Dr Craig Gedye

Dr Craig Gedye

Conjoint Senior Lecturer

School of Biomedical Sciences and Pharmacy

Divide and conquer

Proving cancer to be as unique as its sufferers, Dr Craig Gedye’s fastidious, thoughtful and well-executed scientific research is pursuing a tailored approach to patient care, rather than a ‘one-size-fits-none’ mentality.

Cancer, according to Dr Craig Gedye, is like a jungle - dense, confusing, and, at times, terrifying. No two cancers are exactly alike, and this represents the greatest unmet challenge for patients, their doctors and scientists.

“The challenges drive the themes of my research; the complexity and heterogeneity of cancers,” Craig shares.

“One of the most frustrating things in the world is watching a treatment help one patient and then watching it fail completely in another.”

“It’s far from ideal but unfortunately it’s a reality – cancer is different in every person.”

Craig believes that identifying individuals who won’t benefit from particular therapies is just as important as identifying those who will. With no point offering a treatment that will fail, the solution is to find novel opportunities for specific patients.

Spanning the “whole breadth” of tumour biology, Craig’s efforts are concentrated on six, “very challenging” types of cancer.

“I treat people suffering from melanomas, as well as testicular, kidney, prostate, bladder and brain cancers,” he reveals.

“They’re tricky cancers and very hard to treat, but I think they’re the ones that have the greatest gains to be made.”

Because of the focus of his work, Craig is also an “impromptu spokesperson” for “biobanking”.

“When you have a cancer operation, surgeons cut out the tumour and pathologists put it under the microscope to determine its type, aggressiveness and what ought to be done next,” he explains.

“Once this procedure is finished, anything left over is usually discarded.”

“But this is a terrible waste; any of these peoples’ cancers might teach us about that kind of cancer and the best treatment.”

Adopting the simple saying ‘waste not, want not,’ the multitasking scientist is helping to establish systems for its set up and funding in the Hunter region.

“We want to save samples from every patient’s cancer for research, because I believe they’re extremely valuable,” he affirms.

Skin sins and scientific stumbles

Craig’s research career began in 1990, when he undertook a summer studentship between the University of Canterbury and University of Otago in his native New Zealand.

“After doing medicine,” he comments, “I went back to science and started a PhD in the last semester of my oncology training in 2004.”

Comically labelled as “the best of times and the worst of times,” Craig’s candidature sought to tease out notions of complexity and heterogeneity in melanoma. Under the assumption that different cancer cells are more pivotal than others, his findings were “provocative” but “not conclusive.”

“Normally you have to wait your whole professional life to be proven wrong, but I was humbled just six weeks after submitting my thesis,” he laughs.

“It’s a critical lesson – you must listen to the data.”

“I was forced to let go of an idea I’d been nurturing for three and a half years.”

Proceed with caution

Craig relocated to Canada in 2008, undertaking a Postdoctoral Fellowship at the University of Toronto and Princess Margaret Cancer Centre. Aiming to expand upon his original thesis, he went looking for complexity in kidney cancer – this time forewarned and forearmed.

“We thought cancers might be like beehives,” he says. “If you kill off the worker bees, it doesn’t matter because the queen bee will just make more, so in order to kill a person’s cancer, you need to go straight to the source and eliminate her.”

“Sadly though, this concept, called the cancer stem cell hypothesis, proved to be too nice and neat.”

Testing this hypothesis at each step, Craig spent the first half of his overseas stint exploring “problematic experimental biases” in the idea of cancer stem cells.

“If you look at the idea of a queen bee cancer cell through the lens of all these overlooked biases and problems, the whole idea unravels.” This work has recently been published in Scientific Reports.

While at the Princess Margaret Cancer Centre he simultaneously undertook a Clinical Fellowship in melanoma.

“I was on the ground as the new class of cancer drugs, the checkpoint immunotherapy antibodies, came into the clinic,” he recalls.

“It was mind-blowing to see them work so dramatically in some patients.”

Detect and inspect

Craig moved to Australia in February 2014, signing on to pursue a number of related research interests at the Calvary Mater Newcastle, University of Newcastle and Hunter Medical Research Institute. His main mission is to cement a technical, nuanced understanding of kidney cancer.

“It’s a different disease than most might otherwise imagine,” the School of Biomedical Sciences and Pharmacy affiliate acknowledges.

“To go back a bit, in the first few days of foetal development, the embryo will fold itself into three layers of cells – the endoderm, mesoderm and ectoderm.”

“The first layer becomes the surfaces of our body, such as skin and the lining of the gut, the second forms our internal structure like muscle and bone, and the third is our nerves and wiring.”

“Cancers often revert back to the behaviours of these very primitive cells, so while cancers are found in different parts of the body, they will have originated from one of the three layers, and cancer behaviour is loosely related to these layers too.”

“For example, breast, lung, bowel and ovary cancers all grow from the surface layer (the endoderm); and although they have clear differences, these cancers look a bit like each other and respond to similar chemotherapy treatments.”

Once considered a cancer of the surface layer (the endoderm), Craig’s analyses are suggesting kidney cancer is “better thought of” as a cancer from the middle layer and therefore mesenchymal cancer, or a sarcoma. He is similarly arguing that patients with the commonest form of kidney cancer, could benefit from different courses of treatment.

“Clear cell kidney cancers contain ‘skinny’ mesenchymal cells that hunt for new blood supplies, and ‘fat’ cells that are full of lipids that batten down the hatches to survive,” he elaborates.

“I’m wanting to find out what drives each kidney cancer cell to perform each way.”

“If we can somehow exploit the control of this process, we can look to offer up new ideas for treatment.”

Old, new and used-but-still-useful

In the not-so-distant future, Craig is planning to take a closer look at the 3,500 drugs that are currently licenced for use in humans.

“Where kidney cancer is concerned, we’ll see if any come up as useful treatments that control if we get more fat cells and less skinny cells,” he affirms.

“It might then be possible to write a clinical trial to “repurpose” medications.”

“We are expanding the clinical trials we offer patients at Medical Oncology Research at the Calvary Mater Newcastle, including trials for kidney and brain cancers.”

“It’s hard to start our own clinical trials but in my work with the ANZUP Cancer Trials Group, we are able to work with doctors across the country to devise new treatment ideas.”

“Cancer is tough. But it’s a privilege to be able to pit ourselves against cancer in the lab and in the clinic”.

Craig Gedye

Divide and conquer

Proving cancer to be as unique as its sufferers, Dr Craig Gedye’s fastidious, thoughtful and well-executed scientific research is pursuing a tailored approach t

Read more

Career Summary

Biography

I am a physician/scientist, dual trained as a medical oncologist and as a basic science cancer researcher. I am inspired by working for patients with melanoma, brain, prostate, bladder and kidney cancers at the Calvary Mater Newcastle. I undertake clinical, translational and basic cancer research at the University of Newcastle/HMRI which is supported by the Hunter Cancer Research Alliance.

My research focuses on complexity in cancer, with a particular interest in understanding "intratumoural heterogeneity". In every patient, every cancer cell is a bit different to every other cancer cell. Some cancer cells seem to be able to spread and cause trouble; others are less aggressive. What determines these differences? Can we exploit them to target cancer cells that are behaving differently?

Between different patients, cancers that come from the same organ can behave completely differently, and treatments that help one patient fail the next. Why is this? Why does a cancer lie dormant, then come back? Why does treatment not work in some patients, or work for a time, then fail?

These questions are incredibly important, as we seek to find the treatments that work best for each individual patient. We will do this by using existing treatments more cleverly, as well as by discovering new treatments.

Qualifications

  • PhD (Medicine Denistry & Health Sciences), University of Melbourne
  • Bachelor of Science (Chemistry)(Honours), University of Canterbury - New Zealand
  • Bachelor of Medicine, Bachelor of Surgery, University of Otago - New Zealand

Keywords

  • Biobanking
  • Cancer
  • Cancer biology
  • Cancer immunotherapy
  • Cancer stem cells
  • Cell biology
  • Clinical trials
  • Epigenetic heterogeneity
  • Epithelial-mesenchymal transition
  • Glioblastoma
  • Medical oncology
  • Melanoma
  • Phenotypic plasticity
  • Prostate cancer
  • Renal cell carcinoma

Fields of Research

Code Description Percentage
111204 Cancer Therapy (excl. Chemotherapy and Radiation Therapy) 25
111201 Cancer Cell Biology 50
111209 Solid Tumours 25

Professional Experience

Professional appointment

Dates Title Organisation / Department
28/05/2016 - 30/11/2017 Conjoint Senior Lecturer The University of Newcastle - Faculty of Health and Medicine
Australia
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Publications

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


Journal article (42 outputs)

Year Citation Altmetrics Link
2017 Rowe CW, Paul JW, Gedye C, Tolosa JM, Bendinelli C, McGrath S, Smith R, 'Targeting the TSH receptor in thyroid cancer.', Endocr Relat Cancer, 24 R191-R202 (2017)
DOI 10.1530/ERC-17-0010
Co-authors Roger Smith, Jonathan Paul, Christopher W Rowe Uon
2017 Day F, Kumar M, Fenton L, Gedye C, 'Durable Response of Metastatic Squamous Cell Carcinoma of the Skin to Ipilimumab Immunotherapy', JOURNAL OF IMMUNOTHERAPY, 40 36-38 (2017)
Citations Web of Science - 1
2017 Day F, Kumar M, Fenton L, Gedye C, 'Durable Response of Metastatic Squamous Cell Carcinoma of the Skin to Ipilimumab Immunotherapy', Journal of Immunotherapy, 40 36-38 (2017)

© 2016 Wolters Kluwer Health, Inc. All rights reserved. A 72-year-old male patient was receiving second-line chemotherapy for metastatic squamous cell carcinoma of the skin (SCCS... [more]

© 2016 Wolters Kluwer Health, Inc. All rights reserved. A 72-year-old male patient was receiving second-line chemotherapy for metastatic squamous cell carcinoma of the skin (SCCS) when he was diagnosed with concurrent metastatic melanoma (BRAF G469E mutant). Chemotherapy was ceased and he was treated with 4 cycles of ipilimumab immunotherapy. The patient experienced clinical benefit and durable remission in both malignancies and remains free of cancer progression 8 months after the last cycle of ipilimumab. Response of SCCS to ipilimumab has not been previously described, however this case and recent reports of pembrolizumab efficacy confirm the critical role of the immune system in SCCS pathogenesis and suggest further exploration of checkpoint immunotherapy for the treatment of this disease.

Citations Scopus - 1
2017 Chevrier S, Levine JH, Zanotelli VRT, Silina K, Schulz D, Bacac M, et al., 'An Immune Atlas of Clear Cell Renal Cell Carcinoma', Cell, 169 736-749.e18 (2017) [C1]

© 2017 The Author(s) Immune cells in the tumor microenvironment modulate cancer progression and are attractive therapeutic targets. Macrophages and T¿cells are key components of... [more]

© 2017 The Author(s) Immune cells in the tumor microenvironment modulate cancer progression and are attractive therapeutic targets. Macrophages and T¿cells are key components of the microenvironment, yet their phenotypes and relationships in this ecosystem and to clinical outcomes are ill defined. We used mass cytometry with extensive antibody panels to perform in-depth immune profiling of samples from 73 clear cell renal cell carcinoma (ccRCC) patients and five healthy controls. In 3.5 million measured cells, we identified 17 tumor-associated macrophage phenotypes, 22 T¿cell phenotypes, and a distinct immune composition correlated with progression-free survival, thereby presenting an in-depth human atlas of the immune tumor microenvironment in this disease. This study revealed potential biomarkers and targets for immunotherapy development and validated tools that can be used for immune profiling of other tumor types.

DOI 10.1016/j.cell.2017.04.016
Citations Scopus - 10Web of Science - 3
2017 Day F, Kumar M, Fenton L, Gedye C, 'Durable Response of Metastatic Squamous Cell Carcinoma of the Skin to Ipilimumab Immunotherapy', Journal of Immunotherapy, 40 36-38 (2017)

© 2016 Wolters Kluwer Health, Inc. All rights reserved. A 72-year-old male patient was receiving second-line chemotherapy for metastatic squamous cell carcinoma of the skin (SCCS... [more]

© 2016 Wolters Kluwer Health, Inc. All rights reserved. A 72-year-old male patient was receiving second-line chemotherapy for metastatic squamous cell carcinoma of the skin (SCCS) when he was diagnosed with concurrent metastatic melanoma (BRAF G469E mutant). Chemotherapy was ceased and he was treated with 4 cycles of ipilimumab immunotherapy. The patient experienced clinical benefit and durable remission in both malignancies and remains free of cancer progression 8 months after the last cycle of ipilimumab. Response of SCCS to ipilimumab has not been previously described, however this case and recent reports of pembrolizumab efficacy confirm the critical role of the immune system in SCCS pathogenesis and suggest further exploration of checkpoint immunotherapy for the treatment of this disease.

Citations Scopus - 1
2017 Gedye C, Brook N, 'ANZUP MDT Masterclass Convenor Welcome', Asia-Pacific Journal of Clinical Oncology, 13 5 (2017)
DOI 10.1111/ajco.12708
2016 Khoja L, Atenafu EG, Ye Q, Gedye C, Chappell M, Hogg D, et al., 'Real-world efficacy, toxicity and clinical management of ipilimumab treatment in metastatic melanoma', Oncology Letters, 11 1581-1585 (2016) [C1]

© 2016, Spandidos Publications. All rights reserved. Approved by the Food and Drug Administration in 2011, the anti-cytotoxic T-lymphocyte-associated protein 4 checkpoint inhibit... [more]

© 2016, Spandidos Publications. All rights reserved. Approved by the Food and Drug Administration in 2011, the anti-cytotoxic T-lymphocyte-associated protein 4 checkpoint inhibitor ipilimumab has delivered a survival benefit of =3 years in a subset of metastatic melanoma patients. After participating in the registration trial, patients were treated with this agent in routine practice. Toxicity and efficacy of agents in ¿real world¿ settings may differ from trials. The present study aimed to evaluate, with respect to toxicity and outcome, all patients treated with ipilimumab to date at the Princess Margaret Hospital (Toronto, Canada). Patients treated with ipilimumab between 2008 and 2013 were identified, and patient characteristics (age, gender, tumour burden, oncogenic mutation status, number of treatments received and toxicities from treatment) were collected. Progression-free survival (PFS) and overall survival (OS) were calculated from the commencement of ipilimumab treatment. Associations between clinical characteristics and outcome or toxicity were assessed. Between 2008 and 2013, 129 patients with metastatic cutaneous melanoma were treated. Since, during this period, ipilimumab was approved in the second line setting, ipilimumab was delivered in the second or subsequent line in all patients, and 70% did not receive any further anticancer therapy. Immune-related toxicities were observed, the onset of which varied from 1 to 162 days. The majority resolved within 6 weeks of the final treatment, with the exception of endocrinopathies and bowel related toxicity. The median PFS and OS were 2.83 and 8.44 months, respectively. No pre-treatment factor independently predicted toxicity. The number of infusions (4 vs. =3) and presence of toxicity were significantly associated with superior survival. The onset of toxicity secondary to ipilimumab could occur later than previously reported. Toxicities were manageable, but required long-term vigilance.

DOI 10.3892/ol.2015.4069
Citations Scopus - 7Web of Science - 7
2016 Gedye C, Sirskyj D, Lobo NC, Meens J, Hyatt E, Robinette M, et al., 'Cancer stem cells are underestimated by standard experimental methods in clear cell renal cell carcinoma', Scientific Reports, 6 (2016) [C1]

Rare cancer stem cells (CSC) are proposed to be responsible for tumour propagation and re-initiation and are functionally defined by identifying tumour-initiating cells (TICs) usi... [more]

Rare cancer stem cells (CSC) are proposed to be responsible for tumour propagation and re-initiation and are functionally defined by identifying tumour-initiating cells (TICs) using the xenotransplantation limiting dilution assay (LDA). While TICs in clear cell renal cell carcinoma (ccRCC) appeared rare in NOD/SCID/IL2R¿ 3 -/- (NSG) mice, xenografts formed more efficiently from small tumour fragments, indicating the LDA underestimated ccRCC TIC frequency. Mechanistic interrogation of the LDA identified multiple steps that influence ccRCC TIC quantitation. For example, tissue disaggregation destroys most ccRCC cells, common assays significantly overestimate tumour cell viability, and microenvironmental supplementation with human extracellular factors or pharmacological inhibition of anoikis increase clonogenicity and tumourigenicity of ccRCC cell lines and primary tumour cells. Identification of these previously uncharacterized concerns that cumulatively lead to substantial underestimation of TICs in ccRCC provides a framework for development of more accurate TIC assays in the future, both for this disease and for other cancers.

DOI 10.1038/srep25220
Citations Scopus - 4Web of Science - 4
2016 Gedye C, Fleming J, 'Forsaking cures for cancer: why are we discarding the tumour biospecimens of most patients?', MEDICAL JOURNAL OF AUSTRALIA, 204 297-298 (2016) [C1]
DOI 10.5694/mja15.00961
Citations Web of Science - 2
2016 Chia PL, Gedye C, Boutros PC, Wheatley-Price P, John T, 'Current and Evolving Methods to Visualize Biological Data in Cancer Research', JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 108 (2016) [C1]
DOI 10.1093/jnci/djw031
2016 Lobo NC, Gedye C, Apostoli AJ, Brown KR, Paterson J, Stickle N, et al., 'Efficient generation of patient-matched malignant and normal primary cell cultures from clear cell renal cell carcinoma patients: Clinically relevant models for research and personalized medicine', BMC Cancer, 16 (2016) [C1]
DOI 10.1186/s12885-016-2539-z
Citations Scopus - 1Web of Science - 1
2016 Gedye C, Cardwell T, Dimopoulos N, Tan BS, Jackson H, Svobodová S, et al., 'Mycoplasma Infection Alters Cancer Stem Cell Properties in Vitro', Stem Cell Reviews and Reports, 12 156-161 (2016) [C1]

© 2015, Springer Science+Business Media New York. Cancer cell lines can be useful to model cancer stem cells. Infection with Mycoplasma species is an insidious problem in mammali... [more]

© 2015, Springer Science+Business Media New York. Cancer cell lines can be useful to model cancer stem cells. Infection with Mycoplasma species is an insidious problem in mammalian cell culture. While investigating stem-like properties in early passage melanoma cell lines, we noted poorly reproducible results from an aliquot of a cell line that was later found to be infected with Mycoplasma hyorhinis. Deliberate infection of other early passage melanoma cell lines aliquots induced variable and unpredictable effects on expression of putative cancer stem cell markers, clonogenicity, proliferation and global gene expression. Cell lines established in stem cell media (SCM) were equally susceptible. Mycoplasma status is rarely reported in publications using cultured cells to study the cancer stem cell hypothesis. Our work highlights the importance of surveillance for Mycoplasma infection while using any cultured cells to interrogate tumor heterogeneity.

DOI 10.1007/s12015-015-9630-8
2016 Khoja L, Kibiro M, Metser U, Gedye C, Hogg D, Butler MO, et al., 'Patterns of response to anti-PD-1 treatment: An exploratory comparison of four radiological response criteria and associations with overall survival in metastatic melanoma patients', British Journal of Cancer, 115 1186-1192 (2016) [C1]

© 2016 Cancer Research UK. Background:Radiological assessment of response to checkpoint inhibitors remains imperfect. We evaluated individual lesion and inter-patient response by... [more]

© 2016 Cancer Research UK. Background:Radiological assessment of response to checkpoint inhibitors remains imperfect. We evaluated individual lesion and inter-patient response by response evaluation (RECIST) 1.1, immune-related response criteria (irRC), CHOI and modified CHOI (mCHOI) and correlated response with overall survival (OS).Methods:Thirty-seven patients with 567 measurable lesions treated with pembrolizumab in the Keynote 001 trial were studied. Association of response with OS was determined.Results:Response varied according to site; lung lesions had the highest rate of complete response (69 out of 163 (42%) vs other sites 71 out of 404 (18%), P < 0.0001). Delayed response post first scan was seen in 2 out of 37 (5%) deemed progressive (PD) by RECIST and 2 out of 14 (14%) deemed PD by irRC. Modified CHOI criteria showed response of 38% (14 out of 37). Change in tumour size and density on first follow-up assessment was associated with OS with each 1000 mm 2 increase in tumour size from baseline increasing the hazard of dying by 25.9% (HR=1.259, (95% CI=1.116-1.420), P=0.0002). Similarly, each 20HU increase in density increased the HR by 15% (HR=1.15, (95% CI 1.045-1.260), P=0.004). Response defined by any criteria had superior OS (CHOI P=0.0084; mCHOI P=0.0183; irRC P < 0.0001 and RECIST P=0.0003).Conclusions:Response by any criterion was prognostic. Novel patterns of response and changes on treatment in tumour density suggest complex anti-tumour responses to immunotherapy.

DOI 10.1038/bjc.2016.308
Citations Scopus - 4Web of Science - 5
2015 Gedye C, Boyle FM, 'Optimising treatment for Australian melanoma patients can save taxpayers millions of dollars annually', The Medical journal of Australia, 202 130 (2015) [C3]
Citations Scopus - 2Web of Science - 2
2015 Gedye C, van der Westhuizen A, John T, 'Checkpoint immunotherapy for cancer: superior survival, unaccustomed toxicities.', Intern Med J, 45 696-701 (2015) [C1]
DOI 10.1111/imj.12653
Citations Scopus - 4Web of Science - 4
2014 Gedye CA, Hussain A, Paterson J, Smrke A, Saini H, Meyer M, 'Correction: Cell surface profiling using high-throughput flow cytometry: A platform for biomarker discovery and analysis of cellular heterogeneity', PLoS ONE, 9 (2014)
DOI 10.1371/journal.pone.0114354
Citations Scopus - 3
2014 Gedye C, Hogg D, Butler M, Joshua AM, 'New treatments for metastatic melanoma', CANADIAN MEDICAL ASSOCIATION JOURNAL, 186 754-760 (2014)
DOI 10.1503/cmaj.130989
Citations Scopus - 6Web of Science - 4
2014 Naert K, Al Habeeb A, Gedye C, Ghazarian D, 'Targeted therapy in melanoma: The era of personalized medicine', Diagnostic Histopathology, (2014) [C1]

Malignant melanoma is the most aggressive of all cutaneous tumours, with over 76, 000 new cases and 9700 deaths estimated for 2014 in the United States.1 In Canada, both the incid... [more]

Malignant melanoma is the most aggressive of all cutaneous tumours, with over 76, 000 new cases and 9700 deaths estimated for 2014 in the United States.1 In Canada, both the incidence and mortality of melanoma are increasing, with a risk of developing melanoma being 1 in 59 for men and 1 in 73 for women.2 The incidence of melanoma is higher in Australia, with a risk of 1 in 14 for males and 1 in 23 for females to age 85 reported for 2009.3 Although early melanoma can be managed surgically, until recently there have been few advances in the treatment of advanced melanoma. However, with the introduction of molecular targeted therapies, the landscape of melanoma treatment has changed dramatically in the past five years, resulting in improved survival rates for patients with metastatic disease. In this review, we will discuss the molecular basis and implementation for some of these novel treatments with particular emphasis on BRAF and BRAF inhibitors.

DOI 10.1016/j.mpdhp.2014.10.001
Citations Scopus - 1
2014 Gedye CA, Hussain A, Paterson J, Smrke A, Saini H, Sirskyj D, et al., 'Cell Surface Profiling Using High-Throughput Flow Cytometry: A Platform for Biomarker Discovery and Analysis of Cellular Heterogeneity', PLOS ONE, 9 (2014)
DOI 10.1371/journal.pone.0105602
Citations Scopus - 9Web of Science - 11
2013 Sompallae R, Hofmann O, Maher CA, Gedye C, Behren A, Vitezic M, et al., 'A comprehensive promoter landscape identifies a novel promoter for CD

PROM1 is the gene encoding prominin-1 or CD 133 , an important cell surface marker for the isolation of both normal and cancer stem cells. PROM1 transcripts initiate at a range of... [more]

PROM1 is the gene encoding prominin-1 or CD 133 , an important cell surface marker for the isolation of both normal and cancer stem cells. PROM1 transcripts initiate at a range of transcription start sites (TSS) associated with distinct tissue and cancer expression profiles. Using high resolution Cap Analysis of Gene Expression (CAGE) sequencing we characterize TSS utilization across a broad range of normal and developmental tissues. We identify a novel proximal promoter (P6) within CD 133 + melanoma cell lines and stem cells. Additional exon array sampling finds P6 to be active in populations enriched for mesenchyme, neural stem cells and within CD 133 + enriched Ewing sarcomas. The P6 promoter is enriched with respect to previously characterized PROM1 promoters for a HMGI/Y (HMGA1) family transcription factor binding site motif and exhibits different epigenetic modifications relative to the canonical promoter region of PROM1.© 2013 Sompallae, Hofmann, Maher, Gedye, Behren, Vitezic, Daub, Devalle, Caballero, Carninci, Hayashizaki, Lawlor, Cebon and Hide.

DOI 10.3389/fgene.2013.00209
Citations Scopus - 5
2013 Kurban G, Gedye C, Morales C, Yousef GM, Almatar A, Jewett MAS, 'DIAGNOSIS AND TREATMENT OF SMALL RENAL MASSES: THE ROLE FOR MOLECULAR BIOLOGY', ARCHIVOS ESPANOLES DE UROLOGIA, 66 505-516 (2013) [C1]
Citations Scopus - 5Web of Science - 3
2013 Gedye C, Ailles L, 'Isolation and characterization of cancer stem cells in vitro', Methods in Molecular Biology, 946 181-204 (2013) [B2]

The cancer stem cell hypothesis is an appealing concept to account for intratumoral heterogeneity and the observation that systemic metastasis and treatment failure are often asso... [more]

The cancer stem cell hypothesis is an appealing concept to account for intratumoral heterogeneity and the observation that systemic metastasis and treatment failure are often associated with the survival of a small number of cancer cells. Whilst in vivo evidence forms the foundation of this concept, in vitro methods and reagents are attractive as they offer opportunities to perform experiments that are not possible in an animal model. While there is abundant evidence that existing cancer cell lines are not reliable models of tumor heterogeneity, recent advances based on well validated novel cancer cell lines established de novo in defined serum-free media are encouraging, particularly in the study of glioblastoma multiforme. In this chapter we wish to broadly outline the process of establishing, characterizing, and managing novel cancer cell lines in defined serum-free media, and discuss the limitations and potential opportunities that may arise from these model systems. © 2013 Springer Science+Business Media, LLC.

DOI 10.1007/978-1-62703-128-8-12
Citations Scopus - 7
2013 Behren A, Anaka M, Lo P-H, Vella LJ, Davis ID, Catimel J, et al., 'The Ludwig Institute for Cancer Research Melbourne Melanoma Cell Line Panel', PIGMENT CELL & MELANOMA RESEARCH, 26 (2013)
DOI 10.1111/pcmr.12097
Citations Scopus - 21Web of Science - 21
2013 Reaume MN, Graham GE, Tomiak E, Kamel-Reid S, Jewett MAS, Bjarnason GA, et al., 'Canadian guideline on genetic screening for hereditary renal cell cancers', CUAJ-CANADIAN UROLOGICAL ASSOCIATION JOURNAL, 7 319-323 (2013)
DOI 10.5489/cuaj.1496
Citations Scopus - 10Web of Science - 9
2013 Trapani JA, Thia KYT, Andrews M, Davis ID, Gedye C, Parente P, et al., 'Human perforin mutations and susceptibility to multiple primary cancers', ONCOIMMUNOLOGY, 2 (2013)
DOI 10.4161/onci.24185
Citations Scopus - 29Web of Science - 23
2012 Neel BG, Stewart JM, Bodenmiller B, Ailles L, Gedye C, Bernardini M, et al., 'Phenotypic heterogeneity and instability of human serous ovarian cancer tumor-initiating cells', CANCER RESEARCH, 72 (2012)
DOI 10.1158/1538-7445.AM2012-SY35-02
2012 Anaka M, Freyer C, Gedye C, Caballero O, Davis ID, Behren A, Cebon J, 'Stem Cell Media Culture of Melanoma Results in the Induction of a Nonrepresentative Neural Expression Profile', STEM CELLS, 30 336-343 (2012) [C3]
DOI 10.1002/stem.786
Citations Scopus - 11Web of Science - 11
2011 Stewart JM, Shaw PA, Gedye C, Bernardini MQ, Neel BG, Ailles LE, 'Phenotypic heterogeneity and instability of human ovarian tumor-initiating cells', PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 108 6468-6473 (2011) [C1]
DOI 10.1073/pnas.1005529108
Citations Scopus - 112Web of Science - 107
2010 Roos FC, Roberts AM, Hwang IIL, Moriyama EH, Evans AJ, Sybingco S, et al., 'Oncolytic targeting of renal cell carcinoma via encephalomyocarditis virus', EMBO MOLECULAR MEDICINE, 2 275-288 (2010) [C1]
DOI 10.1002/emmm.201000081
Citations Scopus - 16Web of Science - 14
2010 Gedye C, Davidson A-J, Elmes MR, Cebon J, Bolton D, Davis ID, 'Cancer stem cells in urologic cancers', UROLOGIC ONCOLOGY-SEMINARS AND ORIGINAL INVESTIGATIONS, 28 585-590 (2010) [C1]
DOI 10.1016/j.urolonc.2009.06.010
Citations Scopus - 5Web of Science - 3
2009 Gedye C, Quirk J, Browning J, Svobodová S, John T, Sluka P, et al., 'Cancer/testis antigens can be immunological targets in clonogenic CD133

&quot;Cancer stem cells&quot; that resist conventional treatments may be a cause of therapeutic failure in melanoma. We report a subpopulation of clonogenic melanoma cells that ar... [more]

"Cancer stem cells" that resist conventional treatments may be a cause of therapeutic failure in melanoma. We report a subpopulation of clonogenic melanoma cells that are characterized by high prominin-1/CD133 expression in melanoma and melanoma cell lines. These cells have enhanced clonogenicity and self-renewal in vitro, and serve as a limited in vitro model for melanoma stem cells. In some cases clonogenic CD133 + melanoma cells show increased expression of some cancer/testis (CT) antigens. The expression of NY-ESO-1 in an HLA-A2 expressing cell line allowed CD133 + clonogenic melanoma cells to be targeted for killing in vitro by NY-ESO-1-specific CD8 + T-lymphocytes. Our in vitro findings raise the hypothesis that if melanoma stem cells express CT antigens in vivo that immune targeting of these antigens may be a viable clinical strategy for the adjuvant treatment of melanoma. © Springer-Verlag 2009.

DOI 10.1007/s00262-009-0672-0
Citations Scopus - 43
2008 John T, Caballero OL, Svobodova SJ, Kong A, Chua R, Browning J, et al., 'ECSA/DPPA2 is an embryo-cancer antigen that is coexpressed with cancer-testis antigens in non-small cell lung cancer', CLINICAL CANCER RESEARCH, 14 3291-3298 (2008) [C1]
DOI 10.1158/1078-0432.CCR-07-1322
Citations Scopus - 19Web of Science - 15
2008 John T, Black MA, Toro TT, Leader D, Gedye CA, Davis ID, et al., 'Predicting clinical outcome through molecular profiling in stage III melanoma', CLINICAL CANCER RESEARCH, 14 5173-5180 (2008) [C1]
DOI 10.1158/1078-0432.CCR-07-4170
Citations Scopus - 48Web of Science - 48
2008 Ebert LM, Tan BS, Browning J, Svobodova S, Russell SE, Kirkpatrick N, et al., 'The regulatory T cell-associated transcription factor FoxP3 is expressed by tumor cells', CANCER RESEARCH, 68 3001-3009 (2008) [C1]
DOI 10.1158/0008-5472.CAN-07-5664
Citations Scopus - 127Web of Science - 115
2007 Cebon J, Gedye C, John T, David ID, 'Immunotherapy of advanced or metastatic melanoma', Clinical Advances in Hematology and Oncology, 5 994-1006 (2007)

Melanoma is often evaluated for the development of anticancer immunotherapeutics. Fascinating immune and clinical responses in small numbers of patients have prompted various appr... [more]

Melanoma is often evaluated for the development of anticancer immunotherapeutics. Fascinating immune and clinical responses in small numbers of patients have prompted various approaches, ranging from nonspecific immune stimulation to therapies that target specific antigens Unfortunately, these immune therapies have often shown limited success and objective responses have been seen in only a modest subset of patients. The challenge has been to identify factors that can lead to more consistent clinical benefit and to develop strategies to overcome the obstacles to successful antitumor immunity. Over the last 15 years many immune targets have been identified in cancers and the mechanisms underpinning clinical responses have become better understood. Furthermore, new ways to manipulate anticancer immunity are making it possible to overcome cancer immune evasion and subversion. New therapeutic: strategies are resulting from these emerging insights into the relationship between melanoma and the host immune response.

Citations Scopus - 14
2006 Gedye CA, Stewart J, Cher LM, 'Encephalopathy after cyclophosphamide with response to methylene blue', Asia-Pacific Journal of Clinical Oncology, 2 185-189 (2006)

We present two cases of encephalopathy occurring after chemotherapy containing cyclophosphamide. Patient 1 was receiving vincristine, cisplatin and cyclophosphamide for recurrent ... [more]

We present two cases of encephalopathy occurring after chemotherapy containing cyclophosphamide. Patient 1 was receiving vincristine, cisplatin and cyclophosphamide for recurrent medulloblastoma, whilst patient 2 received cyclophosphamide-containing chemotherapy as adjuvant treatment for early breast cancer. After cumulative doses of 2.8 and 6g/ m 2 of cyclophosphamide both patients developed a gradual onset of fluctuating attention, slowed mentation and decreased consciousness. Extensive investigations excluded other causes of this altered conscious state. Given the similarity of presentation to ifosfamide encephalopathy, methylene blue (50mg i.v.) was administered. Patient 1 experienced an immediate improvement that was not sustained, with a subsequent deterioration over several weeks and became unresponsive before death. Patient 2 experienced a dramatic improvement within 3h and received a second dose of methylene blue with further improvement. To our knowledge, cyclophosphamide has not previously been implicated as a cause of encephalopathy. A review of the literature is presented. We hypothesize that cyclophosphamide may rarely cause encephalopathy and may also contribute to the cognitive dysfunction reported in association with chemotherapy for breast cancer and non-Hodgkin's lymphoma. © 2006 Blackwell Publishing Asia Pty Ltd.

DOI 10.1111/j.1743-7563.2006.00062.x
1997 Kettle AJ, Gedye CA, Winterbourn CC, 'Mechanism of inactivation of myeloperoxidase by 4-aminobenzoic acid hydrazide', BIOCHEMICAL JOURNAL, 321 503-508 (1997)
Citations Scopus - 131Web of Science - 126
1995 Gedye CJ, 'Patient confidentiality in New Zealand', BMJ, 310 127 (1995)
DOI 10.1136/bmj.310.6972.127b
1995 KETTLE AJ, GEDYE CA, HAMPTON MB, WINTERBOURN CC, 'INHIBITION OF MYELOPEROXIDASE BY BENZOIC-ACID HYDRAZIDES', BIOCHEMICAL JOURNAL, 308 559-563 (1995)
Citations Scopus - 104Web of Science - 108
1994 Vasudevan SG, Gedye C, Dixon NE, Cheah E, Carr PD, Suffolk PM, et al., 'Escherichia coli P

The Escherichia coli signal transduction protein P II , product of the glnB gene, was overproduced and purified. The predicted molecular weight of the protein based on the correct... [more]

The Escherichia coli signal transduction protein P II , product of the glnB gene, was overproduced and purified. The predicted molecular weight of the protein based on the correct nucleotide sequence is 12,427 and is very close to the value 12,435 obtained by matrix-assisted laser desorption mass spectrometry. Hexagonal crystals of the unuridylylated form of P II with dimensions 0.2 × 0.2 × 0.3 mm were grown and analysed by X-ray diffraction. The crystals belong to space group P6 3 with a=b=61.6Å,c= 56.3 Å and V m of 2.5 for one subunit in the asymmetric unit. A low-resolution electron density map showed electron density concentrated around a three-fold axis, suggesting the molecule to be a trimer. A sedimentation equilibrium experiment of the meniscus depletion type was used to estimate a molecular weight of 35,000 ± 1,000 for P II in solution. This result is consistent with the native protein being a homotrimer. © 1994.

DOI 10.1016/0014-5793(94)80203-3
Citations Scopus - 26
1993 KETTLE AJ, GEDYE CA, WINTERBOURN CC, 'SUPEROXIDE IS AN ANTAGONIST OF ANTIINFLAMMATORY DRUGS THAT INHIBIT HYPOCHLOROUS ACID PRODUCTION BY MYELOPEROXIDASE', BIOCHEMICAL PHARMACOLOGY, 45 2003-2010 (1993)
DOI 10.1016/0006-2952(93)90010-T
Citations Scopus - 70Web of Science - 69
1992 GEDYE C, HARDING C, MCKEE V, NELSON J, PATTERSON J, 'A NEW GEOMETRY FOR TETRAMANGANESE - FUSED OPEN CUBANES', JOURNAL OF THE CHEMICAL SOCIETY-CHEMICAL COMMUNICATIONS, 392-394 (1992)
DOI 10.1039/c39920000392
Citations Scopus - 27Web of Science - 29
Show 39 more journal articles

Conference (11 outputs)

Year Citation Altmetrics Link
2016 Anthony E, Pearsall E, Holien J, Gedye C, Skelding K, 'PRECLINICAL INVESTIGATION OF A NEW CLASS OF DRUGS FOR THE TREATMENT OF GLIOBLASTOMA MULTIFORME', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
2016 Gedye C, 'BIOMARKERS IN RENAL CELL CARCINOMA: THE TRIANGLE OR THE ORCHESTRA?', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
2015 Laegdsgaard P, Nielsen S, Koegelenberg A, Goode S, Thorne R, Lund D, et al., 'A NEW VENTURE FOR THE HUNTER CANCER BIOBANK-ESTABLISHMENT OF SEQUENTIAL BLOOD COLLECTION FOR BRAIN CANCER RESEARCH', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2015) [E3]
Co-authors Rodney Scott, Rick Thorne
2014 Gedye C, Kurban G, Gallie BL, Leveridge MJ, Musquera M, Morales C, et al., 'Surgical ischemia and detection of clear cell renal cell carcinoma biomarkers', JOURNAL OF CLINICAL ONCOLOGY (2014)
2014 Gedye C, Sirskyj D, Lobo NC, Hyatt E, Evans A, Finelli A, et al., 'Essential experimental steps and estimates of renal carcinoma initiating cells', JOURNAL OF CLINICAL ONCOLOGY (2014)
2014 Gedye C, Sirskyj D, Hyatt E, Lobo N, Lourenco C, Evans A, et al., 'MESENCHYMAL DIFFERENTIATION PROGRAMS GOVERN VHL-MUTANT CLEAR CELL RENAL CANCER BIOLOGY', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
Co-authors Rodney Scott
2014 Koegelenberg AM, Dean S, Nielsen S, Carroll R, Mellon A, Surgeons G, et al., 'THE IMPACT OF INTEGRATING SYSTEM CHANGES INTO ROUTINE HEALTHCARE PRACTICES VIA MODIFICATION OF EXISTING PROCESSES; A LOOK AT BIOBANKING CONSENT IN THE HUNTER REGION', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
Co-authors Chris Paul
2013 Gedye C, Sirskyj D, Lobo NC, Evans A, Fleshner NE, Robinette M, et al., 'VHL-mutant renal cell carcinomas contain cancer cells with mesenchymal phenotypes', JOURNAL OF CLINICAL ONCOLOGY (2013) [E3]
Citations Web of Science - 1
2013 Davidson A, Quirk J, Gedye C, Browning J, Bolton D, Davis I, 'Differential cancer/testis antigen expression in colony forming bladder cancer cell populations', BJU INTERNATIONAL (2013) [E3]
2009 Davidson AJ, Quirk J, Gedye C, Browning J, Bolton DM, Davis ID, 'Differential Cancer/Testis antigen expression in colony forming bladder cancer cell populations', BJU INTERNATIONAL (2009)
2007 Ebert LM, Tan BS, Browning J, Svobodova S, Kirkpatrick N, Gedye C, et al., 'FoxP3 is expressed by tumor cells, virally transformed B cells, and germ cells', JOURNAL OF IMMUNOTHERAPY (2007)
Show 8 more conferences
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Grants and Funding

Summary

Number of grants 12
Total funding $6,498,792

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


20171 grants / $39,874

Sub-Project - Hunter Cancer Research Alliance; HCRA$39,874

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Associate Professor Erica James, Doctor Craig Gedye, Conjoint Associate Professor Jarad Martin, Doctor Nick Zdenkowski, Miss Aoife McGarvey, Professor Ronald Plotnikoff, Doctor Ben Britton, Mrs Merridie Rees, Associate Professor Mitch Duncan, Miss Fiona Stacey
Scheme Translational Cancer Research Centre Grants
Role Investigator
Funding Start 2017
Funding Finish 2018
GNo GS170010
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

20161 grants / $3,049

Bringing CLARITY to Brain Cancer$3,049

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Jamie Flynn, Doctor Craig Gedye
Scheme Project Grant
Role Investigator
Funding Start 2016
Funding Finish 2016
GNo G1600967
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20155 grants / $687,675

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

The Hunter Cancer Biobank (HCB): Maximising community value through validation, annotation and distribution throughout NSW$300,000

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Professor Marjorie Walker, Conjoint Professor Stephen Ackland, Laureate Professor Rodney Scott, Professor John Forbes, Professor Xu Dong Zhang, Doctor Pradeep Tanwar, Doctor Nikola Bowden, Doctor Craig Gedye, Doctor James Lynam, Doctor Kelly Kiejda, Doctor Jennette Sakoff, Mr Loui Rassam, Dr Tara Roberts, Professor Soon Lee, Dr Betty Kan
Scheme Research Infrastructure Grants
Role Investigator
Funding Start 2015
Funding Finish 2018
GNo G1500825
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

Destroying kidney cells that evade current treatments$46,000

Funding body: Kidney Health Australia

Funding body Kidney Health Australia
Project Team Doctor Craig Gedye, Doctor Nikola Bowden, Laureate Professor Rodney Scott
Scheme Medical Research Project Grants
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1401048
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

BAALC - a novel target for the development of new treatments for brain cancer.$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Kathryn Skelding, Doctor Craig Gedye
Scheme Project Grant
Role Investigator
Funding Start 2015
Funding Finish 2015
GNo G1600225
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Too Much of a Good Thing: Application for a triple-gas incubator to allow cell culture under normal conditions$16,675

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Craig Gedye, Laureate Professor Rodney Scott, Doctor Nikola Bowden, Associate Professor Simon Keely, Doctor Kathryn Skelding
Scheme Research Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1500730
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20145 grants / $5,768,194

High Throughput Image Capture Platform for Translational Cancer Research$282,614

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Conjoint Professor Stephen Ackland, Laureate Professor Rodney Scott, Professor John Forbes, Professor Xu Dong Zhang, Professor Marjorie Walker, Professor Hubert Hondermarck, Doctor Craig Gedye, Doctor Rick Thorne, Mr Loui Rassam, Doctor Stephen Braye
Scheme Research Equipment Grant
Role Investigator
Funding Start 2014
Funding Finish 2014
GNo G1400626
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

Embedding patient tissue banking consent into routine clinical practice: To maximize state-wide consent and enable a patient-led approach to tissue banking$265,000

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Laureate Professor Rodney Scott, Doctor Craig Gedye, Associate Professor Christine Paul, Assoc. Prof Nicholas Hawkins, Associate Professor Deborah Marsh, Professor Phil Crowe
Scheme Community of Practice Program
Role Investigator
Funding Start 2014
Funding Finish 2015
GNo G1400792
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

The Virtuous Circle: A Living Brain Cancer BioBank$242,176

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Laureate Professor Rodney Scott, Doctor Craig Gedye
Scheme Project Grant
Role Investigator
Funding Start 2014
Funding Finish 2017
GNo G1401406
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Is Renal Cell Carcinoma Driven by "Cancer Stem Cells"?$173,058

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Doctor Craig Gedye
Scheme Training (Postdoctoral) Fellowships - C.J. Martin Biomedical Fellowships (Overseas)
Role Lead
Funding Start 2014
Funding Finish 2016
GNo G1400027
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y
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Research Supervision

Number of supervisions

Completed0
Current1

Total current UON EFTSL

PhD0.15

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2015 PhD Targeting Thyroid Cancer Cells for Diagnosis and Treatment PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
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Research Collaborations

The map is a representation of a researchers co-authorship with collaborators across the globe. The map displays the number of publications against a country, where there is at least one co-author based in that country. Data is sourced from the University of Newcastle research publication management system (NURO) and may not fully represent the authors complete body of work.

Country Count of Publications
Australia 32
Canada 22
United States 9
New Zealand 7
United Kingdom 4
More...
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News

Study using new tools to unlock secrets of immune cells in cancer

May 25, 2017

An in-depth atlas of the tumour microenvironment has been mapped by an international cancer team involving Hunter researcher Dr Craig Gedye, seeking to build a clearer picture of how the immune system is involved with cancer.

Expanding the horizons of brain cancer research

October 13, 2015

A raft of Mark Hughes Foundation (MHF) travel grants will give Hunter brain cancer researchers the chance to build new clinical trial collaborations at the international COGNO Annual Scientific Meeting in Brisbane this month.

Dr Craig Gedye

More flexibility needed in melanoma treatment

February 16, 2015

Survival rates would be improved by making treatment regimens for metastatic melanoma more flexible, according to HMRI cancer researcher Dr Craig Gedye, a medical oncologist at the Calvary Mater Newcastle.

brain cancer biobank

Brain cancer biobank

October 29, 2014

A new "biobank" for brain cancer is being established at the Hunter Medical Research Institute courtesy of funding from the Mark Hughes Foundation (MHF).

Dr Craig Gedye

Position

Conjoint Senior Lecturer
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Contact Details

Email craig.gedye@newcastle.edu.au
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