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

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

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 (46 outputs)

Year Citation Altmetrics Link
2018 Almazi JG, Pockney P, Gedye C, Smith ND, Hondermarck H, Verrills NM, Dun MD, 'Cell-Free DNA Blood Collection Tubes Are Appropriate for Clinical Proteomics: A Demonstration in Colorectal Cancer.', Proteomics. Clinical applications, 12 e1700121 (2018) [C1]
DOI 10.1002/prca.201700121
Co-authors Nikki Verrills, Matt Dun, Hubert Hondermarck, Peter Pockney
2018 Fradgley EA, Chong SE, Cox ME, Paul CL, Gedye C, 'Enlisting the willing: A study of healthcare professional¿initiated and opt-in biobanking consent reveals improvement opportunities throughout the registration process', European Journal of Cancer, 89 36-41 (2018) [C1]

© 2017 The Authors Biobanking consent processes should accord with patients' preferences and be offered in a consistent and systematic manner. However, these aims can be diff... [more]

© 2017 The Authors Biobanking consent processes should accord with patients' preferences and be offered in a consistent and systematic manner. However, these aims can be difficult to achieve under healthcare professionals' (HCPs) time-constrained workflows, resulting in low participation rates. This current perspective provides a brief overview of HCP involvement in consent and reports new data on participant attrition at each step of the biobanking consent process as experienced by 113 patients at an Australian tertiary cancer centre. To determine attrition in this HCP-driven consent process, we reviewed medical records for the following events: inclusion of biobanking consent forms; visible patient and HCP signatures; consent status selected (decline or accept) and specimen registration with local biobank. Accessible medical records revealed the following data: 75 of 85 records included viewable forms; 22 of 85 records included patient and 19 of 85 included HCP signatures; 15 of 85 records included signed and completed forms and 3 of 85 had samples banked with annotated clinical data. We compared these data with self-reported experiences of being approached to participate by HCPs. Of the 15 participants (17.6%) who successfully completed consent, only five could recall being asked and providing consent. The low enrolment rate is a considerable lost opportunity because most patients (59%) who were not asked to participate indicated they would have consented if asked. Furthermore, in comparing self-reported experiences with medical records, we believe cancer patients' preferences for participation are mismatched with actual biobanking enrolment, which has considerable attrition at each step in the consent process.

DOI 10.1016/j.ejca.2017.10.025
Co-authors Chris Paul, Elizabeth Fradgley
2018 Gedye C, 'ANZUP MDT Masterclass Convenor Welcome', Asia-Pacific Journal of Clinical Oncology, 14 5 (2018)
DOI 10.1111/ajco.13035
2018 Fradgley EA, Chong SE, Cox ME, Gedye C, Paul CL, 'Patients' experiences and preferences for opt-in models and health professional involvement in biobanking consent: A cross-sectional survey of Australian cancer outpatients', Asia-Pacific Journal of Clinical Oncology, (2018)

© 2018 John Wiley & Sons Australia, Ltd. Background: Many biobanks rely upon patients' willingness to donate biospecimens and healthcare professionals to initiate opt-i... [more]

© 2018 John Wiley & Sons Australia, Ltd. Background: Many biobanks rely upon patients' willingness to donate biospecimens and healthcare professionals to initiate opt-in consent processes. This study explored if: (1) patients accept opt-in or opt-out consent models with varying levels of professional involvement; (2) professionals discuss participation with specific patient groups; and (3) this discussion is associated with patient knowledge of biobanking processes. Methods: Outpatients completed surveys at a tertiary cancer center in New South Wales, Australia. Eligible participants were English-speaking adults who recently had cancer-related surgery. Participants completed 27 questions exploring acceptable consent models, biobanking experiences, knowledge, and willingness. Logistic regression and chi-square tests examined differences in the characteristics and knowledge of participants who were offered the opportunity to participate versus those who were not. Results: A total of 113 outpatients participated (97% response). Most participants (92%) found opt-out, patient-initiated consent acceptable; however, high acceptability was reported for all models except for opt-in, patient-initiated consent (58%). University or technical qualifications (P = 0.001) was associated with increased odds (OR = 4.5) of being offered biobanking. The majority did not know what occurred to samples after surgery (59.3%) or pathology review (81.4%) and ability to answer these questions was associated with discussion of participation (P < 0.001). Of the few outpatients who discussed biobanking with their doctor (29%), all consented. Conclusion: Professional-initiated, opt-in consent resulted in a few educated patients being approached; greater professional initiation of consent would be fruitful as most patients were willing to participate if asked. However, other consent approaches minimizing professional involvement were as acceptable to participants warranting further consideration.

DOI 10.1111/ajco.12866
Co-authors Chris Paul, Elizabeth Fradgley
2017 Rowe CW, Paul JW, Gedye C, Tolosa JM, Bendinelli C, McGrath S, Smith R, 'Targeting the TSH receptor in thyroid cancer', Endocrine-Related Cancer, 24 R191-R202 (2017) [C1]

© 2017 Society for Endocrinology Printed in Great Britain. Recent advances in the arena of theranostics have necessitated a re-examining of previously established fields. The exis... [more]

© 2017 Society for Endocrinology Printed in Great Britain. Recent advances in the arena of theranostics have necessitated a re-examining of previously established fields. The existing paradigm of therapeutic thyroid-stimulating hormone receptor (TSHR) targeting in the post-surgical management of differentiated thyroid cancer using levothyroxine and recombinant human thyroid-stimulating hormone (TSH) is well understood. However, in an era of personalized medicine, and with an increasing awareness of the risk profile of longstanding pharmacological hyperthyroidism, it is imperative clinicians understand the molecular basis and magnitude of benefit for individual patients. Furthermore, TSHR has been recently re-conceived as a selective target for residual metastatic thyroid cancer, with pilot data demonstrating effective targeting of nanoparticles to thyroid cancers using this receptor as a target. This review examines the evidence for TSHR signaling as an oncogenic pathway and assesses the evidence for ongoing TSHR expression in thyroid cancer metastases. Priorities for further research are highlighted.

DOI 10.1530/ERC-17-0010
Citations Scopus - 2Web of Science - 2
Co-authors Christopher W Rowe, Roger Smith, Jonathan Paul
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)
DOI 10.1097/CJI.0000000000000146
Citations Scopus - 2Web of Science - 2
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 t... [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 - 54Web of Science - 51
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 inhibito... [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 - 13Web of Science - 12
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 - 5Web of Science - 5
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 Scopus - 1Web 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 Gedye C, Fleming J, 'Forsaking cures for cancer: why are we discarding the tumour biospecimens of most patients?', MEDICAL JOURNAL OF AUSTRALIA, 204 297-+ (2016)
DOI 10.5694/mja15.00961
Citations Web of Science - 3
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 - 3Web of Science - 3
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 mammalia... [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
Citations Scopus - 1Web of Science - 1
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 - 10Web of Science - 14
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 - 3Web of Science - 2
2015 Gedye C, Boyle FM, 'Optimising treatment for Australian melanoma patients can save taxpayers millions of dollars annually', MEDICAL JOURNAL OF AUSTRALIA, 202 I-I (2015)
DOI 10.5694/mja14.01202
Citations Web of Science - 3
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 - 9Web of Science - 10
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 - 7Web of Science - 5
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 - 2
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 - 19Web of Science - 20
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 CD133, an important cell surface marker for the isolation of both normal and cancer stem cells. PROM1 transcripts initiate at a range of t... [more]

PROM1 is the gene encoding prominin-1 or CD133, 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 CD133+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 CD133+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 - 6
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 - 8
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 - 24Web of Science - 24
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 - 14Web of Science - 13
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 - 35Web of Science - 27
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 - 120Web of Science - 116
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 - 45
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 - 22Web of Science - 16
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 - 51Web of Science - 50
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 - 134Web of Science - 120
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/ m2of 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)
DOI 10.1042/bj3210503
Citations Scopus - 140Web of Science - 134
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)
DOI 10.1042/bj3080559
Citations Scopus - 113Web of Science - 114
1994 Vasudevan SG, Gedye C, Dixon NE, Cheah E, Carr PD, Suffolk PM, et al., 'Escherichia coli P

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

The Escherichia coli signal transduction protein PII, 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 PIIwith dimensions 0.2 × 0.2 × 0.3 mm were grown and analysed by X-ray diffraction. The crystals belong to space group P63with a=b=61.6Å,c= 56.3 Å and Vmof 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 PIIin 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 43 more journal articles

Conference (22 outputs)

Year Citation Altmetrics Link
2018 Mersiades A, Tognela A, Haber PS, Stockler M, Lintzeris N, Simes J, et al., 'Pilot and Definitive Randomised Double-Blind Placebo-Controlled Trials Evaluating an Oral Cannabinoid-Rich THC/CBD Cannabis Extract for Chemotherapy-Induced Nausea and Vomiting (CINV)', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2018)
2018 Rowe C, Dill T, Clarke M, Paul J, Gedye C, King S, Hondermarck H, 'A methodology for validating automated digital whole-slide analysis of immunohistochemical biomarkers using open source software (QuPath).', Newcastle, Australia (2018)
Co-authors Hubert Hondermarck, Christopher W Rowe, Jonathan Paul
2018 Rowe C, Dill T, Clarke M, Paul JW, Gedye C, King S, Hondermarck H, 'A methodology for validating automated digital whole-slide analysis of immunohistochemical biomarkers using open source software (QuPath)', HMRI, Newastle (2018)
Co-authors Hubert Hondermarck
2018 Rowe CW, Dill T, Faulkner S, Griffin N, Jobling P, King S, et al., 'Increased nerve density around papillary thyroid cancers and primary thyroid cancers with nodal metastases.', Adelaide (2018)
Co-authors Phillip Jobling, Hubert Hondermarck, Jonathan Paul, Roger Smith, Christopher W Rowe
2018 Rowe C, Dill T, King S, Gedye C, Paul J, Tolosa JM, Smith R, 'Thyroid cancers resected in patients with concurrent TSH-receptor stimulation have higher levels of sodium-iodide symporter (NIS) expression', CLINICAL ENDOCRINOLOGY, Perth, AUSTRALIA (2018)
Co-authors Jonathan Paul, Roger Smith, Christopher W Rowe
2017 Rowe C, King S, Tolosa J, Paul J, Gedye C, Smith R, 'Overexpression of the Sodium-Iodide Symporter in thyroid cancer co-existing with Graves¿ disease', Perth, Western Australia (2017)
Co-authors Jonathan Paul, Roger Smith
2017 Gedye C, 'New Indications in GU Cancers', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2017)
2017 Mersiades A, Tognela A, Haber P, Stockler M, Lintzeris N, Simes J, et al., 'Pilot and Definitive Randomised Double-Blind Placebo-Controlled Trials Evaluating an Oral Cannabinoid-Rich THC/CBD Cannabis Extract for Secondary Prevention of Chemotherapy-Induced Nausea and Vomiting (CINV)', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2017)
2017 Rowe C, Tolosa Gonzalez JT, Faulkner S, Paul JW, Gedye C, McGrath S, et al., 'The precursor for nerve growth factor (proNGF) is detectable in the rinse of fine needle aspiration biopsy of thyroid cancer', Boston, Massachussetts (2017)
Co-authors Roger Smith, Hubert Hondermarck, Jonathan Paul, Christopher W Rowe
2017 Gedye C, 'CATCHING-UP: OPPORTUNITIES AND CHALLENGES FOR KIDNEY CANCER BIOMARKERS TO ENABLE TRANSLATIONAL RESEARCH', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2017)
2017 Mersiades A, Haber P, Stockler M, Lintzeris N, Simes J, McGregor I, et al., 'Pilot and Definitive Randomized Double-Blind Placebo-Controlled Trials Evaluating an Oral Cannabinoid-Rich THC/CBD Cannabis Extract for Secondary Prevention of Chemotherapy-Induced Nausea and Vomiting (CINV)', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2017)
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)
Co-authors Kathryn Skelding
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 Rick Thorne, Rodney Scott
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, Chicago, IL (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, Chicago, IL (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, Chicago, IL (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, Melbourne, AUSTRALIA (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, Gold Coast, AUSTRALIA (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, Boston, MA (2007)
Show 19 more conferences
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Grants and Funding

Summary

Number of grants 10
Total funding $1,502,786

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


20181 grants / $99,997

Investigating a new class of drugs for the treatment of brain cancer$99,997

Funding body: Mark Hughes Foundation

Funding body Mark Hughes Foundation
Project Team Doctor Kathryn Skelding, Doctor Craig Gedye
Scheme Research Funding
Role Investigator
Funding Start 2018
Funding Finish 2018
GNo G1701638
Type Of Funding C3120 - Aust Philanthropy
Category 3120
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 Dr 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 / $612,675

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, Associate Professor 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 C2210 - Aust StateTerritoryLocal - Own Purpose
Category 2210
UON Y

The Hunter Cancer Biobank (HCB): Maximising community value through validation, annotation and distribution throughout NSW$225,000

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Professor Marjorie Walker, Conjoint Professor Stephen Ackland, Laureate Professor Rodney Scott, Emeritus Professor John Forbes, Professor Xu Dong Zhang, Associate Professor Pradeep Tanwar, Associate Professor 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 2017
GNo G1500825
Type Of Funding C2210 - Aust StateTerritoryLocal - Own Purpose
Category 2210
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, Associate Professor Nikola Bowden, Laureate Professor Rodney Scott
Scheme Medical Research Project Grants
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1401048
Type Of Funding C3112 - Aust Not for profit
Category 3112
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: The Honda Foundation

Funding body The Honda Foundation
Project Team Doctor Craig Gedye, Laureate Professor Rodney Scott, Associate Professor Nikola Bowden, Associate Professor Simon Keely, Doctor Kathryn Skelding
Scheme Research Funding
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1500730
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

20143 grants / $787,065

The Virtuous Circle: A Living Brain Cancer BioBank$331,393

Funding body: Mark Hughes Foundation

Funding body Mark Hughes Foundation
Project Team Laureate Professor Rodney Scott, Doctor Craig Gedye, Professor Marjorie Walker
Scheme Research Funding
Role Investigator
Funding Start 2014
Funding Finish 2018
GNo G1401406
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

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, Emeritus 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

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 2015
GNo G1400027
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y
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Research Supervision

Number of supervisions

Completed0
Current1

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 42
Canada 22
New Zealand 7
United States 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

Expanding the horizons of brain cancer research

October 13, 2015

Mark Hughes Foundation travel grants give Hunter researchers the chance to build clinical trial collaborations.

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 m

Brain cancer biobank

October 29, 2014

MHF BIOBANK AN INVESTMENT IN BRAIN CANCER RESEARCH, University of Newcastle, news

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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