="text-align:justify;text-justify:inter-ideograph;line-height:150%;"><span lang="EN-US" style="color:windowtext;">Breast cancer is a major national and global health concern. While the overall survival for breast cancer has significantly improved over the past decades, outcomes for patients with triple negative (TNBC) or Luminal B subtype tumuors remains poor. Recent studies have shown that some TNBCs display inactivation of key DNA damage repair (DDR) pathways which renders them hypersensitive to specific DNA damaging chemotherapy. Whether other breast cancer subtypes also have altered DDR pathways is not known, in part because an effective tool for quantifying the activity of DDR pathways is not available. Therefore, we aimed to develop a robust and sensitive assay to quantitate the activity of DDR pathways in breast cancer.</span><span style="color:windowtext;"> Recent studies indicate that </span><span style="color:windowtext;">a targeted proteomics approach, utilising </span><span style="color:windowtext;">quantitative mass spectrometry-based </span><span style="color:windowtext;">parallel reaction monitoring (PRM), may be a useful technique for identification and quantification of such pathways. PRM is a highly selective and specific method for targeted peptide quantification, including peptides with post-translational modifications such as phosphorylation. It is beginning to be implemented for the quantitative study of changes in protein components within cancer cells. Given that cancer associated signalling pathways are regulated by phosphorylation of key protein mediators, we hypothesized that</span><span style="color:windowtext;"> the development of</span><span style="color:windowtext;"> a multiplexed PRM assay for quantitation of key phosphoproteins involved in activated signalling pathways could be a powerful tool for the identification of activated, and potentially &lsquo;druggable&rsquo; pathways in human breast tumours. </span></p><p style="text-align:justify;text-justify:inter-ideograph;line-height:150%;"><span>Sample preparation is the crucial starting point to obtain high-quality mass spectrometry data, therefore a major focus of this thesis was to determine the optimal sample preparation procedure for PRM-based quantitation of phospho-peptides. To do this,</span><span style="color:windowtext;"> the human breast cancer cell line, </span><span lang="EN-US" style="color:windowtext;">BT474, was </span><span style="color:windowtext;">treated +/- bleomycin to induce double stranded DNA breaks (DSBs) and activate DSB repair pathways. Proteins were extracted in either a sodium carbonate buffer or via the commercially available </span><span lang="EN-US">ProteaseMax<sup>TM</sup></span><span style="color:windowtext;"> kit, and enzymatically digested into peptides using trypsin and lysozyme C, and identified by liquid chromatography tandem mass spectrometry (LC-MS/MS). Analysis of the identified peptides demonstrated </span><span lang="EN-US">enhanced tryptic/Lys C digestion efficiency with the sodium carbonate method, and as such this was used for all subsequent experiments. However, phosphorylated peptides only constituted ~1% of the total peptides identified, and the peak intensity for most phospho-peptides was low, making accurate quantitation difficult. Recent studies have shown <a name="OLE_LINK41">enrichment of phosphopeptides</a> using titanium dioxide chromatography (TiO2) significantly increases the number of phosphoproteins identified in discovery MS projects. Whether phospho-peptide enrichment is required for targeted PRM MS approaches however has not been determined. Therefore, a direct comparison of non-enriched versus phospho-peptide enrichment using a range of TiO2 procedures were performed in the BT474 cells. This resulted in high abundance of non-modified peptides in the non-enriched and flow through lysates, while the majority of phosphopeptides were found in TiO2 eluates. The enrichment enabled improved quantitation of specific phosphopeptides by PRM, and thus confirmed that enrichment with at least one TiO2 step was required for quantitative detection of phosphopeptides. </span></p><p style="text-align:justify;text-justify:inter-ideograph;line-height:150%;"><span lang="EN-US">This optimized procedure was then used to quantitate key phosphoproteins involved in growth, survival and DNA damage repair pathways in breast cancer. </span><span style="color:windowtext;">As a positive control we analysed H2AX, a key marker of DSBs, and as expected found increased phosphorylation of pSer139-H2AX in response to bleomycin. We further found increased phosphorylation of </span><span lang="EN-US" style="color:windowtext;">Protein Kinase B (AKT; Thr307 and Ser473), </span><span style="color:windowtext;">checkpoint kinase 2 (CHK2) at Thr386, and the ataxia-telangiectasia mutated (ATM) protein (double phosphorylation at Y175 and S179). In contrast H2AX doubly phosphorylated at S139/Y140, pThr68-CHK2 and pSer367-ATM was reduced. This provides novel insight into the cellular response to DSBs. Importantly, t</span><span lang="EN-US" style="color:windowtext;">his analysis was achieved from average 2 &micro;g of peptides, therefore we believe this assay will be useful for primary patient tissues and hence may be a powerful approach for identifying activated and druggable pathways in human breast tumuors.</span></p>
Medical Science, Faculty of Health and Medicine, University of Newcastle Co-Supervisor
2015 Honours The Role of Reduced Protein Phosphatase 2A Subunit, PPP2R2A (B55α), Expression in Breast Cancer.
&lt;p style="margin-bottom:0cm;margin-bottom:.0001pt;line-height:150%;"&gt;&lt;span style="font-size:12.0pt;line-height:150%;font-family:'Times New Roman',serif;"&gt;Breast Cancer is a disease of global concern, with current treatments lacking selectivity and not showing a response in many patients. Patients with luminal-B like breast cancers in particular have shown reduced sensitivity to endocrine therapies, and have a more aggressive phenotype similar to Triple Negative breast tumours and worse prognosis than luminal-A like breast tumours. A marker and potential therapeutic target was thus need to distinguish these particular patients, as current methods of classification have been shown to be ineffective, especially in distinguishing between luminal-A and B tumours. Recent studies have shown that reduced expression of the &lt;em&gt;PPP2R2A&lt;/em&gt; gene, encoding the B55a subunit of Protein Phosphatase 2a (PP2A), may be such a marker, with highly reduced expression in a majority of luminal-B tumours studied. Reduced expression of this subunit has been found to impair the DNA damage Homologous Recombination (HR) repair pathway in HeLa cervical cancer cells, and furthermore, reduced B55a expression and impaired DNA damage repair in lung carcinomas was found to sensitise these cells to the PARP inhibitor (PARPi) ABT888, through synthetic lethality. &lt;/span&gt;&lt;/p&gt;&lt;p style="margin-bottom:0cm;margin-bottom:.0001pt;line-height:150%;"&gt;&lt;span style="font-size:12.0pt;line-height:150%;font-family:'Times New Roman',serif;"&gt;&lt;/span&gt;&lt;/p&gt;&lt;p style="margin-bottom:0cm;margin-bottom:.0001pt;line-height:150%;"&gt;&lt;span style="font-size:12.0pt;line-height:150%;font-family:'Times New Roman',serif;"&gt;This study therefore investigated the role reduced B55a expression may play in breast cancer cells, to determine whether this is a potential treatment target for low-B55a expressing luminal-B tumours. It was first hypothesised, based on past studies, that reduced B55a expression in breast cancer cells would impair their DNA damage repair pathways. To investigate this, two B55a knockdown models were created in both&lt;span&gt;&amp;nbsp; &lt;/span&gt;MCF7 and ZR751breast cancer cell lines, as well as a control cell line to compare back to. DNA repair efficiency was then examined by inducing DNA damage via Bleomycin and analysing expression of important HR repair proteins. Changes in expression and phosphorylation mediated activation of many of these proteins, as well as prolonged increase of ɣH2AX (marker for DSBs) in B55a-low cells compared to control cells supported the hypothesis that DN repair was impaired in these B55a-low cells. &lt;/span&gt;&lt;/p&gt;&lt;p style="margin-bottom:0cm;margin-bottom:.0001pt;line-height:150%;"&gt;&lt;span style="font-size:12.0pt;line-height:150%;font-family:'Times New Roman',serif;"&gt;&lt;/span&gt;&lt;/p&gt;&lt;p style="margin-bottom:0cm;margin-bottom:.0001pt;line-height:150%;"&gt;&lt;span style="font-size:12.0pt;line-height:150%;font-family:'Times New Roman',serif;"&gt;It was then hypothesised that impaired DNA repair in B55a-low breast cancer cells would further sensitise these cells to DNA damaging agents. To examine this, B55a knockdown and control cells were treated with DNA damaging agents (ɣ-irradiation, Bleomycin, Cisplatin, ABT888), at various doses. However the hypothesis was not supported, as there was no significantly increased sensitivity to these agents in B55a-low cells compared to the control cells.&lt;/span&gt;&lt;/p&gt;&lt;p style="margin-bottom:0cm;margin-bottom:.0001pt;line-height:150%;"&gt;&lt;span style="font-size:12.0pt;line-height:150%;font-family:'Times New Roman',serif;"&gt;&lt;/span&gt;&lt;/p&gt;&lt;span style="font-size:12.0pt;line-height:107%;font-family:'Times New Roman',serif;"&gt;Therefore while this study suggests that DNA repair may be altered and impaired in B55a-low breast cancer cells (and hence luminal-B tumours), this finding is currently not translatable to use as a potential treatment target for patient with luminal-B tumours. However future studies using altered dosage and time course of DNA damaging agents may find a heightened sensitivity of B55a-low breast cancer cell lines, allowing for specific personalised treatment of patients with aggressive luminal-B tumours, using therapeutics that already currently available. &lt;/span&gt;
Medical Science, Faculty of Health and Medicine, University of Newcastle Co-Supervisor
2014 Honours Investigation of the function of tetraspanins CD9 and CD151 on prostate exosomes
Exosomes are nanosized, membranous vesicles secreted by most cells that have been shown to be important for cellular communication. Whilst most research into exosomes has focussed on their function in a diseased state, such as cancer, their role in normal cellular functioning has not been thoroughly investigated. Tetraspanins are a family of transmembrane proteins, including CD9 and CD151, that are abundantly expressed on exosomes, however, their function within exosomes is yet to be fully elucidated. CD9 and CD151 have opposing roles in many solid tumours, including prostate, where CD9 is typically downregulated and CD151 is typically upregulated and both being indicative of poor prognosis. Therefore, this study was designed to investigate the effects that altered CD9 and CD151 in exosomes have on a normal cellular population, and whether alteration of these tetraspanins can make a normal cell more metastatic.&lt;br /&gt;CD9 and CD151 expression was altered in a normal, non-tumourigenic cell line (RWPE1) to express either low CD9 (CD9 low) or high CD151 (CD151 high). Western blot and flow cytometry were used to confirm that these cell lines displayed altered expression of CD9 and CD151 and that their control lines (Scram and Zeo respectively) displayed similar expression to RWPE1 cells. An invasive and metastatic derivative cell line of RWPE1 cells, WPE1-NB26, was used as a tumourigenic control. Exosomes from these cells were then assessed for their ability to attach to and internalise into RWPE1 cells before being used as treatments for RWPE1 cells in a range of functional assays, including adhesion, proliferation, migration and invasion, to assess whether the altered exosomal expression of CD9 and CD151 can influence these cellular behaviours. Exosomes from RWPE1, CD9 low, CD151 high and WPE1-NB26 cell lines were also analysed using a quantitative mass spectroscopy approach to determine changes in their proteome.&lt;br /&gt;There were no differences observed between exosome populations in regards to attachment and internalisation into RWPE1 cells. Treating RWPE1 cells with exosomes also showed no difference in the proliferation of RWPE1 cells over a 72&lt;br /&gt;6&lt;br /&gt;hour period. RWPE1 cell adhesion to Collagen-IV, Fibronectin and Laminin 1 was assessed and revealed no difference for CD9 low exosome treated cells, however, an increase in adhesion was seen with the CD151 high exosome treated cells at 1 (p = 0.0023) and 4 hours (p = 0.0279). Only CD151 high exosome treated RWPE1 cells showed an increase in migration at 20 (p = 0.0186), 24 (p = 0.0068) and 30 hours (p = 0.0038), however no differences were observed in an invasion assay. Proteomic analysis of exosomes revealed that there were 101 proteins with a greater than 2 fold increase and 18 proteins with a greater than 2 fold decrease in abundance compared to RWPE1 exosomes.&lt;br /&gt;The results of this study suggest that alterations of CD9 and CD151 in exosomes have only limited functional effects on a normal cellular population. This study also identified that altering the expression of CD9 and CD151 in exosomes affects their entire proteome. Further characterisation of the effects of CD9 and CD151 expression in exosomes needs to be performed, utilising a panel of tumourigenic cell lines. Therefore due to the alterations on cellular function upon the addition of CD151 high exosomes, it suggests that modified exosomes could represent a therapeutic strategy for prostate cancer.
Medical Science, Faculty of Health and Medicine, University of Newcastle Co-Supervisor
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News

Dr Matthew Dun

Strengthening the defence against Leukaemia

September 25, 2017

Research from the University of Newcastle (UON) has revealed a more targeted way of treating T-cell acute lymphoblastic leukaemia (T-ALL), an aggressive type of cancer typically prevalent in children and adolescents.

PHD Scholarship: Anticancer Properties of Low-THC containing Medicinal Cannabis

September 25, 2017

There is an opportunity within the UON School of Biomedical Sciences and Pharmacy in the Faculty of Health and Medicine for a PhD research student to study the anticancer properties of Low-THC containing Medicinal Cannabis, under the supervision of Dr Matthew Dun and Dr Mengna Chi.

Matt Dun

$1.5m to Newcastle researchers to unlock cancer secrets

February 21, 2014

Three University of Newcastle cancer researchers have been recognised with Cancer Institute NSW Early Career Fellowships, totalling more than $1.5 million.

Dr Matt Dun

Position

Cancer Institute NSW EC Fellow
Molecular Oncology
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Contact Details

Email matt.dun@newcastle.edu.au
Phone (02) 4921 5693
Fax (02) 4921 6903

Office

Room LS3.33
Building Life Sciences Building
Location Callaghan
University Drive
Callaghan, NSW 2308
Australia
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