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Dr Christopher Scarlett

Senior Lecturer

School of Environmental and Life Sciences (Applied Sciences)

Career Summary

Biography

I undertook my Bachelor of Science (Hons I) studies at the University of Newcastle. I then completed my PhD through the University of Sydney, Faculty of Medicine where I established a novel proteomic initiative with the specific aim of using proteomics as a tool to answer clinically relevant questions. Using this approach I identified unique markers of pancreatic and bile duct cancer by creating powerful new diagnostic models for the improved diagnosis of pancreatico-biliary malignancies. I then continued my interest in pancreatic cancer research by joining the Pancreatic Cancer Research Group at the Garvan Institute of Medical Research in 2007.

In my early post-doctoral years, I was awarded an NHMRC Postdoctoral Training Fellowship (Peter Doherty) and was funded as a Cancer Institute NSW Early Career Development Fellow at the Garvan Institute. My research interests primarily focussed on signalling pathways in pancreatic cancer to identify novel therapeutic and chemopreventative strategies, as well as defining the role of bone marrow derived cells in the development of the normal pancreas, pancreatic injury and regeneration, and pancreatic cancer.

Recognition of these contributions included a feature article in the CINSW Cancer Research Achievement Report 2008; A celebration of the outstanding contributions made to cancer research in NSW. I am also is a Cancer Institute NSW Career Development Fellow investigating novel therapeutic approaches to pancreatic cancer, and was awarding the Cancer Research Network Innovation Award (Sydney Cancer Conference 2010).

I am also investigating the personalised treatment of metastatic pancreatic cancer based on genomic sequence data acquired through the Australian Pancreatic Cancer Genome Initiative, as part of the International Cancer Genome Consortium.

I moved to the University of Newcastle in early 2012 to take a position within the School of Environmental and Life Sciences,and am now driving a research program investigating aberrations in nutrient-gene interactions to define clinically relevant phenotypes of pancreatic cancer, as well as examining the efficacy of bioactive compounds as novel therapeutics in the treatment of pancreatic cancer.

Research Expertise
My research interests have primarily focused on signalling pathways in pancreatic cancer to identify novel therapeutic and chemopreventative strategies, as well as defining the role of bone marrow derived cells in the development of the normal pancreas, pancreatic injury and regeneration, and pancreatic cancer.

I am also investigating novel therapeutic approaches to pancreatic cancer in addition to investigating personalised treatment of metastatic pancreatic cancer based on genomic sequence data acquired through the Australian Pancreatic Cancer Genome Initiative, as part of the International Cancer Genome Consortium (ICGC). Upon my move to the University of Newcastle, School of Environmental and Life Sciences, I have been investigating aberrations in nutrient-gene interactions to define clinically relevant phenotypes of pancreatic cancer, as well as examining the efficacy of bioactive compounds as novel therapeutics in the treatment of pancreatic cancer.

Teaching Expertise
I have been involved in coordinating and teaching core courses for the Bachelor of Food Science and Human Nutrition Program, in particular BIOL2011 - Fundamentals of Biology and Biochemistry; and FSHN2100 - Microbiology, Food Safety and Immunology.

Collaborations
I am an Associate Investigator for the Australian Pancreatic Cancer Network, based at the Garvan Institute of Medical Research, which provides direct links to the clinical management of patients facilitating rapid translation of scientific discoveries to patient care, providing a unique opportunity for translational research efforts in pancreatic cancer in Australia.

I am also contributing to the Australian Pancreatic Cancer Genome Initiative (APGI), which aims to sequence ~400 individual pancreatic cancers as part of the International Cancer Genome Consortium (ICGC).

I have been awarded project grant funding through the Priority-driven Collaborative Cancer Research Scheme, co-funded by Cancer Australia and the Cure Cancer Australia Foundation (CIA; 2012-1013). I am also a Co-Investigator on a successful NHMRC program grant ($11,128,320; 2009-2013), and a Co-Chief Investigator on successful project grants through the NHMRC (CI-B; 2011-2013) and The Cancer Council NSW (CI-C; 2010-2012) in collaboration with Dr Tao Liu at the Children’s Cancer Institute Australia.


Qualifications

  • PhD, University of Sydney
  • Bachelor of Science, University of Newcastle
  • Bachelor of Science (Honours), University of Newcastle

Keywords

  • Biochemistry
  • Carcinogenesis
  • Metastases
  • Microbiology
  • Mouse Models
  • Novel Therapeutics
  • Pancreatic Cancer
  • Research Methods

Fields of Research

CodeDescriptionPercentage
111201Cancer Cell Biology20
111204Cancer Therapy (excl. Chemotherapy and Radiation Therapy)20
111299Oncology and Carcinogenesis not elsewhere classified60

Professional Experience

UON Appointment

DatesTitleOrganisation / Department
30/01/2015 - Senior LecturerUniversity of Newcastle
School of Environmental and Life Sciences
Australia
5/07/2014 - 5/07/2014Casual AcademicUniversity of Newcastle
School of Environmental and Life Sciences
Australia
25/06/2011 - 5/12/2011Casual AcademicUniversity of Newcastle
School of Environmental and Life Sciences
Australia
1/03/2010 - 3/12/2010LecturerUniversity of Newcastle
School of Environmental and Life Sciences
Australia
23/11/2009 - 30/11/2009Casual AcademicUniversity of Newcastle
School of Environmental and Life Sciences
Australia
3/09/2009 - 3/09/2009Casual MiscellaneousUniversity of Newcastle
Centre for Teaching and Learning
Australia

Academic appointment

DatesTitleOrganisation / Department
1/06/2012 - 1/02/2013Fellow
Cancer Institute NSW:- Career Development Fellowship
University of Newcastle
School of Environmental and Life Sciences
Australia
1/03/2012 - Honorary ScientistGarvan Institute of Medical Research
Cancer Research Program
Australia
1/01/2007 - 1/03/2012Senior Research OfficerGarvan Institute of Medical Research
Cancer Research Program
Australia
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Publications

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


Book (1 outputs)

YearCitationAltmetricsLink
2015Scarlett CS, Vuong QV, Plant Bioactive Compounds for Pancreatic Cancer Prevention and Treatment, Nova Science Publishers, Inc., New York (2015)

Chapter (5 outputs)

YearCitationAltmetricsLink
2015Vuong QV, Scarlett CJ, 'Selected Australian Flora As Potential Sources of Anti-Cancer Agents', Plant Bioactive Compounds for Pancreatic Cancer Prevention and Treatment, Nova Science Publishers , Inc., New York 195-217 (2015)
Co-authorsVanquan Vuong
2015Scarlett CJ, Vuong QV, McCluskey A, Bowyer MC, 'Pancreatic Cancer Drugs: Case Studies in Synthesis and Production', Plant Bioactive Compounds for Pancreatic Cancer Prevention and Treatment, Nova Science Publishers , Inc., New York 145-193 (2015)
Co-authorsMichael Bowyer, Vanquan Vuong, Adam Mccluskey
2015Vuong QV, Scarlett CJ, 'Selected Australian Flora As Potential Sources of Anti-Cancer Agents', Plant Bioactive Compounds for Pancreatic Cancer Prevention and Treatment, Nova Science Publishers , Inc., New York 195-217 (2015)
Co-authorsVanquan Vuong
2015Scarlett CJ, Vuong QV, McCluskey A, Bowyer MC, 'Pancreatic Cancer Drugs: Case Studies in Synthesis and Production', Plant Bioactive Compounds for Pancreatic Cancer Prevention and Treatment, Nova Science Publishers , Inc., New York 145-193 (2015)
Co-authorsVanquan Vuong, Michael Bowyer, Adam Mccluskey
2013Vuong QV, Scarlett CJ, Roach PD, 'Green tea and pancreatic cancer chemoprevention', Green Tea: Varieties, Production and Health Benefits, Nova Science Publishers, New York 75-90 (2013) [B1]
Co-authorsPaul Roach, Vanquan Vuong
Show 2 more chapters

Journal article (55 outputs)

YearCitationAltmetricsLink
2015Vuong QV, Van TN, Dang TT, Bhuyan DJ, Goldsmith CD, Sadeqzadeh E, et al., 'Optimization of ultrasound-assisted extraction conditions for euphol from the medicinal plant, Euphorbia tirucalli, using response surface methodology', INDUSTRIAL CROPS AND PRODUCTS, 63 197-202 (2015)
DOI10.1016/j.indcrop.2014.09.057Author URL
Co-authorsVanquan Vuong, Michael Bowyer
2015Nguyen VT, Bowyer MC, Vuong QV, Altena IA, Scarlett CJ, 'Phytochemicals and antioxidant capacity of Xao tam phan (Paramignya trimera) root as affected by various solvents and extraction methods', Industrial Crops and Products, 67 192-200 (2015)

Xao tam phan (. Paramignya trimera (Oliv.) Guillaum) is a Vietnamese traditionally medicinal plant used in the treatment of numerous cancers. The preparation of Xao tam phan extracts including solvent type and extraction method have significant effects on extraction efficiency, phytochemical profile and biological activity. This study aimed to investigate the effects of five various solvents (water, acetonitrile, methanol, ethyl acetate and hexane) and three different extraction methods (conventional, ultrasound-assisted and microwave-assisted) on phytochemical yield and antioxidant capacity of P. trimera root from Vietnam. The results indicate that methanol extracted the maximal yield of phytochemicals from P. trimera and exhibited the greatest antioxidant capacity, with eleven compounds were identified and quantified. Microwave-assisted extraction produced the maximal phytochemical yields (except for total flavonoids) and antioxidant capacity, when compared to conventional and ultrasound-assisted extractions. These data reveal that the use of methanol and microwave-assisted extraction are recommended for extraction of biologically active phytochemicals from P. trimera root for application in the nutraceutical and/or pharmaceutical industries.

DOI10.1016/j.indcrop.2015.01.051
Co-authorsVanquan Vuong, Michael Bowyer
2015Vuong QV, Hirun S, Chuen TLK, Goldsmith CD, Murchie S, Bowyer MC, et al., 'Antioxidant and anticancer capacity of saponin-enriched Carica papaya leaf extracts', International Journal of Food Science and Technology, 50 169-177 (2015)

Summary: The papaya (Carica papaya) leaf (PL) contains high levels of saponins and polyphenolic compounds, and historically, it has been used as a folk medicine for numerous ailments, including cancer. PL is traditionally prepared by hot water extraction; however, optimised extraction conditions have not been assessed. This study optimised conditions for the extraction of saponins from PL and assessed their antioxidant capacity and antipancreatic cancer activity. Optimisation was achieved using response surface methodology. Saponins and total phenolic compounds were assessed for their antioxidant, free radical scavenging, ion-reducing capacity, and antipancreatic cancer activity. Optimal aqueous extraction conditions were 85 °C, 25 min. and a water-to-leaf ratio of 20:1 mL g-1. Ethanol extracts demonstrated higher antioxidant, free radical scavenging and ion-reducing capacity, as well as antipancreatic cancer activity. This study revealed that the PL contains numerous bioactive compounds, with significant anticancer activity warranting further studies on the isolation and characterisation of individual bioactive compounds from the PL.

DOI10.1111/ijfs.12618
Co-authorsVanquan Vuong, Michael Bowyer
2015Vuong QV, Hirun S, Chuen TLK, Goldsmith CD, Munro B, Bowyer MC, et al., 'Physicochemical, antioxidant and anti-cancer activity of a Eucalyptus robusta (Sm.) leaf aqueous extract', INDUSTRIAL CROPS AND PRODUCTS, 64 167-174 (2015)
DOI10.1016/j.indcrop.2014.10.061Author URL
Co-authorsMichael Bowyer, Vanquan Vuong, Jennette Sakoff, Anita Chalmers
2015Vuong QV, Hirun S, Chuen TLK, Goldsmith CD, Murchie S, Bowyer MC, et al., 'Antioxidant and anticancer capacity of saponin-enriched Carica papaya leaf extracts', INTERNATIONAL JOURNAL OF FOOD SCIENCE AND TECHNOLOGY, 50 169-177 (2015)
DOI10.1111/ijfs.12618Author URL
Co-authorsMichael Bowyer, Vanquan Vuong
2015Susanto JM, Colvin EK, Pinese M, Chang DK, Pajic M, Mawson A, et al., 'The epigenetic agents suberoylanilide hydroxamic acid and 5-AZA-2' deoxycytidine decrease cell proliferation, induce cell death and delay the growth of MiaPaCa2 pancreatic cancer cells in vivo', International Journal of Oncology, 46 2223-2230 (2015)

Despite incremental advances in the diagnosis and treatment for pancreatic cancer (PC), the 5-year survival rate remains <5%. Novel therapies to increase survival and quality of life for PC patients are desperately needed. Epigenetic therapeutic agents such as histone deacetylase inhibitors (HDACi) and DNA methyltransferase inhibitors (DNMTi) have demonstrated therapeutic benefits in human cancer. We assessed the efficacy of these epigenetic therapeutic agents as potential therapies for PC using in vitro and in vivo models. Treatment with HDACi [suberoylanilide hydroxamic acid (SAHA)] and DNMTi [5-AZA-2' deoxycytidine (5-AZA-dc)] decreased cell proliferation in MiaPaCa2 cells, and SAHA treatment, with or without 5-AZA-dc, resulted in higher cell death and lower DNA synthesis compared to 5-AZA-dc alone and controls (DMSO). Further, combination treatment with SAHA and 5-AZA-dc significantly increased expression of p21WAF1, leading to G1 arrest. Treatment with epigenetic agents delayed tumour growth in vivo, but did not decrease growth of established pancreatic tumours. In conclusion, these data demonstrate a potential role for epigenetic modifier drugs for the management of PC, specifically in the chemoprevention of PC, in combination with other chemotherapeutic agents.

DOI10.3892/ijo.2015.2894
2015Hirun S, Choi J-H, Ayarungsaritkul J, Pawsaut C, Sutthiwanjampa C, Vuong QV, et al., 'Optimization of far-infrared vacuum drying conditions for Miang leaves (Camellia sinensis var. assamica) using response surface methodology', Food Science and Biotechnology, 24 461-469 (2015)

Far-infrared (FIR) vacuum is an advanced drying technique that has recently been applied in food processing. Optimal drying conditions for processing tea from Miang leaves using FIR vacuum drying were investigated. Response surface methodology with a central composite design was used to design, analyze, and predict the optimal time and temperature conditions for FIR vacuum drying, taking into account the physicochemical properties of Miang leaves. When the temperature increased from 50 to 65°C and the time from 60 to 120 min, the amount of epicatechin, epicatechin gallate, epigallocatechin gallate, and total catechins significantly (p<0.05) increased while the moisture content and water activity significantly (p<0.05) decreased, compared with controls. The physicochemical properties of dried Miang leaves were significantly (p>0.05) influenced by time and temperature, compared with controls. Drying conditions of 65°C for 120 min are recommended for optimization of drying.

DOI10.1007/s10068-015-0061-8
Co-authorsVanquan Vuong
2015Bhuyan DJ, Quan VV, Chalmers AC, van Altena IA, Bowyer MC, Scarlett CJ, 'Microwave-assisted extraction of Eucalyptus robusta leaf for the optimal yield of total phenolic compounds', INDUSTRIAL CROPS AND PRODUCTS, 69 290-299 (2015)
DOI10.1016/j.indcrop.2015.02.044Author URL
Co-authorsAnita Chalmers, Michael Bowyer, Vanquan Vuong
2015Nguyen VT, Van Vuong Q, Bowyer MC, Van Altena IA, Scarlett CJ, 'Effects of Different Drying Methods on Bioactive Compound Yield and Antioxidant Capacity of Phyllanthus amarus', Drying Technology, 33 1006-1017 (2015)

Phyllanthus amarus (P. amarus) has been used as a herbal medicine, particularly for liver support, in many countries and its extracts have been shown to possess potent antioxidant and anticancer properties in vitro. The preparation of dried sample is crucial for further extraction and isolation of phytochemicals. In this study, the effects of six different drying methods (hot air, low-temperature air, infrared, microwave, sun, and vacuum drying) on the phytochemical yield and antioxidant capacity were determined to identify the optimal drying method for P. amarus. The results showed that different drying methods, as well as different drying conditions within each method, significantly affected phytochemical yield and antioxidant capacity of P. amarus extracts. Infrared drying at 30°C was the best method for both retention of bioactive compound yield and antioxidant capacity of P. amarus extract, with 12 compounds were identified. In contrast, low-temperature-air drying at 25°C not only required the longest drying time but also significantly reduced the levels of bioactive compounds and antioxidant capacity of P. amarus. Therefore, infrared drying at 30°C is suggested for drying P. amarus for subsequent assessment of bioactivity.

DOI10.1080/07373937.2015.1013197
Co-authorsMichael Bowyer, Vanquan Vuong
2015Vuong QV, Zammit N, Munro BR, Murchie S, Bowyer MC, Scarlett CJ, 'Effect of drying conditions on physicochemical and antioxidant properties of vitex agnus-castus leaves', Journal of Food Processing and Preservation, (2015)

Vitex agnus-castus (VitexAC) leaves have been used for medicinal purposes for many years. Drying is important to prepare starting materials for further processing, as it is associated with production cost and quality of the materials. Herein, the effects of five different drying conditions on the physical, chemical and antioxidant properties of VitexAC were evaluated. The results showed that 30% of dried leaves with moisture content of less than 7% could be produced from fresh leaves. VitexAC leaves dried by freeze and vacuum drying at 65C had higher levels of bioactive compounds as well as higher antioxidant capacity in comparison with other drying conditions, revealing that these drying conditions are more suitable for drying VitexAC leaves. However, freeze drying is costly and time-consuming; thus, vacuum drying at 65C is suggested for drying the VitexAC leaves as the starting materials for further processing steps. Practical Applications: As drying is an important process to prepare starting materials for further processing steps, it is important to compare different drying methods to identify the most suitable method with low cost and less effect on material quality. The results showed that inappropriate drying conditions resulted in big loss of bioactive compounds and antioxidant capacity. Vacuum drying at 65C was found to be the most suitable method, which can be easily applied for drying Vitex agnus-castus leaves in the industrial scale.

DOI10.1111/jfpp.12506
Co-authorsVanquan Vuong, Michael Bowyer
2015Waddell N, Pajic M, Patch AM, Chang DK, Kassahn KS, Bailey P, et al., 'Whole genomes redefine the mutational landscape of pancreatic cancer.', Nature, 518 495-501 (2015)
DOI10.1038/nature14169Author URL
CitationsScopus - 1
2015Vuong QV, Chalmers AC, Jyoti Bhuyan D, Bowyer MC, Scarlett CJ, 'Botanical, Phytochemical, and Anticancer Properties of the Eucalyptus Species.', Chem Biodivers, 12 907-924 (2015)
DOI10.1002/cbdv.201400327Author URL
Co-authorsVanquan Vuong, Anita Chalmers, Michael Bowyer
2014Shahbazi J, Scarlett CJ, Norris MD, Liu B, Haber M, Tee AE, et al., 'Histone Deacetylase 2 and N-Myc reduce p53 protein phosphorylation at serine 46 by repressing gene transcription of tumor protein 53-induced nuclear protein 1', Oncotarget, 5 4257-4268 (2014) [C1]

Myc oncoproteins and histone deacetylases (HDACs) exert oncogenic effects by modulating gene transcription. Paradoxically, N-Myc induces p53 gene expression. Tumor protein 53-induced nuclear protein 1 (TP53INP1) phosphorylates p53 protein at serine 46, leading to enhanced p53 activity, transcriptional activation of p53 target genes and programmed cell death. Here we aimed to identify the mechanism through which N-Myc overexpressing p53 wild-type neuroblastoma cells acquired resistance to apoptosis. TP53INP1 was found to be one of the genes most significantly repressed by HDAC2 and N-Myc according to Affymetrix microarray gene expression datasets. HDAC2 and N-Myc reduced TP53INP1 gene expression by direct binding to the TP53INP1 gene promoter, leading to transcriptional repression of TP53INP1, p53 protein de-phosphorylation at serine 46, neuroblastoma cell proliferation and survival. Moreover, low levels of TP53INP1 expression in human neuroblastoma tissues correlated with high levels of N-Myc expression and poor patient outcome, and the BET bromodomain inhibitors JQ1 and I-BET151 reduced N-Myc expression and reactivated TP53INP1 expression in neuroblastoma cells. These findings identify TP53INP1 repression as an important co-factor for N-Myc oncogenesis, and provide further evidence for the potential application of BET bromodomain inhibitors in the therapy of N-Myc-induced neuroblastoma.

CitationsScopus - 2Web of Science - 2
2014Nagrial AM, Chang DK, Nguyen NQ, Johns AL, Chantrill LA, Humphris JL, et al., 'Adjuvant chemotherapy in elderly patients with pancreatic cancer', British Journal of Cancer, 110 313-319 (2014) [C1]

Background:Adjuvant chemotherapy improves survival for patients with resected pancreatic cancer. Elderly patients are under-represented in Phase III clinical trials, and as a consequence the efficacy of adjuvant therapy in older patients with pancreatic cancer is not clear. We aimed to assess the use and efficacy of adjuvant chemotherapy in older patients with pancreatic cancer.Methods:We assessed a community cohort of 439 patients with a diagnosis of pancreatic ductal adenocarcinoma who underwent operative resection in centres associated with the AUSn Pancreatic Cancer Genome Initiative.Results:The median age of the cohort was 67 years. Overall only 47% of all patients received adjuvant therapy. Patients who received adjuvant chemotherapy were predominantly younger, had later stage disease, more lymph node involvement and more evidence of perineural invasion than the group that did not receive adjuvant treatment. Overall, adjuvant chemotherapy was associated with prolonged survival (median 22.1 vs 15.8 months; P<0.0001). Older patients (aged =70) were less likely to receive adjuvant chemotherapy (51.5% vs 29.8%; P<0.0001). Older patients had a particularly poor outcome when adjuvant therapy was not delivered (median survival=13.1 months; HR 1.89, 95% CI: 1.27-2.78, P=0.002).Conclusion:Patients aged =70 are less likely to receive adjuvant therapy although it is associated with improved outcome. Increased use of adjuvant therapy in older individuals is encouraged as they constitute a large proportion of patients with pancreatic cancer. © 2014 Cancer Research UK.

DOI10.1038/bjc.2013.722
CitationsScopus - 2Web of Science - 3
2014Morran DC, Wu J, Jamieson NB, Mrowinska A, Kalna G, Karim SA, et al., 'Targeting mTOR dependency in pancreatic cancer', Gut, 63 1481-1489 (2014)
DOI10.1136/gutjnl-2013-306202
CitationsScopus - 2
2014Morran DC, Wu J, Jamieson NB, Mrowinska A, Kalna G, Karim SA, et al., 'Targeting mTOR dependency in pancreatic cancer', Gut, 63 1481-1489 (2014) [C1]

Objective: Pancreatic cancer is a leading cause of cancer-related death in the Western world. Current chemotherapy regimens have modest survival benefit. Thus, novel, effective therapies are required for treatment of this disease. Design Activating KRAS mutation almost always drives pancreatic tumour initiation, however, deregulation of other potentially druggable pathways promotes tumour progression. PTEN loss leads to acceleration of Kras G12Ddriven pancreatic ductal adenocarcinoma (PDAC) in mice and these tumours have high levels of mammalian target of rapamycin (mTOR) signalling. To test whether these KRAS PTEN pancreatic tumours show mTOR dependence, we compared response to mTOR inhibition in this model, to the response in another established model of pancreatic cancer, KRAS P53. We also assessed whether there was a subset of pancreatic cancer patients who may respond to mTOR inhibition. Results: We found that tumours in KRAS PTEN mice exhibit a remarkable dependence on mTOR signalling. In these tumours, mTOR inhibition leads to proliferative arrest and even tumour regression. Further, we could measure response using clinically applicable positron emission tomography imaging. Importantly, pancreatic tumours driven by activated KRAS and mutant p53 did not respond to treatment. In human tumours, approximately 20% of cases demonstrated low PTEN expression and a gene expression signature that overlaps with murine KRAS PTEN tumours. Conclusions: KRAS PTEN tumours are uniquely responsive to mTOR inhibition. Targeted anti-mTOR therapies may offer clinical benefit in subsets of human PDAC selected based on genotype, that are dependent on mTOR signalling. Thus, the genetic signatures of human tumours could be used to direct pancreatic cancer treatment in the future.

DOI10.1136/gutjnl-2013-306202
CitationsScopus - 3Web of Science - 4
2014Vuong QV, Hirun S, Phillips PA, Chuen TLK, Bowyer MC, Goldsmith CD, Scarlett CJ, 'Fruit-derived phenolic compounds and pancreatic cancer: Perspectives from Australian native fruits', JOURNAL OF ETHNOPHARMACOLOGY, 152 227-242 (2014) [C1]
DOI10.1016/j.jep.2013.12.023Author URL
CitationsScopus - 2Web of Science - 2
Co-authorsVanquan Vuong, Michael Bowyer
2014Hirun S, Utama-ang N, Vuong QV, Scarlett CJ, 'Investigating the Commercial Microwave Vacuum Drying Conditions on Physicochemical Properties and Radical Scavenging Ability of Thai Green Tea', DRYING TECHNOLOGY, 32 47-54 (2014) [C1]
DOI10.1080/07373937.2013.811249Author URL
CitationsScopus - 2Web of Science - 1
Co-authorsVanquan Vuong
2014Sun Y, Liu PY, Scarlett CJ, Malyukova A, Liu B, Marshall GM, et al., 'Histone deacetylase 5 blocks neuroblastoma cell differentiation by interacting with N-Myc', Oncogene, 33 2987-2994 (2014)
DOI10.1038/onc.2013.253
CitationsScopus - 2
2014Sun Y, Liu PY, Scarlett CJ, Malyukova A, Liu B, Marshall GM, et al., 'Histone deacetylase 5 blocks neuroblastoma cell differentiation by interacting with N-Myc', Oncogene, 33 2987-2994 (2014) [C1]

The N-Myc oncoprotein induces neuroblastoma, which arises from undifferentiated neuroblasts in the sympathetic nervous system, by modulating gene and protein expression and consequently causing cell differentiation block and cell proliferation. The class IIa histone deacetylase 5 (HDAC5) represses gene transcription, and blocks myoblast, osteoblast and leukemia cell differentiation. Here we showed that N-Myc upregulated HDAC5 expression in neuroblastoma cells. Conversely, HDAC5 repressed the ubiquitin-protein ligase NEDD4 gene expression, increased Aurora A gene expression and consequently upregulated N-Myc protein expression. Genome-wide gene expression analysis and protein co-immunoprecipitation assays revealed that HDAC5 and N-Myc repressed the expression of a common subset of genes by forming a protein complex, whereas HDAC5 and the class III HDAC SIRT2 independently repressed the expression of another common subset of genes without forming a protein complex. Moreover, HDAC5 blocked differentiation and induced proliferation in neuroblastoma cells. Taken together, our data identify HDAC5 as a novel co-factor in N-Myc oncogenesis, and provide the evidence for the potential application of HDAC5 inhibitors in the therapy of N-Myc-induced neuroblastoma and potentially other c-Myc-induced malignancies.. © 2014 Macmillan Publishers Limited All rights reserved 0950-9232/14.

DOI10.1038/onc.2013.253
CitationsScopus - 4Web of Science - 3
2014Colyin EK, Scarlett CJ, 'A historical perspective of pancreatic cancer mouse models', SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY, 27 96-105 (2014) [C1]
DOI10.1016/j.semcdb.2014.03.025Author URL
CitationsScopus - 2
2014Vuong QV, Sadeqzadeh E, Hirun S, Goldsmith CD, Zammitt N, Bowyer MB, et al., 'Phenolic Compounds, Antioxidant and Anti-Cancer Properties of the Australian Maroon Bush Scaevola spinescens (Goodeniaceae)', Journal of Bioanalysis & Biomedicine, S12 (2014) [C1]
DOI10.4172/1948-593X.S12-002
Co-authorsJennette Sakoff, Michael Bowyer, Rick Thorne, Vanquan Vuong, Judith Weidenhofer
2014Vuong QV, Hirun S, Chuen TLK, Goldsmith CD, Bowyer MC, Chalmers AC, et al., 'Physicochemical composition, antioxidant and anti-proliferative capacity of a lilly pilly (Syzygium paniculatum) extract', JOURNAL OF HERBAL MEDICINE, 4 134-140 (2014)
DOI10.1016/j.hermed.2014.04.003Author URL
CitationsWeb of Science - 1
Co-authorsMichael Bowyer, Vanquan Vuong, Anita Chalmers
2014Vuong QV, Hirun S, Chuen TLK, Goldsmith CD, Bowyer MC, Chalmers AC, et al., 'Physicochemical composition, antioxidant and anti-proliferative capacity of a lilly pilly (Syzygium paniculatum) extract', Journal of Herbal Medicine, 4 134-140 (2014) [C1]

Lilly pilly (LP) fruit (Syzygium paniculatum Gaertn.) is widely grown in eastern Australia and has been used as food by indigenous Australians. However, there is limited information on its bioactivity. This study investigated the physicochemical and antioxidant properties of the crude fruit extract, identified its bioactive compounds and also assessed its potential anti-proliferative effect on pancreatic cancer cells. Our data showed that the LP extract was water-soluble and possessed a total phenolic content of 96 mg of gallic acid equivalents (GAE)/g, flavonoid levels of 52 mg catechin equivalents (CAE)/g, proanthocyanidin levels of 29 mg CAE/g. Several phenolic compounds such as gallic acid, chlorogenic acid, catechin and epicatechin were identified in the LP extract with levels of 0.39, 2.35, 0.47 and 2.9 mg/g, respectively. Results from six different antioxidant assays revealed that the LP extract pocessed potent antioxidant and free radical scavenging capacity. Although antioxidant capacity of the extract was lower than that of vitamin E, vitamin C and BHT, it could be significantly improved if the extract was to be further purified. We also showed that the LP extract (200 µg/mL) significantly reduced the viability of MiaPaCa-2 and ASPC-1 pancreatic cancer cells to levels comparable to that of the chemotherapeutic agent gemcitabine. For this reason lilly pilly should be further investigated for its health promoting and potential anti-cancer benefits, particularly for pancreatic cancer. © 2014 Elsevier GmbH.

DOI10.1016/j.hermed.2014.04.003
Co-authorsVanquan Vuong, Michael Bowyer, Anita Chalmers
2014Goldsmith C, Vuong Q, Stathopoulos C, Roach P, Scarlett C, 'Optimization of the Aqueous Extraction of Phenolic Compounds from Olive Leaves', Antioxidants, 3 700-712 (2014) [C1]
DOI10.3390/antiox3040700
Co-authorsPaul Roach, Vanquan Vuong
2014Vuong Q, Goldsmith C, Dang T, Nguyen V, Bhuyan D, Sadeqzadeh E, et al., 'Optimisation of Ultrasound-Assisted Extraction Conditions for Phenolic Content and Antioxidant Capacity from Euphorbia tirucalli Using Response Surface Methodology', Antioxidants, 3 604-617 (2014) [C1]
DOI10.3390/antiox3030604
Co-authorsMichael Bowyer, Vanquan Vuong
2013Scarlett CJ, 'Contribution of bone marrow derived cells to the pancreatic tumor microenvironment', Frontiers in Physiology, 4 (2013) [C1]
DOI10.3389/fphys.2013.00056
CitationsScopus - 2Web of Science - 3
2013Chang DK, Jamieson NB, Johns AL, Scarlett CJ, Pajic M, Chou A, et al., 'Histomolecular Phenotypes and Outcome in Adenocarcinoma of the Ampulla of Vater', JOURNAL OF CLINICAL ONCOLOGY, 31 1348-1356 (2013) [C1]
DOI10.1200/JCO.2012.46.8868Author URL
CitationsScopus - 11Web of Science - 10
2013Liu PY, Xu N, Malyukova A, Scarlett CJ, Sun YT, Zhang XD, et al., 'The histone deacetylase SIRT2 stabilizes Myc oncoproteins', CELL DEATH AND DIFFERENTIATION, 20 503-514 (2013) [C1]
DOI10.1038/cdd.2012.147Author URL
CitationsScopus - 31Web of Science - 28
Co-authorsXu Zhang
2013Vuong QV, Hirun S, Roach PD, Bowyer MC, Phillips PA, Scarlett CJ, 'Effect of extraction conditions on total phenolic compounds and antioxidant activities of Carica papaya leaf aqueous extracts', JOURNAL OF HERBAL MEDICINE, 3 104-111 (2013) [C1]
DOI10.1016/j.hermed.2013.04.004Author URL
CitationsScopus - 8Web of Science - 9
Co-authorsVanquan Vuong, Michael Bowyer, Paul Roach
2012Biankin AV, Waddell N, Kassahn KS, Gingras M-C, Muthuswamy LB, Johns AL, et al., 'Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes', Nature, 491 399-405 (2012) [C1]
CitationsScopus - 266Web of Science - 270
2012Das A, Musgrove EA, Sutherland RL, Biankin AV, Humphris JL, Chang DK, et al., 'The prognostic and predictive value of serum CA19.9 in pancreatic cancer', Annals of Oncology, 23 1713-1722 (2012) [C1]
CitationsScopus - 45Web of Science - 38
2011Marshall GM, Liu PY, Gherardi S, Scarlett CJ, Bedalov A, Xu N, et al., 'SIRT1 promotes N-Myc oncogenesis through a positive feedback loop involving the effects of MKP3 and ERK on N-Myc protein stability', PLoS Genetics, 7 (2011) [C1]
DOI10.1371/journal.pgen.1002135
CitationsScopus - 54Web of Science - 46
2011Colvin EK, Susanto JM, Kench JG, Ong VN, Mawson A, Pinese M, et al., 'Retinoid signaling in pancreatic cancer, injury and regeneration', PLoS ONE, 6 e29075 (2011) [C1]
DOI10.1371/journal.pone.0029075
2011Chong JJH, Chandrakanthan V, Xaymardan M, Asli NS, Li J, Ahmed I, et al., 'Adult cardiac-resident MSC-like stem cells with a proepicardial origin', Cell Stem Cell, 9 527-540 (2011) [C1]
DOI10.1016/j.stem.2011.10.002
CitationsScopus - 102Web of Science - 92
2011Scarlett CJ, Colvin EK, Pinese M, Chang DK, Morey AL, Musgrove EA, et al., 'Recruitment and activation of pancreatic stellate cells from the bone marrow in pancreatic cancer: A model of tumor-host interaction', PLoS One, 6 1-8 (2011) [C1]
DOI10.1371/journal.pone.0026088
CitationsScopus - 18
2011Kwong RA, Scarlett CJ, Kalish LH, Cole IE, Kench JG, Sum EY, et al., 'LMO4 expression in squamous cell carcinoma of the anterior tongue', Histopathology, 58 477-480 (2011) [C3]
DOI10.1111/j.1365-2559.2011.03765.x
CitationsScopus - 2
2011Nguyen NQ, Johns AL, Gill AJ, Ring N, Chang DK, Clarkson A, et al., 'Clinical and immunohistochemical features of 34 solid pseudopapillary tumors of the pancreas', Journal of Gastroenterology and Hepatology, 26 267-274 (2011) [C1]
CitationsScopus - 14Web of Science - 9
2010Xue A, Scarlett CJ, Chung L, Butturini G, Scarpa A, Gandy R, et al., 'Discovery of serum biomarkers for pancreatic adenocarcinoma using proteomic analysis', British Journal of Cancer, 103 391-400 (2010) [C1]
DOI10.1038/sj.bjc.6605764
CitationsScopus - 21Web of Science - 21
2010Marshall GM, Gherardi S, Xu N, Neiron Z, Trahair T, Scarlett CJ, et al., 'Transcriptional upregulation of histone deacetylase 2 promotes Myc-induced oncogenic effects', Oncogene, 29 5957-5968 (2010) [C1]
CitationsScopus - 37Web of Science - 34
2009Pinese M, Scarlett CJ, Kench JG, Colvin EK, Segara D, Henshall SM, et al., 'Messina: A novel analysis tool to identify biologically relevant molecules in disease', PLoS One, 4 (2009) [C1]
DOI10.1371/journal.pone.0005337
CitationsScopus - 4Web of Science - 3
2009Biankin AV, Kench JG, Colvin EK, Segara D, Scarlett CJ, Nguyen NQ, et al., 'Expression of S100A2 Calcium-Binding Protein Predicts Response to Pancreatectomy for Pancreatic Cancer', Gastroenterology, 137 558-568 (2009) [C1]
DOI10.1053/j.gastro.2009.04.009
CitationsScopus - 33Web of Science - 31
2009Chang DK, Johns AL, Merrett ND, Gill AJ, Colvin EK, Scarlett CJ, et al., 'Margin Clearance and Outcome in Resected Pancreatic Cancer', Journal of Clinical Oncology, 27 2855-2862 (2009) [C1]
DOI10.1200/JCO.2008.20.5104
CitationsScopus - 101Web of Science - 87
2008Murphy NC, Scarlett CJ, Kench JG, Sym EYM, Segara D, Colvin EK, et al., 'Expression of LMO4 and outcome in pancreatic ductal adenocarcinoma', British Journal of Cancer, 98 537-541 (2008) [C1]
DOI10.1038/sj.bjc.6604177
CitationsScopus - 18
2008Kuo SCL, Gananadha S, Scarlett CJ, Gill A, Smith RC, 'Sporadic pancreatic polypeptide secreting tumors (PPomas) of the pancreas', World Journal of Surgery, 32 1815-1822 (2008) [C1]
DOI10.1007/s00268-008-9499-7
CitationsScopus - 8Web of Science - 6
2008Xue A, Scarlett CJ, Jackson CJ, Allen BJ, Smith RC, 'Prognostic significance of growth factors and the urokinase-type plasminogen activator system in pancreatic ductal adenocarcinoma', Pancreas, 36 160-167 (2008) [C1]
DOI10.1097/MPA.0b013e31815750f0
CitationsScopus - 28
2007Smith R, Xue A, Gill A, Scarlett C, Saxby A, Clarkson A, Hugh T, 'High expression of plasminogen activator inhibitor-2 (PAI-2) is a predictor of improved survival in patients with pancreatic adenocarcinoma', WORLD JOURNAL OF SURGERY, 31 493-503 (2007) [C1]
DOI10.1007/s00268-006-0289-9Author URL
CitationsWeb of Science - 21
2007Scarlett CJ, Samra SJ, Xue A, Baxter RC, Smith RC, 'Classification of pancreatic cystic lesions using SELDI-TOF mass spectrometry', ANZ Journal of Surgery, 77 648-653 (2007) [C1]
DOI10.1111/j.1445-2197.2007.04179.x
2007O'Leary MJ, Xue A, Scarlett CJ, Sevette A, Kee AJ, Smith RC, 'Parenteral versus enteral nutrition: Effect on serum cytokines and the hepatic expression of mRNA of suppressor of cytokine signaling proteins, insulin-like growth factor-1 and the growth hormone receptor in rodent sepsis', CRITICAL CARE, 11 (2007) [C1]
DOI10.1186/cc5972Author URL
CitationsWeb of Science - 5
2006Scarlett CJ, Saxby AJ, Nielsen A, Bell C, Samra JS, Hugh T, et al., 'Proteomic profiling of cholangiocarcinoma: Diagnostic potential of SELDI-TOF MS in malignant bile duct stricture', Hepatology, 44 658-666 (2006) [C1]
DOI10.1002/hep.21294
2006Scarlett CJ, Smith RC, Saxby A, Nielsen A, Samra JS, Wilson SR, Baxter RC, 'Proteomic Classification of Pancreatic Adenocarcinoma Tissue Using Protein Chip Technology', Gastroenterology, 130 1670-1678 (2006) [C1]
DOI10.1053/j.gastro.2006.02.036
2005Saxby AJ, Nielsen A, Scarlett CJ, Clarkson A, Morey A, Gill A, Smith RC, 'Assessment of HER-2 status in pancreatic adenocarcinoma: Correlation of immunohistochemistry, quantitative real-time RT-PCR, and FISH with aneuploidy and survival', American Journal of Surgical Pathology, 29 1125-1134 (2005) [C1]
DOI10.1097/01.pas.0000160979.85457.73
2005Nielsen A, Scarlett CJ, Samra JS, Gill A, Li Y, Allen BJ, Smith RC, 'Significant overexpression of urokinase-type plasminogen activator in pancreatic adenocarcinoma using real-time quantitative reverse transcription polymerase chain reaction', Journal of Gastroenterology and Hepatology, 20 256-263 (2005) [C1]
DOI10.1111/j.1440-1746.2004.03531.x
2004Scarlett CJ, O'Leary MJ, Kee AJ, Nielsen A, Sevette A, Baxter RC, Smith RC, 'A study of parenteral versus enteral nutrition following caecal ligation and puncture in the rat: Influence on survival and tissue protein turnover', Clinical Nutrition, 23 1135-1145 (2004) [C1]
DOI10.1016/j.clnu.2004.02.008
2001Scarlett CJ, Lin M, Aitken RJ, 'Actin polymerisation during morphogenesis of the acrosome as spermatozoa undergo epididymal maturation in the tammar wallaby (Macropus eugenii)', Journal of Anatomy, 198 93-101 (2001) [C1]
DOI10.1017/S0021878200007299
CitationsScopus - 9Web of Science - 8
Co-authorsMinjie Lin, John Aitken
Show 52 more journal articles

Review (3 outputs)

YearCitationAltmetricsLink
2011Scarlett CJ, Biankin A, 'S100A2 (S100 calcium binding protein A2; 1q21)', Atlas of Genetics and Cytogenetics in Oncology and Haematology (2011) [D2]
2011Scarlett CJ, Salisbury EL, Biankin AV, Kench J, 'Precursor lesions in pancreatic cancer: Morphological and molecular pathology', Pathology (2011) [D1]
DOI10.1097/PAT.0b013e3283445e3a
CitationsScopus - 22Web of Science - 17
2011Pajic M, Scarlett CJ, Chang DK, Sutherland RL, Biankin AV, 'Preclinical strategies to define predictive biomarkers for therapeutically relevant cancer subtypes', Human Genetics (2011) [D1]
DOI10.1007/s00439-011-0990-0
CitationsScopus - 8Web of Science - 8

Conference (6 outputs)

YearCitationAltmetricsLink
2014Shahbazi J, Scarlett CJ, Norris M, Liu B, Haber M, Tee AE, et al., 'Histone deacetylase 2 and N-Myc reduce p53 protein phosphorylation at serine 46 by repressing gene transcription of tumor protein 53-induced nuclear protein 1', CANCER RESEARCH, San Diego, CA (2014) [E3]
DOI10.1158/1538-7445.AM2014-5138Author URL
2014Sun Y, Liu PY, Scarlett CJ, Malyukova A, Liu B, Marshall GM, et al., 'Histone deacetylase 5 blocks neuroblastoma cell differentiation by forming a protein complex with N-Myc and repressing target gene transcription', INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE (2014) [E3]
Author URL
2014Faulkner S, Roselli S, Thorne RF, Scarlett CJ, Walker MM, Hondermarck H, 'PRONGF AND SORTILIN EXPRESSION AND FUNCTION IN PANCREATIC CANCER', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
Author URL
Co-authorsHubert Hondermarck, Rick Thorne, Marjorie Walker
2014Goldsmith CD, Vuong QV, Sadeqzadeh E, Stathopoulos CE, Roach PD, Scarlett CJ, 'ANTI-PROLIFERATIVE CAPACITY OF OLEUROPEIN RICH OLIVE LEAF EXTRACTS AGAINST PANCREATIC CANCER CELLS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
Author URL
Co-authorsPaul Roach, Vanquan Vuong
2014Sadeqzadeh E, Vuong QV, Goldsmith CD, Nguyen VT, Bhuyan DJ, Trung TD, et al., 'A NATURAL PRODUCT DRUG DISCOVERY PIPELINE FOR NOVEL PANCREATIC CANCER THERAPIES: A NEW CANCER RESEARCH HUB FOR THE HUNTER REGION OF NSW', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
Author URL
Co-authorsTroy Gaston, Vanquan Vuong, Michael Bowyer, Judith Weidenhofer, Rick Thorne, Natalie Moltschaniwskyj, Anita Chalmers
2012Chantrill L, Gill A, Johns A, Wu J, Scarlett CJ, Biankin A, Australian Pancreatic Cancer Genome Initiative, 'The outliers of pancreatic cancer: Preliminary data for timeless expression as a prognostic biomarker', Asia-Pacific Journal of Clinical Oncology: Special Issue: Medical Oncology Group of Australia Incorporated Annual Scientific Meeting, Program and Abstracts: Targeting Cancer from Diagnosis to Cure, Melbourne, Vic (2012) [E3]
Show 3 more conferences
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Grants and Funding

Summary

Number of grants20
Total funding$5,059,128

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


20151 grants / $8,000

Novel Drug Leads for Pancreatic Cancer Treatment$8,000

Funding body: Calvary Mater Newcastle

Funding bodyCalvary Mater Newcastle
Project TeamDoctor Christopher Scarlett, Dr Jennette Sakoff
SchemeProject Grant
RoleLead
Funding Start2015
Funding Finish2015
GNoG1500436
Type Of FundingContract - Aust Non Government
Category3AFC
UONY

20146 grants / $2,292,372

Food & Beverage Supply Chain Optimisation Industrial Transformation Training Centre$2,119,872

Funding body: ARC (Australian Research Council)

Funding bodyARC (Australian Research Council)
Project TeamProfessor Rick Middleton, Associate Professor Regina Berretta, Associate Professor Michael Bowyer, Doctor Ali Eshragh, Doctor Christopher Scarlett, Doctor Masoud Talebian, Associate Professor Behnam Fahimnia, Professor Mathieu Savelsbergh, Professor Natashia Boland, Dr Costas Stathopoulos, Professor John Bartholdi, Doctor John Golding, Doctor Simon Dunstall, Mrs Carlee McGowan, Mr Robert McMahon, Mr Robert Scoines, Mr Tim Norris
SchemeIndustrial Transformation Training Centres
RoleInvestigator
Funding Start2014
Funding Finish2014
GNoG1301004
Type Of FundingAust Competitive - Commonwealth
Category1CS
UONY

Food & Beverage Supply Chain Optimisation Industrial Transformation Training Centre$90,000

Funding body: Coca Cola Amatil (Australia)

Funding bodyCoca Cola Amatil (Australia)
Project TeamProfessor Rick Middleton, Associate Professor Regina Berretta, Associate Professor Michael Bowyer, Doctor Ali Eshragh, Doctor Christopher Scarlett, Doctor Masoud Talebian, Associate Professor Behnam Fahimnia, Professor Mathieu Savelsbergh, Professor Natashia Boland, Dr Costas Stathopoulos, Professor John Bartholdi, Doctor John Golding, Doctor Simon Dunstall, Mrs Carlee McGowan, Mr Robert McMahon, Mr Robert Scoines, Mr Tim Norris
SchemeARC IC Partner Funding
RoleInvestigator
Funding Start2014
Funding Finish2014
GNoG1301129
Type Of FundingAust Competitive - Commonwealth
Category1CS
UONY

Food & Beverage Supply Chain Optimisation Industrial Transformation Training Centre$30,000

Funding body: Sanitarium Health and Wellbeing Company

Funding bodySanitarium Health and Wellbeing Company
Project TeamProfessor Rick Middleton, Associate Professor Regina Berretta, Associate Professor Michael Bowyer, Doctor Ali Eshragh, Doctor Christopher Scarlett, Doctor Masoud Talebian, Associate Professor Behnam Fahimnia, Professor Mathieu Savelsbergh, Professor Natashia Boland, Dr Costas Stathopoulos, Professor John Bartholdi, Doctor John Golding, Doctor Simon Dunstall, Mrs Carlee McGowan, Mr Robert McMahon, Mr Robert Scoines, Mr Tim Norris
SchemeARC IC Partner Funding
RoleInvestigator
Funding Start2014
Funding Finish2014
GNoG1301130
Type Of FundingAust Competitive - Commonwealth
Category1CS
UONY

Food & Beverage Supply Chain Optimisation Industrial Transformation Training Centre$30,000

Funding body: Sunrice

Funding bodySunrice
Project TeamProfessor Rick Middleton, Associate Professor Regina Berretta, Associate Professor Michael Bowyer, Doctor Ali Eshragh, Doctor Christopher Scarlett, Doctor Masoud Talebian, Associate Professor Behnam Fahimnia, Professor Mathieu Savelsbergh, Professor Natashia Boland, Dr Costas Stathopoulos, Professor John Bartholdi, Doctor John Golding, Doctor Simon Dunstall, Mrs Carlee McGowan, Mr Robert McMahon, Mr Robert Scoines, Mr Tim Norris
SchemeARC IC Partner Funding
RoleInvestigator
Funding Start2014
Funding Finish2014
GNoG1301131
Type Of FundingAust Competitive - Commonwealth
Category1CS
UONY

Identification and evaluation of anti-pancreatic cancer activity of cytotoxic compounds extracted from Australian sea sponges: a pilot study$20,500

Funding body: Hunter Medical Research Institute

Funding bodyHunter Medical Research Institute
Project TeamDoctor Christopher Scarlett, Doctor Quan Vuong, Doctor Jude Weidenhofer, Doctor Rick Thorne, Associate Professor Michael Bowyer, Doctor Troy Gaston
SchemeProject Grant
RoleLead
Funding Start2014
Funding Finish2014
GNoG1401452
Type Of FundingGrant - Aust Non Government
Category3AFG
UONY

2013 Vice Chancellor's Award for Research Excellence - Regional$2,000

Funding body: University of Newcastle

Funding bodyUniversity of Newcastle
Project TeamDoctor Christopher Scarlett
SchemeAward for Research Excellence
RoleLead
Funding Start2014
Funding Finish2014
GNoG1301445
Type Of FundingInternal
CategoryINTE
UONY

20133 grants / $42,303

Gastro-pancreatic cancer research$20,050

Funding body: Terrigal Trotters Inc. Running Club

Funding bodyTerrigal Trotters Inc. Running Club
Project TeamDoctor Christopher Scarlett
SchemeBay to Bay Running Festival
RoleLead
Funding Start2013
Funding Finish2013
GNoG1301010
Type Of FundingGrant - Aust Non Government
Category3AFG
UONY

Extraction and identification of cytotoxic compounds from Australian sea sponges as novel therapeutic agents for pancreatic cancer.$14,749

Funding body: University of Newcastle - Faculty of Science & IT

Funding bodyUniversity of Newcastle - Faculty of Science & IT
Project TeamDoctor Christopher Scarlett, Doctor Quan Vuong
SchemeStrategic Small Grant
RoleLead
Funding Start2013
Funding Finish2013
GNoG1401071
Type Of FundingInternal
CategoryINTE
UONY

Faculty Visiting Fellowship 2013$7,504

Funding body: University of Newcastle - Faculty of Science & IT

Funding bodyUniversity of Newcastle - Faculty of Science & IT
Project TeamDoctor Christopher Scarlett
SchemeVisiting Fellowship
RoleLead
Funding Start2013
Funding Finish2013
GNoG1401145
Type Of FundingInternal
CategoryINTE
UONY

20125 grants / $583,826

The therapeutic potential of targeting S100A2 calcium-binding protein in pancreatic cancer$177,451

Funding body: Cancer Australia

Funding bodyCancer Australia
Project TeamDoctor Christopher Scarlett
SchemePriority-driven Collaborative Cancer Research Scheme
RoleLead
Funding Start2012
Funding Finish2012
GNoG1200404
Type Of FundingAust Competitive - Commonwealth
Category1CS
UONY

The therapeutic potential of targeting S100A2 calcium-binding protein in pancreatic cancer$177,450

Pancreatic cancer (PC) is the fourth leading cause of cancer death in Western societies with an overall 5-year survival rate of less than 5%. Consequently, there is an urgent need to develop novel therapeutic strategies. Analysis of clinical material by our group demonstrate that S100A2 calcium-binding protein defines a specific pancreatic cancer phenotype, and suggests that S100A2 calcium-binding protein may either play a key role, or is a surrogate marker of a metastatic phenotype. In addition, our preliminary experiments suggest that S100A2 does play a key role in the metastatic process in PC. Gain of function studies showed increased invasion in vitro, and in vivo analyses demonstrated marked increased potential to develop liver metastases, the major cause of death for pancreatic cancer. Consequently, the overall aim of this proposal is to test the hypothesis that S100A2 plays a role in pancreatic cancer metastasis, and may be suitable as a therapeutic target in pancreatic cancer.
Funding body: Cure Cancer Australia Foundation

Funding bodyCure Cancer Australia Foundation
Project Team
SchemeResearch Grant
RoleLead
Funding Start2012
Funding Finish2013
GNo
Type Of FundingNot Known
CategoryUNKN
UONY

Novel Targeted Therapies for Pancreatic Cancer$149,877

Funding body: Cancer Institute NSW

Funding bodyCancer Institute NSW
Project TeamDoctor Christopher Scarlett
SchemeCareer Development Fellowship
RoleLead
Funding Start2012
Funding Finish2012
GNoG1200531
Type Of FundingOther Public Sector - State
Category2OPS
UONY

Establishment of a pancreatic cancer research program for screening the activity and efficacy of natural bioactive compounds$74,048

Funding body: Ramaciotti Foundations

Funding bodyRamaciotti Foundations
Project TeamDoctor Christopher Scarlett
SchemeEstablishment Grant
RoleLead
Funding Start2012
Funding Finish2012
GNoG1200739
Type Of FundingGrant - Aust Non Government
Category3AFG
UONY

Project support to develop pancreatic cancer research within the School$5,000

Funding body: University of Newcastle

Funding bodyUniversity of Newcastle
Project TeamDoctor Christopher Scarlett
SchemeNew Staff Grant
RoleLead
Funding Start2012
Funding Finish2012
GNoG1200559
Type Of FundingInternal
CategoryINTE
UONY

20111 grants / $344,208

Targeting histone deacetylases for the therapy of Myc-induced malignancies$344,208

BACKGROUND: N-Myc and c-Myc oncoproteins are over-expressed in tumour tissues from neuroblastoma (N-Myc) and pancreatic cancer (c-Myc) patients, induce oncogenesis by modulating gene transcription (CIA, PNAS 2007), and are stabilized when phosphorylated by ERK. By repressing target gene transcription, histone deacetylase 2 (HDAC2) induces proliferation and blocks apoptosis in cancer cells, and HDAC5 blocks stem cell differentiation. HDAC inhibitors including panobinostat are highly effective anti-cancer agents in clinical trials. However, some patients are insensitive. The ERK inhibitor PD0325901 reduces Myc expression, induces tumour cell growth arrest and apoptosis, and blocks tumour growth in mice and in clinical trials. PRELIMINARY DATA: We have found in neuroblastoma and pancreatic cancer cells that Myc oncoproteins up-regulate HDAC2 and HDAC5 expression, that HDAC2 promotes cell proliferation and HDAC5 blocks cell differentiation, and that HDAC2 and Myc commonly repress the transcription of a subset of genes and form a protein complex. Moreover, HDAC2 protein expression is up-regulated in Myc over-expressing neuroblastoma and pancreatic cancer tissues, and panobinostat and PD0325901 exert synergistic anti-cancer effects in vitro. AIMS: To define the roles of HDAC2 up-regulation in Myc-induced transcriptional repression, cell proliferation and/or apoptosis, HDAC5 up-regulation in Myc-induced cell differentiation block, HDAC2 and HDAC5 in the initiation and progression of neuroblastoma and pancreatic cancer in vivo, and the anti-cancer efficacy of panobinostat and PD0325901 combination therapy against neuroblastoma and pancreatic cancer in vitro and in vivo. SIGNIFICANCE: This innovative project addresses an unrecognised interaction between HDAC2, HDAC5 and Myc. Successful completion of this project will provide direct evidence for clinical trials of the combination therapy for the treatment of neuroblastoma and pancreatic cancer patients.
Funding body: NHMRC (National Health & Medical Research Council)

Funding bodyNHMRC (National Health & Medical Research Council)
Project Team
SchemeProject Grant
RoleInvestigator
Funding Start2011
Funding Finish2013
GNo
Type Of FundingNot Known
CategoryUNKN
UONY

20102 grants / $919,181

Novel Targeted Therapies for Pancreatic Cancer$599,681

Funding body: Cancer Institute NSW

Funding bodyCancer Institute NSW
Project Team
SchemeCareer Development Fellowship
RoleLead
Funding Start2010
Funding Finish2012
GNo
Type Of FundingNot Known
CategoryUNKN
UONY

Targeting Myc onco-protein degradation for the treatment of Myc-induced malignancies$319,500

Neuroblastoma is the commonest solid tumour in early childhood. Pancreatic cancer is the fourth leading cause of cancer death in adults with a 5-year survival rate of less than 5%. We will define how proteins called histone deacetylases promote cancer initiation and progression, and whether specific inhibitors of the histone deacetylases exert anti-cancer effects in animal models of neuroblastoma and pancreatic cancer.
Funding body: Cancer Council NSW

Funding bodyCancer Council NSW
Project Team
SchemeResearch Grant
RoleInvestigator
Funding Start2010
Funding Finish2012
GNo
Type Of FundingNot Known
CategoryUNKN
UONY

20091 grants / $330,000

Continuing infrastructure support for the ACRF Genomics Facility$330,000

Continuing infrastructure support for the ACRF Genomics Facility
Funding body: Cancer Instititue NSW

Funding bodyCancer Instititue NSW
Project Team
SchemeResearch Infrastructure Grants
RoleInvestigator
Funding Start2009
Funding Finish2011
GNo
Type Of FundingNot Known
CategoryUNKN
UONY

20071 grants / $539,238

Adult Haematopoietic Stem Cells in The Evolution of Pancreatic Cancer$539,238

This project sought to define the role for bone marrow-derived cells in normal pancreatic development, pancreatic injury and regeneration and pancreatic cancer.
Funding body: Cancer Instititue NSW

Funding bodyCancer Instititue NSW
Project Team
SchemeEarly Career Fellowship
RoleLead
Funding Start2007
Funding Finish2009
GNo
Type Of FundingNot Known
CategoryUNKN
UONY
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Research Supervision

Current Supervision

CommencedResearch Title / Program / Supervisor Type
2015Anticancer Compounds from Plants Against Pancreatic Cancer Cells: Extraction, Purification and Characterization
Food Science & Biotechnology, Faculty of Science and Information Technology
Principal Supervisor
2014Identification of Biomarkers and Novel Targets for Prostate Cancer from Exosomes
Medical Science, Faculty of Health and Medicine
Co-Supervisor
2014Developing Synthetic Exosomes to Target and Deliver Anti-Cancer Agents to Prostate Cancer Cells
Medical Science, Faculty of Health and Medicine
Co-Supervisor
2014Evaluation of Edible Coating Application on Different Fruits
Food Science & Biotechnology, Faculty of Science and Information Technology
Principal Supervisor
2014Brown Algae as a Source of Bioactive Compounds for Pancreatic Cancer Treatment
Food Science & Biotechnology, Faculty of Science and Information Technology
Principal Supervisor
2014Bioactive Compounds, Antioxidant and Anti-Pancreatic Cancer Capacity of Two Vietnamese Medicinal Plants: Phyllanthus Amarus and Paramignya Trimera
Food Science & Biotechnology, Faculty of Science and Information Technology
Principal Supervisor
2014Phytochemicals Derived From Australian Eucalypts as Anticancer Agents for Pancreatic Malignancies
Food Science & Biotechnology, Faculty of Science and Information Technology
Principal Supervisor
2013Olive Waste Products as a Source of Phenolic Compounds with Chemotherapeutic and Chemopreventative Efficacy Against Pancreatic Cancer
Food Science & Biotechnology, Faculty of Science and Information Technology
Principal Supervisor
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Dr Christopher Scarlett

Position

Senior Lecturer
Food Science & Human Nutrition
School of Environmental and Life Sciences
Faculty of Science and Information Technology

Focus area

Applied Sciences

Contact Details

Emailc.scarlett@newcastle.edu.au
Phone(02) 4348 4680

Office

RoomSO E1.46
BuildingScience Offices
LocationOurimbah
10 Chittaway Road
Ourimbah, NSW 2258
Australia
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