Dr Craig Gedye
Conjoint Associate Professor
School of Medicine and Public Health
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”.
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.
- 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
- Cancer biology
- Cancer immunotherapy
- Cancer stem cells
- Cell biology
- Clinical trials
- Epigenetic heterogeneity
- Epithelial-mesenchymal transition
- Medical oncology
- Phenotypic plasticity
- Prostate cancer
- Renal cell carcinoma
Fields of Research
|111204||Cancer Therapy (excl. Chemotherapy and Radiation Therapy)||25|
|111201||Cancer Cell Biology||50|
|Dates||Title||Organisation / Department|
|28/5/2016 - 30/11/2017||Conjoint Senior Lecturer||The University of Newcastle - Faculty of Health and Medicine
For publications that are currently unpublished or in-press, details are shown in italics.
Journal article (55 outputs)
Rush A, Matzke L, Cooper S, Gedye C, Byrne JA, Watson PH, 'Research Perspective on Utilizing and Valuing Tumor Biobanks', BIOPRESERVATION AND BIOBANKING, 17 219-229 (2019)
Gedye C, Brook N, 'ANZUP MDT Masterclass Convenor Welcome', Asia-Pacific Journal of Clinical Oncology, 15 5 (2019)
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, 15 31-37 (2019) [C1]
© 2018 John Wiley & Sons Australia, Ltd Background: Many biobanks rely upon patients¿ willingness to donate biospecimens and healthcare professionals to initiate opt-in cons... [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.
Rowe CW, Faulkner S, Paul JW, Tolosa JM, Gedye C, Bendinelli C, et al., 'The precursor for nerve growth factor (proNGF) is not a serum or biopsy-rinse biomarker for thyroid cancer diagnosis.', BMC endocrine disorders, 19 128 (2019) [C1]
Rowe CW, Dill T, Faulkner S, Gedye C, Paul JW, Tolosa JM, et al., 'The precursor for nerve growth factor (ProNGF) in thyroid cancer lymph node metastases: Correlation with primary tumour and pathological variables', International Journal of Molecular Sciences, 20 1-13 (2019) [C1]
Peters S, Clézardin P, Márquez-Rodas I, Niepel D, Gedye C, 'The RANK RANKL axis: an opportunity for drug repurposing in cancer?', Clinical and Translational Oncology, 21 977-991 (2019) [C1]
|2018||Gedye C, 'The diverse landscape of genitourinary cancer immunotherapy', Cancer Forum, 42 29-39 (2018) [C1]|
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]
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.
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.
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.
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.
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.
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]
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]
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)
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]
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.
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.
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]
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)
Gedye C, van der Westhuizen A, John T, 'Checkpoint immunotherapy for cancer: superior survival, unaccustomed toxicities.', Intern Med J, 45 696-701 (2015) [C1]
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)
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.
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.
|Show 52 more journal articles|
Conference (33 outputs)
|2019||Cathomas R, Merseburger AS, Loriot Y, James N, Choy E, Castellano D, et al., 'Primary results from the SAUL study: atezolizumab for locally advanced or metastatic urothelial carcinoma (UC) or non-UC', SWISS MEDICAL WEEKLY (2019)|
|2019||de Bono JS, Fizazi K, Saad F, Shore N, Sandhu SK, Mehra N, et al., 'Central, prospective detection of homologous recombination repair gene mutations (HRRm) in tumour tissue from \ 4000 men with metastatic castration-resistant prostate cancer (mCRPC) screened for the PROfound study', ANNALS OF ONCOLOGY, Barcelona, SPAIN (2019)|
Sternberg CN, Merseburger AS, Choy E, Castellano DE, Lopez-Rios F, James N, et al., 'Clinical outcomes according to PD-L1 status and age in the prospective international SAUL study of atezolizumab (atezo) for locally advanced or metastatic urothelial carcinoma (UC) or non-UC of the urinary tract.', JOURNAL OF CLINICAL ONCOLOGY, Chicago, IL (2019)
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)
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)
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]
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)
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)
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]
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]
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]
|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]|
|Show 30 more conferences|
Number of supervisions
|Commenced||Level of Study||Research Title||Program||Supervisor Type|
|2015||PhD||The Precursor for Nerve Growth Factor and Innervation in Thyroid Cancer||PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle||Co-Supervisor|
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|
May 25, 2017
October 13, 2015
February 16, 2015
October 29, 2014