2015_Postgraduate_Symposium_booklet

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ContentsOrganising Committee and Welcome �� 2About Cancer Research Network �� 3 Program �� 4Keynote speaker ��7Abstracts �� 8Attendee list �� 23

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The Cancer Research Network is a cross-Faculty initiative of the University of Sydney, formed in 2006, that links cancer researchers at the University of Sydney, its teaching hospitals and its affiliated research institutes and institutions� It encompasses a wide range of researchers who share a commitment to cancer research, collaborative research and research development� Their core values include a willingness to collaborate and share expertise, openness to multiple disciplines, and an interest in the translation of research findings into improvements in cancer control� The Network’s membership has grown to over 900 active cancer researchers�

The Network fosters communication with and among members to facilitate multidisciplinary collaboration across research groups, with an emphasis on research translation� This builds a sense of community among cancer researchers across discipline and geographical boundaries�

The Network adapts and responds to the needs of cancer researchers, and through its activities stimulates knowledge transfer within the Network, the University and to the Government and public�

Membership is open to employees and postgraduate research students of the University of Sydney, people employed by teaching hospitals and Institutes of the University of Sydney, or people holding an academic title award from the University of Sydney, who are active in the area of cancer research�

For further information, please contact the Cancer Research Network OfficePhone: +61 2 8627 1532Email: cancer-research@med�usyd�edu�ausydney�edu�au/cancer-research/

Organising committee

Sarah Frost (Chair) Sydney Medical School, The University of Sydney

Juliana Andrici Sydney Medical School, The University of Sydney

Ali Azimi Sydney Medical School, The University of Sydney

Merilyn Heuschkel Cancer Research Network, The University of Sydney

Monira Hoque Faculty of Pharmacy, The University of Sydney

Rebecca Mercieca-Bebber

Sydney Medical School, The University of Sydney

Rosita Pang School of Medical Sciences, Bosch Institute, The University of Sydney

Tomas Richardson-Sanchez

Sydney Medical School, The University of Sydney

Welcome message from the Symposium chairs

Welcome to the 7th Annual Postgraduate Cancer Research Symposium, hosted by the Postgraduate Student Working Group of the University of Sydney Cancer Research Network� We would also like to extend a warm welcome to Professor Tim Shaw, who has been invited to give today’s plenary address� Cancer research conducted across the University of Sydney and affiliated research institutes is remarkably varied� The Postgraduate Student Working Group aims to bring together students from these diverse disciplines and campuses to facilitate networking, encourage collaboration, and provide access to a supportive peer community� The Postgraduate Cancer Research Symposium is an exciting forum for students to present their research to their peers, as well as their academic colleagues� The program features work from a broad range of research areas – basic science, public health, clinical, psychosocial – and will be presented by

students at various stages of their candidature� This inter-disciplinary format will showcase the breadth of cancer research across the Network and allow students the opportunity to broaden their own knowledge� We would like to thank the Cancer Research Network and, in particular, Merilyn Heuschkel, for its support and sponsorship� I would also like to thank the other members of the Postgraduate Student Working Group for all of their hard work, both in the lead up to the Symposium and throughout the year� On behalf of the Postgraduate Student Working Group, I hope that you enjoy today’s talks, learn something new, and leave with a few more bright ideas!

Sarah FrostChair, Postgraduate Student Working Group Cancer Research Network

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Organising Committee and Welcome 2015 Postgraduate Cancer Research Symposium

About the Cancer Research Network

Plenary sessionNew Law Lecture Theatre 026 Chair – Sarah Frost

9�30am Welcome and introduction

9�40am K1: Plenary address Professor Tim ShawProfessor of eHealth, Faculty of Health Sciences, The University of Sydney

10�00am Q & A

Concurrent sessions (session 2 & 3)

Session 2 – Clinical research and therapy New Law Seminar Room 020 Chair: Tomas Richardson-Sanchez

Session 3 - Molecular biology and biomarkers New Law Seminar Room 022 Chair – Monira Hoque

10�10am P1: Work after breast cancer: Identification of cognitive difficulties using the perceive, recall, plan perform system of task analysisJoanne LewisFaculty of Health Sciences, The University of Sydney

P6: The long noncoding RNA - prins as a novel recurrence biomarker and tumour suppressor for adrenocotical carcinomaLauren JooNorthern Clinical School, Kolling Institute of Medical Research

10�25am P2: Appropriate selection for colorectal cancer resection but no need for therapeutic gloom in nonagenarians Steven Schlichtemeier Royal North Shore Hospital

P7: Comparative proteomic analysis of cutaneous squamous cell carcinoma for the identification of novel biomarkersAli AzimiDepartment of Dermatology, The University of Sydney

10�40am P3: Patterns of use and clinical benefit of endocrine therapy in women with epithelial ovarian cancer Cristina Mapagu Centre for Cancer Research, Westmead Millennium Institute, The University of Sydney

P8: MK2 inhibition sensitises glioblastoma cells to chemotherapyFadi GurgisDiscipline of Pharmacology, The University of Sydney

10�55am P4: Cutaneous adverse events of anti-programmed cell death 1 therapy in patients with metastatic melanoma; A single-institution cohort Shelley Ji Eun Hwang Westmead Hospital, The University of Sydney

P9: TGF-beta signalling during vaccinia infection: a novel mechanism of activationChristopher McKenzie School of Molecular Bioscience, The University of Sydney

11�10am P5: Breast cancer amongst gulf women Salman Mohammed Al-Beshan Discipline Of Medical Radiation Sciences, Faculty of Health Sciences, The University of Sydney

P10: The effect of atherogenic diet on hepatocellular carcinomaGhazal Alipour TaleshStorr Liver Unit, Westmead Millennium Institute, The University of Sydney

11.25am Morning Tea


Session 4 – Public health and cancer screening New Law Seminar Room 020 Chair – Rebecca Mercieca-Bebber

Session 5 – Cell biology New Law Seminar Room 022 Chair – Sarah Frost

11�40am P11: How non-statisticians can reduce the instance and impact of missing patient-reported outcome data in cancer clinical trials: a systematic reviewRebecca Mercieca-BebberSydney Medical School, The University of Sydney

P16: A novel mechanism for sustained proliferation of neuroblastoma cellsRebecca DaggThe Children’s Hospital at Westmead

11�55am P12: Volumetric breast density assessment using quantraErnest EkpoFaculty of Health Sciences, The University of Sydney

P17: The role of ascorbate and the metastasis suppressor N-Myc downstream regulated gene 1 (ndrg1) in stress-induced autophagy in neoplastic cellsDong-Hun BaeDiscipline of Pathology, The University of Sydney

12�10pm P13: Mammographic density variations in China: causal agents and potential implicationsTong LiMedical Imaging & Radiation Sciences, Faculty of Health Sciences, The University of Sydney

P18: Development of a whole genome sequencing based classifier to determine telomere maintenance mechanism in tumoursMichael LeeChildren’s Medical Research Institute

12�25pm P14: Addressing overtreatment of ductal carcinoma in situ (DCIS): a qualitative study of how terminology affects women’s concern and management preferencesBrooke NickelSchool of Public Health, The University of Sydney

P19: The role of actomyosin dynamics during T cell migrationJorge Luis Galeano Nino Centenary Institute of Cancer Medicine & Cell Biology

12�40pm P15: Trends in genital warts by socioeconomic factors after the introduction of HPV vaccination in Australia: Analysis of national hospital dataMegan SmithSydney Medical School, The University of Sydney

P20: Dipeptidyl Peptidase 9: Noval nautral substrates and association with cell adhesion, focal adhesion kinase and paxillinHui ZhangCentenary Institute of Cancer Medicine & Cell Biology

12.55pm Lunch

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Program2015 Postgraduate Cancer Research Symposium


Session 6 – Genomics and novel treatmentsNew Law Seminar Room 020Chair – Rosita Pang

Session 7 – Anti-cancer agents New Law Seminar Room 022Chair – Ali Azimi

1�45pm P21: Pharmacogenetics and chemotherapy: the role of transporter genes in actinomycin D pharmacokinetics in paediatric cancer patientsHannah Yejin KimFaculty of Pharmacy, The University of Sydney

P26: Sourcing novel anticancer drugs by the enzymatic fragmentation of natural productsTomas Richardson-SanchezDiscipline of Pharmacology, The University of Sydney

2�00pm P22: MRNA electroporated CMRF-56 blood dendritic cells: an anti-tumour vaccination strategyMichael PapadimitriousANZAC Research Institute

P27: Development of novel anti-cancer metastasis agents derived from omega-3 fatty acid metabolitesNooshin KoolajiSydney Medical School, The University of Sydney

2�15pm P23: Investigation into lymphoma predisposition in Australian bullmastiffsSally MortlockFaculty of Veterinary Science, The University of Sydney

P28: Glucose conjugation for targeted delivery of metal based anticancer agentsAlexandra GlenisterSchool of Chemistry, The University of Sydney

2�30pm P24: Gadolinium as a novel nano-probe to enhance image-guided targeted x-ray therapyHilary ByrneFaculty of Science, The University of Sydney

P29: The design of stabilised platinum(iv) complexes for targeted drug deliveryCatherine ChenFaculty of Science, The University of Sydney

2�45pm P25: BRAF mutations and response to BRAF inhibition in epithelial ovarian cancerTania Moujaber Westmead Millennium Institute, The University of Sydney

P30: Biological speciation of the anticancer rh(iii)-dimethylsulfoxide complexes via x-ray absorption spectroscopyJun LiangSchool of Chemistry, The University of Sydney

3.00pm Afternoon tea

Awards ceremonyNew Law Seminar Room 020Chair – Sarah Frost

3�15pm Most outstanding student presenter within each of the following sessions:

− Clinical research and therapy

− Molecular biology and biomarkers

− Public health and cancer screening

− Cell biology

− Genomics and novel treatments

− Anti-cancer agents

3.30pm Finish

Keynote speaker

Professor Tim ShawTim is the inaugural Professor of eHealth and Director of the Research in Implementation Science and eHealth Group (RISe) in the Faculty of Health Sciences at the University of Sydney� Tim leads implementation science across Sydney Catalyst and Sydney West Translational Cancer Research Centres and has an active research and development program both in Australia and Internationally�

Tim’s research interests lie at the intersection of implementation science and quality improvement and how ICT and health data is impacting on practice, professional development and system improvement�

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P1 Work after breast cancer: identification of cognitive difficulties using the perceive, recall, plan perform system of task analysisJoanne Lewis, Lynette Mackenzie, Chris Chapparo

The University of Sydney

Introduction: A high proportion of women report subtle cognitive changes that negatively impact their capacity to participate in work after breast cancer chemotherapy intervention� Evidence comprising neuropsychological assessment results of cognitive changes following breast cancer is equivocal� No systematic investigation has targeted the particular cognitive difficulties experienced by women on return to work� Difficulty is thought to stem from a disorder in cognitive strategy application rather than cognitive deficit per se� Few workplace assessment tools capture the effect of inefficient cognitive strategy use upon work performance in situ�

Purpose: To describe the cognitive strategy use strengths and difficulties women who survive breast cancer experience after return to work� Method: Ten women who returned to work post-breast cancer intervention (42 – 54 years) were previously interviewed about cognitive changes they experienced after treatment� A secondary analysis of this data was conducted using the Perceive, Recall, Plan and Perform System of Task Analysis - PRPP@WORK (Questionnaire/Interview)� This interview format provides a structure to explore women’s perceptions of their ability to carry out both procedural (steps) and strategy application (cognitive) components of the job� Information about 34 cognitive strategy items were obtained relative to attention, sensory perception, memory, planning, and performance monitoring�

Results: While all women rated themselves competent with their work performance, they all experienced high level cognitive strategy application disturbance which impacted their ability to work to the level they desired relative to amount, effort, or quality� They likened the disturbance to ‘a hidden disability’ which was experienced by them, but not observable to others� Thematic analysis of the data indicated particular patterns of cognitive strategy use which were most and least challenging�

Conclusion: Women who undergo chemotherapy for breast cancer may experience difficulties with cognitive strategy application upon return to work� Further research is required to determine how common this phenomenon is and establish the PRPP as a valid and reliable tool for assessing the cognitive demands of work and identification of cognitive strategy problems for women with breast cancer�

P2 Appropriate selection for colorectal cancer resection but no need for therapeutic gloom in nonagenarians

Steven Schlichtemeier1,3, Anthony J. Gill1,2, Alexander Engel1,3

1Sydney Medical School, The University of Sydney

2Department of Anatomical Pathology, Royal North Shore Hospital

3Department of Colorectal Surgery, Royal North Shore Hospita

Aims: The nonagenarian population is a rapidly growing segment of the Australian population� Surgical resection continues to offer the best chance of long-term survival in colorectal cancer�

Methods: All patients 90 years of age or older undergoing surgical resection for colorectal cancer from 1998 to 2012 were identified in a centralized multihospital database� Gender, tumour size, key lymph node data, TNM stage, 90-day mortality and overall long-term survival were recorded for each patient�

Results: Of the 122 identified patients the mean age was 92�4 years and 72�7% were female� In this group mean tumour size was 45�5 mm, mean total lymph nodes harvested was 15�5, mean involved lymph nodes was 1�4 and apical node positivity was 6�3%� The distribution of TNM stage in these patients was Stage I: 10%, Stage II: 35%, Stage III: 28% and Stage IV: 27%� The 90-day mortality was 8�2% (10/122) and the actuarial mean overall survival was 46�6 months� In comparison to younger age groups, there was no difference in mean tumour size or apical node positivity though nonagenarians had a statistically lower TNM stage� Conclusion: Surgical resection in the appropriate selected nonagenarian continues to offer acceptable mortality and good overall survival�

Abstracts

P3 Patterns of use and clinical benefit of endocrine therapy in women with epithelial ovarian cancerCristina Mapagu1,2, Sian Fereday3, David Bowtell3,4,5, Paul Harnett1,6,7, Anna deFazio1,2,6,7

1Centre for Cancer Research, Westmead Millennium Institute, The University of Sydney, Australia 2Department of Gynaecological Oncology, Westmead Hospital3Peter MacCallum Cancer Centre, East Melbourne4Department of Pathology, University of Melbourne5Sir Peter MacCallum Cancer Centre Department of Oncology, University of Melbourne 6Sydney West Translational Cancer Research Centre, The University of Sydney7Crown Princess Mary Cancer Centre, Westmead Hospital

Background: Most epithelial ovarian carcinomas express hormone receptors, however receptor positivity does not predict response to endocrine therapy and its role in the management of ovarian cancer remains unclear� In this study, we determined the patterns of use of endocrine agents and response rates in ovarian cancer patients in a real-world setting�

Methods: Our cohort consisted of 1,424 women with ovarian cancer recruited nationally to the Australian Ovarian Cancer Study (AOCS) between 2002-2006� We identified all patients treated with endocrine therapy for ovarian cancer and determined clinical predictors of endocrine therapy use� Where possible, recognized CA125 response criteria (Gynaecologic Cancer InterGroup) were used to assign response� Survival was assessed by Cox-regression and Kaplan-Meier analysis�

Results: In AOCS, 16�6% (236/1424) of patients were treated with endocrine therapy for their ovarian cancer, with tamoxifen being the most common agent� Progressive or relapsed disease was the most significant predictor of endocrine treatment� More than 1/3 (34�7%, 82/236) of patients received endocrine treatment at first relapse� An overall clinical benefit rate of 43�1% (ORR + SD = 10�5% + 32�6%) was observed in cases evaluable by CA125 criteria (n = 86)� In women with advanced stage (Stage III/IV), high-grade (grade 3), serous ovarian cancer (n = 438), Kaplan-Meier survival analysis showed that treatment with endocrine treatment at first relapse was associated with increased overall survival (HR 0�52, 95% CI 0�36 - 0�75, p=0�001)�

Conclusion: Despite a modest response rate, the overall clinical benefit of endocrine therapy was comparable to more toxic chemotherapy usually used in relapsed disease� The improved overall survival associated with endocrine treatment warrants further clinical trials to investigate the use of endocrine therapy and further research to identify predictive biomarkers to select ovarian cancer patients most likely to derive a clinical benefit from treatment with endocrine agents such as tamoxifen�

P4 Cutaneous adverse events of anti-programmed cell death 1 therapy in patients with metastatic melanoma; a single-institution cohortShelley Ji Eun Hwang1,2, Giuliana Carlos1,2, Deepal Wakade1,2, Karen Byth2,3, Benjamin Y. Kong4, Shaun Chou5, Matteo S. Carlino2,4,6, Richard Kefford4,6, Pablo Fernandez-Penas1,2

1Department of Dermatology, Westmead Hospital2Sydney Medical School, The University of Sydney3Research and Education Network, Westmead Hospital4Crown Princess Mary Cancer Centre, Westmead Hospital5Tissue Pathology and Diagnostic Oncology, Westmead Hospital6Melanoma Institute Australia

Introduction: Anti-Programmed cell Death 1 therapy is emerging as the backbone of new standard of care immunotherapy for metastatic melanoma� Immune related cutaneous events are observed in these patients� Aim To describe cutaneous adverse events observed in patients with metastatic melanoma on anti-Programmed cell Death 1 therapy�

Methods: We performed the skin evaluation and reviewed all clinical information of patients with metastatic melanoma treated with single agent anti-Programmed cell Death 1 therapy at Westmead Hospital, Sydney, Australia from May 2012 to February 2015�

Results: Forty of 82 patients (49%) developed a form of anti-Programmed cell Death 1 associated cutaneous adverse event� 17% of the population developed lichenoid reactions and eczema, and 15% of the population developed vitiligo� An estimated 25% of patients is expected to develop their first lichenoid reactions within 8�3 months, and eczema and vitiligo within 10�3 months� There was statistically significant evidence of an association between the presence of lichenoid reaction, eczema and vitiligo�

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Conclusion: Anti-Programmed cell Death 1 therapy is associated with the development of immune related cutaneous events� Lichenoid reactions, eczema and vitiligo are the three most prevalent lesions observed in our population� There is a tendency for lichenoid reactions and eczema to occur with vitiligo�

P5 Breast cancer amongst Gulf womenSalman Mohammed Al-Beshan

Discipline of Medical Radiation Sciences, Faculty of Health Sciences, The University of Sydney

Background: Breast cancer is the most frequently diagnosed female malignant disease and it is the leading cause of death among the Gulf women� The present review aims to highlight similarities and variations in terms of breast cancer incidence, age at diagnosis, clinic-pathological features as well as molecular characteristics with data from westernised countries and non-Gulf Arab with an attempt to explain possible underlying risk factors�

Method: All available electronic articles about breast cancer epidemiology among Arab women either within the context of that article or as its main subject have been reviewed�

Results: This review showed that the majority of Gulf women diagnosed with breast cancer are in their 40s and 50s age groups (mean age 48) compared with the 50-69 years old and those individuals older than 75 years age groups from westernised nations (mean age 60)� It also revealed that aggressive clinico-pathological patterns of breast cancer, including invasive ductal carcinoma, advance stages and higher pathological grades are more predominant among the Gulf women� These disparities are not only confined to clinic-pathological features, but also found at molecular levels with relatively higher prevalence of aggressive breast cancer subtypes such as Human Epidermal Growth factor Receptor 2 and triple negatives�

Conclusions: The data presented whilst having important implications for health policy, highlights the need for further research�Such research would ensure that detection and treatment strategies are tailored to the specific needs of the Gulf region so that the management of breast cancer is optimised�

P6 The long noncoding RNA - prins as a novel recurrence biomarker and tumour suppressor for adrenocotical carcinomaLauren Jin Suk Joo, Anthony R Glover, Jing Ting Zhao, Anthony J Gill, Bruce G Robinson, Stan B Sidhu1Cancer Genetics Laboratory, Kolling Institute, Northern Sydney Local Health District2Sydney Medical School Northern, Royal North Shore Hospital, The University of Sydney3University of Sydney Endocrine Surgery Unit, Royal North Shore Hospital,4Sydney Vital, Kolling Institute, Northern Sydney Local Health District

Background: Adrenocortical carcinoma (ACC) has high recurrence rates� Novel prognostic biomarkers are needed to tailor adjuvant therapy� We have shown expression of PRINS, a long noncoding RNA (lncRNA) can predict ACC recurrence, which is the first clinical association in cancer� In the skin, PRINS interacts with the protein nucleophosphmin (NPM) allowing NPM to move from the cytoplasm to the nucleus� In the nucleus NPM binds to TP53 to increase its transcriptional activity� TP53 is a key driver of ACC�

Aims: To establish a biological basis for PRINS as a biomarker by investigating a tumour suppressor RNA action in ACC�

Method: PRINS expression in ACC cells (NCI-H295R) was restored using the mammalian expression vector containing full length of PRINS cDNA transcript� Cell phenotypes were compared to cells transfected with an empty vector� Transcriptome analysis was performed on clinical samples of ACC (n=10) and normal adrenal cortex (n=6) using the ArrayStar Human LncRNA V3�0 microarray� Results: Restoring PRINS expression in NCI-H295R cells induced apoptosis, assessed by Annexin V assays (P<0�05) and cPARP protein expression and reduced cell proliferation by MTS assays (P<0�05)� Using RNA FISH, PRINS was localised to the cell cytoplasm� Correlation of ~26,000 mRNA transcripts found PRINS expression to be correlated with 48 mRNAs (Pearson Correlation Coefficients > 80%, corrected P<0�05), including p53 related genes – TNFRSF11B, MKI-67 and TTK� Following PRINS restoration in NCI-H295R cells, TP53 was increased (Fold change 1�5, P<0�001) and TNFRSF11B reduced (Fold change 0�56,P<0�05) supporting a mechanism of increased apoptosis�

Conclusions: This first report of PRINS acting as a tumour suppressor supports the association with ACC recurrence and offers a novel mechanism of TP53 action in cancer� As PRINS is also under-expressed in breast and prostate cancer it offers potential as a biomarker of recurrence in other cancers to improve quality of life�

P7 Comparative proteomic analysis of cutaneous squamous cell carcinoma for the identification of novel biomarkersAli Azimi1, Kim L. Kaufman2, 3, Marina Ali1, Steven Kossard4, Pablo Fernandez-Penas1

1Dermatology, The University of Sydney2School of Molecular Bioscience, Faculty of Science, The University of Sydney3Brain and Mind Research Institute, The University of Sydney4Dermatopathology, Skin and Cancer Foundation Australia

Background: Cutaneous Squamous Cell Carcinoma (cSCC) is the most common type of non-melanoma skin cancer� Histopathologic variants of cSCC show significantly different clinical behaviour and their correct classification is critical for diagnosis, prognosis and therapy� This study aimed to test the viability of using archival formalin-fixed paraffin embedded (FFPE) cSCC material for proteomic investigations that could provide more reliable biomarkers for the clinical management of cSCC�

Methods: We obtained FFPE cSCC samples from five patients and employed laser capture microdissection to separate tumour cell populations from surrounding normal tissue� Protein extracts from tumour and matched normal tissues were solubilised by rounds of heating and sonication followed by reduction, alkylation and proteolytic digestion� The resulting peptides were desalted prior to analysis by reverse phased liquid chromatography coupled with a Q-Exactive™ Plus Hybrid Quadrupole-Orbitrap™ Mass Spectrometer (MS)� The MS data was captured in triplicate and searched against the SwissPROT database for protein identification and label-free relative quantification was performed using Scaffold™ software� Pair-wise comparisons were performed between tumour and surrounding normal tissue proteomes for each patient� Ingenuity Pathway Analysis (IPA) bioinformatics suite was used to interpret the roles of common de-regulated proteins in cSCC pathophysiology�

Results: In total, 1341 unique protein species were identified across all five patients� Of these, an average of 182 proteins were significantly increased and 82�6 proteins decreased in the tumor samples compared to their normal counterparts (p<0�05)� IPA analysis revealed the disruptions are in proteins associated with the MAPK pathway and the regulation and control of cell proliferation, differentiation, apoptosis, and cell movement�

Conclusions: Significant proteins identified have roles in tumorigenesis and will be assessed for their use as cSCC biomarkers that could aid in diagnosis, therapy, or drug development� This study will be expanded to identify protein markers of cSCC subtypes to aid clinical management�

P8 MK2 inhibition sensitises glioblastoma cells to chemotherapyFadi Gurgis, Lenka Munoz

Discipline of Pharmacology, Faculty of Medicine, The University of Sydney

Glioblastoma is a challenging disease to treat and is considered to be one of the most lethal solid tumours� Patients diagnosed with glioblastoma have a median survival of 12 to 14 months with most tumours featuring a high rate of recurrence and resistance to the current chemotherapeutic agent temozolomide used in the clinic� Much research has been ongoing to improve glioblastoma therapy� Mitogen-activated protein kinase (MAPK) activated-protein kinase 2 (MK2) is a downstream substrate of the p38 MAPK responsible for the signalling events influencing inflammation, cell division and differentiation, apoptosis as well as cell motility in response to a wide range of extracellular stimuli� Recent studies have highlighted a role of MK2 as a cell cycle checkpoint kinase� MK2 is activated following DNA damage and results in cell cycle arrest so that cells have the capacity to repair their DNA and continue to proliferate� As this mechanism underlies resistance to chemotherapy, MK2 inhibitors could serve as anti-cancer agents that improve efficacy of chemotherapy� Using specific pharmacological inhibitors and genetic knockdown experiments, we examined whether MK2 inhibition improves temozolomide efficacy in various glioblastoma cell lines� We show that MK2 inhibition sensitised a number of glioblastoma cells including patient derived cell lines to the anti-proliferative effects of temozolomide� Furthermore, MK2 inhibition resulted in an enhanced inhibition of clonogenicity of glioblastoma cells when combined with temozolomide� Mechanistic studies revealed that MK2 inhibition abrogated the G2/M arrest caused by temozolomide and resulted in marked cell death� MK2 inhibition reduced the temozolomide-induced phosphorylation of Cdc25C (S216) and Cdk1 (Tyr 15) explaining the underlying cause of cell cycle abrogation� We propose that MK2 inhibition sensitises glioblastoma cells to temozolomide by inducing mitotic catastrophe� In conclusion, our results demonstrate that targeting MK2 could improve glioblastoma response to chemotherapy�

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P9 TGF-beta signalling during vaccinia infection: a novel mechanism of activationChristopher D. McKenzie, Anjali Gowripalan, Timothy P. Newsome

School of Molecular Bioscience, The University of Sydney

Tumour cells possess many features which predispose them to viral infections, including an abundance of replication resources, a defective interferon response and localised evasion of host immune cells� Oncolytic viruses exploit these characteristics to preferentially replicate within tumour cells, multiplying rapidly and targeting cells for destruction by the host immune system� Vaccinia virus (VACV) is a well characterised oncolytic virus and has been studied extensively due to its role in the smallpox vaccine� To improve safety and specificity of its use in oncolytic therapy, numerous genetic modifications have been made, giving rise to a therapeutic strain known as JX-594� Unfortunately there are still dangers associated with treatment, including the intratumoral route of administration, which dislodges malignant cells and encourages distal tumour formation� Recent work has focused on mining important elements of the VACV replication cycle to dig up novel targets to improve tumour selectivity� Observations made in our lab have demonstrated potent upregulation of TGF-β signalling upon VACV infection� These pathway components can be detected at both the transcript and protein level, via qPCR, immunoblot and immunofluorescence assays� Furthermore, using both CRISPR-Cas9 and siRNA technologies, we have demonstrated a novel role for Smad4, a transcription factor in this cascade, in a number of aspects of infection, including virus-induced cell invasion� As high levels of TGF-ß signalling are associated with numerous tumours, including but not limited to colon, prostate, breast and hepatocellular carcinoma, understanding how VACV recruits this pathway could assist in shifting infection away from healthy cells and towards tumours�

P10 The effect of atherogenic diet on hepatocellular carcinomaGhazal Alipour Talesh, Mahmoud Karimi Azar Daryani, Mehdi Ramezani-Moghadam, Jacob George, Saeed Esmaili

Storr Liver Unit, Westmead Millennium Institute, The University of Sydney

Introduction: Hepatocellular carcinoma (HCC) is the most common form of liver cancer and the fastest growing solid organ tumour in Australia� HCC has an abysmal prognosis with 5 year survival rate of <10%� Epidemiological studies have demonstrated different degrees of correlation between diet and cancer risk/or rate of tumour free survival� However, the underlying mechanisms are poorly understood to date� Cancer cells induce a tolerogenic (rather than a pro-inflammatory) environment to escape immune-surveillance� Therefore, it is plausible that the mechanisms that activate inflammatory responses can increase the immune-surveillance and restrict growth of HCC� We aimed to find a diet that has the potential to increase the survival of HCC patients�

Method: Male C57BL6 mice fed an atherogenic diet containing 2% cholesterol to induce liver inflammation or a normal chow diet for 12 weeks� Subsequently, liver tissue was collected and the immune response was characterised within the liver using nCounter nanostring gene expression panel for inflammation and immunostaining�

Results: By hematoxylin eosin staining we detected infiltration of inflammatory cells within the liver which formed foci� Nanostring expression profiling demonstrated higher levels of macrophage marker F4/80, CD3 (pan-T cell marker), CD4 and CD8 (T cell markers), and B220 (B cell marker) in mice fed the atherogenic diet� Immunofluorescence staining confirmed the presence of macrophages, T cells, and B cells within the foci as well as spread throughout the liver�

Conclusion and future plan: We demonstrate that atherogenic diet increases the inflammatory response within the liver� The future direction of the project is to investigate the effect of atherogenic diet in the context of DEN induced Hepatocellular carcinoma in mice�

P11 How non-statisticians can reduce the instance and impact of missing patient-reported outcome data in cancer clinical trials: a systematic reviewRebecca Mercieca-Bebber1,2, Michael J Palmer3, Michael Brundage3, Melanie Calvert4, Madeleine King1,2

1Central Clinical School, Sydney Medical School, The University of Sydney2Psycho-oncology Co-operative Research Group, School of Psychology, The University of Sydney3Cancer Care and Epidemiology, Cancer Research Institute, Queen’s University, Kingston, Ontario, Canada 4Primary Care and Clinical Sciences, University of Birmingham, Birmingham, United Kingdom

Aims: Patient-reported outcomes (PROs) in cancer clinical trials provide important information about treatment impact from the patient’s perspective� However the potential for PROs to inform clinical practice may be limited by missing data, which continues to be a problem in cancer trials� While statisticians can address missing data at the analysis stage, these strategies are far from ideal� Thus, we undertook a systematic review to collate strategies to minimise the problem of missing PRO data in cancer trials�

Methods: We searched Medline and CINAHL databases (inception-Mar2014) for English articles providing recommendations for reducing the instance and/or potential for bias of missing PRO data� Two reviewers independently screened titles and abstracts against pre-defined eligibility criteria� Discrepancies were discussed with the research team� Recommendations were extracted and coded using framework analysis�

Results: Our database search retrieved 5996 unique articles� An additional 41 references were identified by experts and hand-searching reference lists� 112 articles met criteria for inclusion, encompassing 1222 recommendations� Design and methodological strategies for reducing the risk of missing PRO data include: incorporating PROs completely into the protocol, involving trial staff in study design, clearly defining PRO assessment schedules and end-rules, minimising patient burden, appointing a PRO coordinator, PRO-specific training for trial staff, appropriately resourcing the study and continuous monitoring of completion rates� Strategies for minimising bias caused by missing PRO data include collecting auxiliary data to inform analysis decisions, collecting reasons for missing data and transparently reporting baseline PRO scores, rates and reasons for missing data and methods for handling missing PRO data�

Conclusions: All members of the trial team can assist in reducing the instance and potential for bias of missing PRO data in cancer trials by implementing thoughtful design, methodology and transparent reporting strategies�

P12 Volumetric breast density assessment using quantraErnest U. Ekpo, Mark McEntee, Mary Rickard, Patrick Brennan, Claudia Mello-Thoms

Faculty of Health Sciences, The University of Sydney

Background: Breast density (BD) is a determinant of breast cancer (BC) risk, interval cancer, and mammographic sensitivity� BD is related to traditional BC risk factors; it is also a biomarker for the efficacy of chemopreventive strategies on BC risk, and lower BD is associated with lower BC risk� Therefore, BD information is important for BC risk assessment, screening personalization, and monitoring the efficacy of chemopreventive strategies� The widely used BIRADS approach for assessing BD is observer dependant and causes differences in clinical decision-making, and underscores the need for automated volumetric BD measurement� However, it is important that volumetric measures reflect radiologists’ opinion�

Aims: To assess the accuracy of Quantra in reproducing BIRADS assessment and the cut off value for Quantra that best differentiates high- and low-grade BIRADS categories�

Methods: Two methods of mammographic breast density measurement were used (Quantra and BIRADS)� Automated BD assessment from 292 raw projection images was performed using Quantra software� These cases were also assessed by three radiologists and a majority report was generated� Inter-reader agreement (κ) and the sensitivity, specificity, and accuracy (Area under curve) of Quantra in reproducing the majority BIRADS report were calculated�

Results: Inter-reader agreement (κ) was substantial (0�66 – 0�75) on a four-grade scale and substantial to almost perfect (0�77 – 0�89) on a two-grade scale� Quantra correctly classified 35�7%, 91�2%, 88�6%, and 50�3% of BIRADS 1, 2, 3, and 4 respectively on a four-grade scale and 83�6% of BIRADS1–2 and 91�3% of BIRADS3–4 on a two-grade scale� A cut off value of 20�5% allowed best differentiation between BIRADS3–4 and BIRADS1–2�

Conclusion: Quantra has limited accuracy in reproducing BIRADS categories on a four-grade scale, however accurately reproduces BIRADS assessment on a dichotomous scale that is used in clinical decision-making�

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P13 Mammographic density variations in china: causal agents and potential implicationsTong Li, Claudia Mello-Thoms, Patrick C. Brennan

Medical Image Optimisation and Perception Group (MIOPeG), Department of Medical Imaging & Radiation Sciences, Faculty of Health Sciences, The University of Sydney

Background: The characteristics of breast of women and presentation of cancer are not fully understood in China� Identification of breast cancer relies on accurate early detection using appropriate imaging technologies; however the efficacy of these imaging solutions depends on the presentation of the breast and the types of breast cancer in the population� Until breast presentation (particularly breast density) and breast cancer profile are comprehensively assessed within China, breast screening strategies cannot be optimised, since current imaging paradigms are based on image data gathered from Westernised countries� Therefore, this study aims to characterise the breast presentation/density and cancer image appearances in Chinese women and based on this information, to determine the optimum imaging technology for early detection of breast cancer�

Methods: Cases for 5000 women (both normal and abnormal) were collected retrospectively from Cancer Institute and Hospital, Chinese Academy of Medical Sciences in China� All mammograms were de-identified, and the mammograms and clinical notes/reports were coded in a matched way� Other morphological features were recorded such as BIRADS scores, as well as demographic features such as age and BMI� The lesion characteristics and location of the cancers were also detailed� In addition, ethnic details for each woman were noted since a proportion of women may not be of Han origin� Breast density will be evaluated on all cranio-caudal and mediolateral images of both breasts using the AutoDensity algorithm and a single density value for each woman will be established� Correlation analyses using a Spearman test will be performed to compare density values across each of the groupings with demographic data� Expected results and output: Breast density and other morphological characteristics of women in China will be provided� The data will lead to recommendations on the most effective imaging approach and suitable optimisation strategy for breast cancer screening in China�

P14 Addressing overtreatment of ductal carcinoma in situ (DCIS): a qualitative study of how terminology affects women’s concern and management preferencesBrooke Nickel, Alex Barratt, Jolyn Hersch, Ray Moynihan, Les Irwig, Kirsten McCaffery

The University of Sydney and Bond University

Background: There are increasing rates of mastectomy and bilateral mastectomy in women diagnosed with ductal carcinoma in situ (DCIS)� To help women avoid decisions that lead to unnecessary aggressive treatments, there have been recent calls to remove the cancer terminology from descriptions of DCIS� We investigated how different proposed terminologies for DCIS affect women’s perceived level of concern and management preferences� Methods: Qualitative study using semi-structured interviews conducted between June and August 2014 with a community sample of 26 Australian women varying by education and cancer screening experience� Women responded to a hypothetical scenario using terminology with and without the cancer term to describe DCIS�

Results: Among a sample of women with no experience of a DCIS diagnosis, a hypothetical scenario involving a diagnosis of DCIS elicited high levels of concern regardless of the terminology used to describe it� Women exhibited stronger negative reactions when a cancer term was used to describe DCIS compared to that of a non-cancer term, and preferred the diagnosis be given as a description of abnormal cells� Overall women expressed interest in watchful waiting for DCIS but displayed preferences for very frequent monitoring with this management approach�

Conclusions: Communicating a diagnosis of DCIS using terminology that does not include the cancer term may help to decrease patients’ high levels of concern, which in turn may enable discussions about more conservative treatment options� However, preferences for a higher frequency of monitoring during watchful waiting of DCIS may have implications for providing confidence to women when making decisions about management�

P15 Trends in genital warts by socioeconomic factors after the introduction of HPV vaccination in Australia: analysis of national hospital dataMegan Smith1, Bette Liu2, Peter McIntyre3, Robert Menzies2, Aditi Dey3, Karen Canfell1

1The University of Sydney, Cancer Council NSW 2UNSW Australia3NCIRS

Objectives: To examine genital warts trends by socioeconomic status (SES) in Australia around the time of the National HPV Vaccination Program� Methods: Hospital admissions involving a diagnosis of genital warts were obtained from a comprehensive national database� We compared sex- and age-specific admission rates in July 2006-June 2007 (pre-vaccination) and July 2010-June 2011 (post-vaccination) according to SES of the individual’s area of residence, nationally and stratified by inside versus outside major cities, using Poisson/ negative binomial models�

Results: Admission rates per 100,000 population in females aged 10-19 years (predominantly vaccinated at school), reduced from 42�2 to 6�0 (rate reduction 86�7%;95%CI:82�2-90�0%) in more disadvantaged areas and from 26�8 to 4�0 (85�0%;95%CI:79�7-88�9%) in less disadvantaged areas� In females aged 20-29 years (predominantly vaccinated in the community), the decreases were from 73�9 to 26�4 (66�0%;95%CI:57�7-72�6%) and from 61�9 to 23�8 (61�6%;95%CI:52�9-68�7%) in more and less disadvantaged areas, respectively� The reductions were similar in more versus less disadvantaged areas both inside major cities (88�6%;95%CI: 82�2-92�7% vs 87�9%; 95%CI:82�6-91�6% in females aged 10-19 years; 64�0%; 95%CI:57�0-69�9% vs 63�8%;95%CI:52�9-72�1% for females aged 20-29 years) and outside major cities (88�8%;95%CI: 83�7-92�3% vs 85�8%;95%CI:73�5-92�4% in females aged 10-19 years; 71�1%;95%CI:58�8-79�7% vs 67�6%;95%CI:48�2-79�8% for females aged 20-29 years)� Admission rates in males aged 20-29 years also reduced, by 23�0% (95%CI:4�8-37�8%) and 39�4% (95%CI:28�9-48�3%) in more versus less disadvantaged areas respectively)�

Conclusions: The relative reduction in genital warts appears similar in young females across different levels of disadvantage, including for females vaccinated at school and in the community�

P16 A novel mechanism for sustained proliferation of neuroblastoma cellsRebecca Dagg1,2, Christine Napier2,3, Roger Reddel2,3, and Loretta Lau1,2

1Children’s Cancer Research Unit, The Children’s Hospital at Westmead2Sydney Medical School, The University of Sydney3Cancer Research Unit, Children’s Medical Research Institute

The end of chromosomes are characterised by a repeat telomeric sequence� Normal somatic cell division results in telomere erosion, ultimately triggering senescence� Cancer cells bypass senescence via activation of a telomere lengthening mechanism (TLM), either telomerase or the Alternative Lengthening of Telomeres (ALT)� Identification of ALT relies on the observation of unique phenotypic characteristics including lack of telomerase, abundance of c-circles, presence of APBs, and long and heterogeneous telomere lengths� During a screen of 35 neuroblastoma cell lines we identified two cultures that were neither telomerase nor ALT positive but were still capable of proliferating >300 population doublings� Examination of telomere length by mean terminal restriction fragment revealed an exceptionally long mean telomere length (35kb) and 50 to 80 base pairs were lost during each population doubling� All immortalised cell lines to date have a TLM so this is an unprecedented finding� Gene mutations associated with ALT (TP53, ATRX, DAXX, IDH1/2, H3�3) were not present in the cell lines� A cohort of 149 high risk neuroblastoma tumours were screened for ALT by identification of long telomere lengths and active ALT markers (c-circles)� We found 24% of the tumours were ALT positive but another subset (11%) of tumours had long telomeres with no active ALT mechanism and a similar telomere phenotype to the two cell lines� This unique group had a better 5 year overall survival (45 vs 26%; P<0�05) compared to the poor outcome high risk neuroblastoma groups (ALT and MYCN amplified tumours)� This is the first report of sustained proliferation of aggressive, malignant and fatal human cancer irrespective of continuous telomere shortening, and that TLM negative tumours form a distinct prognostic subgroup of neuroblastoma� These discoveries have implications for the use of telomere maintenance inhibitors clinically and in our understanding of the role that immortalisation plays in carcinogenesis�

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P17 The role of ascorbate and the metastasis suppressor N-Myc downstream regulated gene 1 (NDRG1) in stress-induced autophagy in neoplastic cellsDong-Hun Bae, Darius J.R. Lane, Des R. Richardson

Department of Pathology and Bosch Institute, The University of Sydney

Ascorbate is an essential nutrient obtained exogenously in humans� It stimulates dietary iron absorption and is required for normal iron metabolism� A number of studies have shown that at pharmacologic (millimolar) concentrations, ascorbate induces autophagy mediated by H2O2 production, which promotes cell death� However, autophagy is mainly a pro-survival mechanism regulated via the protein kinase-like endoplasmic reticulum kinase (PERK)/eukaryotic initiation factor 2α (eIF2α)-mediated endoplasmic reticulum (ER) stress pathway� We have recently shown that NDRG1 suppresses basal autophagic initiation via the ER stress pathway and induces apoptosis� The possible interaction between ascorbate and NDRG1 was important to assess as little is known about the molecular mechanisms of ascorbate-induced neoplastic cell death� In our study, we investigated the mechanisms of ascorbate-induced autophagy and neoplastic cell death, and the involvement of NDRG1 in these processes� We observed that, at pharmacologic concentrations in various cell lines, ascorbate promoted an early, but transitory, increase in the autophagic marker, light chain 3 (LC3)-II� Moreover, corresponding bright-field imaging indicated significant cell death� Interestingly, recent studies have suggested sensitivity to ascorbate cytotoxicity is dependent on hypoxia inducible factor- 1α (HIF1α) levels� Importantly, our studies have shown that the combined treatment of pharmacologic ascorbate and novel anti-cancer thiosemicarbazones (TSCs) was more cytotoxic than either treatment alone, which may result from the ability of TSCs to increase HIF-1α levels� Additionally, this effect was further enhanced with silencing of endogenous NDRG1 expression� Thus, these studies indicate that ascorbate promotes neoplastic cell death that is: (1) associated with an early and transient increase in autophagic initiation; (2) may be potentiated by an increase in HIF1α levels; and (3) enhanced by silencing of NDRG1� In summary, this study provides crucial insights into the mechanisms of pharmacologic ascorbate-induced neoplastic cell death, and the possible role of ascorbate as an adjuvant for novel anti-cancer therapeutics�

P18 Development of a whole genome sequencing based classifier to determine telomere maintenance mechanism in tumoursMichael Lee1, Rebecca A. Dagg2,3, Loretta M. Lau2,3, Nic Waddell4, John V. Pearson5, Sean Grimmond6, Roger R. Reddel7, Jonathan Arthur8, Hilda A. Pickett1

1Telomere Length Regulation Group, Children’s Medical Research Institute, The University of Sydney2Children’s Cancer Research Unit, The Children’s Hospital at Westmead3Sydney Medical School, The University of Sydney4Medical Genomics Group, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia 5Genome Informatics Group, QIMR Berghofer Medical Research Institute 6Wolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow7Cancer Research Unit, Children’s Medical Research Institute, The University of Sydney8Bioinformatics Unit, Children’s Medical Research Institute, The University of Sydney

Telomeres are terminal repetitive DNA sequences at the ends of chromosomes, and are considered to consist almost exclusively of the hexameric sequence TTAGGG� Telomere variant repeat sequences have been identified at elevated levels in a subset of human cancers which use the Alternative Lengthening of Telomeres (ALT) pathway of telomere maintenance� We analysed whole genome sequencing (WGS) data from a panel of ALT and telomerase-positive tumours along with matched normal tissue� Telomere reads were extracted and filtered, and the number of variant repeats were quantitated� Statistical analysis was performed and the most statistically significant variant repeats were selected to generate a random forest classifier� We identified a subset of variant telomeric repeats that are able to classify ALT and telomerase tumours with 90% accuracy� To further support this we performed hierachical clustering on the dataset and found that two clusters were formed representing the ALT and telomerase-positive groups� We also found that including the telomeric data extracted from the matched normal samples did not improve the classifier, suggesting that sequencing the tumour DNA alone is sufficient to identify the telomere maintenance mechanism� We propose that using telomeric variant repeat profiles from WGS data is sufficient to determine the telomere maintenance mechanism of a tumour�

P19 The role of actomyosin dynamics during T cell migrationJorge L. Galeano Niño1,2, Rain Y Kwan1, Adam J Cook1,2, Wolfgang Weninger1,3,4, Maté Biro1,2,1Centenary Institute of Cancer Medicine and Cell Biology2Sydney Medical School, The University of Sydney3Discipline of Dermatology, The University of Sydney4Department of Dermatology, Royal Prince Alfred Hospital

Cytotoxic T cells (CTLs) play a key role in the immune surveillance against tumours� They constitutively patrol organs for cognate antigen� These cells display a polarised shape with a dynamic leading edge and a uropod at the rear� The actomyosin cortex generates the mechanical forces that drive cell migration� The polymerization of actin filaments, mediated by Arp2/3 complex or formins (actin nucleators), and the contractility of myosin motor proteins, determines the morphology and underpins the migration of cells� However it is still unknown how the actomyosin cortex is involved in determining T cell scanning for antigens� Using migration assays based on collagen matrices, we found that by inhibiting specific components of the actomyosin cortex, CTLs can be forced to adopt different migration modes and extend distinct sets of protrusions� These findings suggest that the inhibition of a particular actin nucleator or myosin contractility regulator modifies the migration behaviour of T cells, which is determined by the type of protrusion that they extend�

P20 Dipeptidyl Peptidase 9: noval nautral substrates and association with cell adhesion, focal adhesion kinase and paxillinHui Zhang1, Sadiqa Maqsudi2, Andrew Stephens2, Carol Wadham3, Ruth Geiss-Friedlander4, Geoffrey W McCaughan1, Fiona M. Keane1, Mark D. Gorrell1

1Centenary Institute, The University of Sydney2Prince Henrys Institute for Medical Research, Monash University3Children’s Cancer Institute Australia, Lowy Cancer Research Centre, University of New South Wales4Georg-August-University of Goettingen, Germany

Dipeptidyl Peptidase 9 (DPP9) is a ubiquitously expressed member of the DPP4 protease family� DPP9 influences cellular interactions with extracellular matrix, and regulates cell apoptosis and proliferation via the EGF/PI3K/Akt pathway� Our homozygous mice lacking DPP9 enzyme activity (KI; knockin Ser-to-Ala) die soon after birth� Confocal and super-resolution microscopy revealed that while some DPP9-EGFP is associated with mitochondria and the strongest co-localization was with microtubules� Upon EGF stimulation, some DPP9 re-distributed towards the ruffling membrane at the leading edge of the migrating cell, where it co-localised with the focal adhesion proteins integrin-β1 and talin� DPP9 gene silencing or enzyme inhibition reduced cell adhesion and migration and reduced expression of integrin-β1 and talin and the phosphorylation of focal adhesion kinase (FAK) and paxillin� Moreover, enzyme inhibition suppressed the viability of Huh7 cells (MTS assay)� Mass spectrometry of 2D-DIGE spots identified 111 novel DPP9 substrates in KI mouse embryonic fibroblasts: 56 of these substrates contain an N-terminal Xaa-Pro and 55 contain Xaa-Ala� Xaa-Ala was not hydrolysed by DPP8� DPP9-mediated cleavage of nine peptides and full length proteins was confirmed by MALDI-TOF or immunoblotting� Those proteins are associated with immunity and cellular secretory processes� Cell adhesion and migration are a key process in both tumour angiogenesis and cancer cell metastasis, so our data provides novel insights into how the DPP9 enzyme may contribute to liver cancer progression�

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P21 Pharmacogenetics and chemotherapy: the role of transporter genes in actinomycin d pharmacokinetics in paediatric cancer patientsHannah Y Kim1, Ting Chan1, Fanfan Zhou1, Amanda Low1, Alan V Boddy1

1Faculty of Pharmacy, The University of Sydney

Background: Actinomycin D is a major component of treatment regimen for paediatric cancers such as Wilms tumour, rhabdomyosarcoma and Ewings sarcoma� However, despite 40 years of clinical use, pharmacokinetics (PK) of actinomycin D is still inadequately understood and inter-patient variability in PK and hepatotoxicity pose a clinical concern� Elimination of actinomycin D is believed to be mediated by transporter mechanisms, as the drug does not undergo significant metabolism� Initial screening data identified four members of solute carrier (SLC) transporter family: organic anion transporter 4 (OAT4), organic cation transporter 2 and 3 (OCT2 and OCT3), and proton-coupled oligopeptide transporter 2 (PEPT2) to have the greatest inhibition by actinomycin D on probe-substrate uptake� The current study aims to characterise actinomycin D uptake in order to identify potential transporter genes, which may be involved in actinomycin D pharmacokinetics�

Methods: Human embryonic kidney 293T (HEK293T) cells were transfected with plasmid DNAs of OAT4, OCT2, OCT3 and PEPT2� The transfected and WT cells were then incubated with 0�1uM actinomycin D� Intracellular accumulation of actinomycin D was analysed in cell lysates after 1hr, 2hr and 6hr incubation, using liquid chromatography-mass spectrometry (LCMS)�

Results: Intracellular accumulation of actinomycin D was observed in all the transfected cell lines� The time-course of actinomycin D accumulation could be characterized for up to 6hrs post incubation in WT and transfected cell lines� Actinomycin D uptake was selectively mediated by individual SLC transporters�

Conclusions: Results showed that actinomycin D is a potential substrate for members of SLC family, and that OAT4, OCT2, OCT3 and PEPT2 appear to be implicated in actinomycin D uptake� Further studies will be conducted through PK modelling and genotyping in order to identify genetic contributers involved in actinomycin D PK and ultimately to improve dosing and monitoring recommendations for actinomycin D in cancer patients�

P22 mRNA electroporated CMRF-56 blood dendritic cells: an anti-tumour vaccination strategyMichael S Papadimitrious1,2, Phillip D. Fromm1,2, Jennifer L Hsu1, Nicolas Van Kooten Losio1,2, Nirupama Verma1,2, Kevin Lo1,2, Pablo Silveira1,2, Christian Bryant1,2, Cameron Turtle3, Rebecca Prue4, Peter Vukovic4, David Munster4, Tomoko Nagasaki4, Ross Barnard5, Stephen Mahler6, Sébastien A. Anguille7, Zwi Berneman7, Lisa G. Horvath8,9,10, Kenneth Bradstock1,2,13, Douglas Joshua2,11, Georgina Clark1,2, Derek NJ Hart1,2,12

1ANZAC Research Institute, Gate 3, Hospital Road, Concord Repatriation General Hospital2Sydney Medical School, The University of Sydney3Program in Immunology, Fred Hutchinson Cancer Research Centre, USA4Mater Medical Research Institute5School of Chemistry and Molecular Biosciences, University of Queensland6Australian Institute for Bioengineering and Nanotechnology, University of Queensland7Antwerp University Hospital, Centre for Cell Therapy and Regenerative Medicine, Belgium8Department of Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital9The Kinghorn Cancer Centre / Garvan Institute of Medical Research10Chris O’Brien Lifehouse, Department of Medical Oncology, Royal Prince Alfred Hospital11Department of Haematology, Concord Repatriation General Hospital12Department of Haematology, Royal Prince Alfred Hospital13Haematology Department, Westmead Hospital

Clinical trials using tumor associated antigen (TAA) mRNA loaded monocyte derived dendritic cells (MoDC) have established this modality as a valid therapeutic to treat cancer� The in vitro manufactured MoDC have been shown to be fundamentally different from blood dendritic cells (BDC)� The use of primary BDC has the potential to dramatically improve overall objective clinical responses by targeting superior antigen presenting cells� We used a human IgG4 chimeric CMRF-56 antibody in a clinically appropriate protocol to purify BDC for loading with TAA mRNA� The CMRF-56 antibody targets a cell surface marker on human BDC subsets and other antigen presenting cells� We evaluated CMRF-56 enriched BDC as an improved clinical preparation for DC immune therapy by: 1) assessing the effect of mRNA transfection on BDC, 2) comparing the migration capacity of both CMRF-56+ BDC and MoDC and 3) assessing their ability to present mRNA antigens and initiate antigen specific immune responses� GM-CSF treatment and mRNA transfection of BDC

resulted in prolonged TAA expression and up-regulation of immune co-stimulatory molecules� Transfected CMRF-56+ BDC exhibited uninhibited in vitro migration capacity and migrated to draining lymph nodes in a preclinical xeno-SCID mouse model� BDC loaded with mRNA for Influenza matrix protein or a leukaemic antigen (Wilms Tumor antigen 1) had the capacity to stimulate autologous antigen specific CD4+ and CD8+ T cells� Our data suggests that human CMRF-56+ cells may be a superior source of DC for therapeutic vaccination� Furthermore, CMRF-56+ BDC can be transfected with TAA mRNA demonstrating their efficacy for future anti-cancer clinical studies�

P23 Investigation into lymphoma predisposition in Australian BullmastiffsSally Mortlock, Mehar Khatkar, Peter Williamson

Faculty of Veterinary Science, The University of Sydney

Lymphoma is the most common haematopoietic malignancy seen in dogs� Bullmastiffs are one of a number of breeds with a high incidence of lymphoma, suggesting a genetic predisposition� The aim of this study was investigate the incidence of lymphoma in the Australian Bullmastiff population, characterise the genetic structure and diversity of the population and identify risk loci predisposing the breed to lymphoma� A survey conducted on Australian Bullmastiffs revealed a high incidence of lymphoma in dogs ≤6 years, contributing to reduced longevity in the breed� Genealogical analysis of diversity was conducted using a database consisting of 16,378 Bullmastiff pedigrees from year 1980 to 2013� Genealogical parameters revealed a mean inbreeding coefficient of 0�047; 142 total founders (f); an effective number of founders (fe) of 79; an effective number of ancestors (fa) of 62; and an effective population size of 41� Genetic diversity and the degree of genome-wide homogeneity were investigated using molecular data� A total of 188 Bullmastiff dogs were genotyped using the 170,000 SNP Illumina CanineHD Beadchip� Fine-scale population structure was analysed using NETVIEW, a population analysis pipeline� Multilocus heterozygosity (MLH) was equal to 0�206; runs of homozygosity (ROH) as proportion of the genome, averaged 16�44%; effective population size was 29�1, with an average inbreeding coefficient of 0�035� Information on genetic structure and diversity was incorporated into a genome wide association study (16 cases, 22 controls) to detect loci associated with disease risk� An association was detected across a 5 Mb region on chromosome 13 (15 SNPs p<1�7x10-4)� Risk haplotypes within this region were identified, 75% cases homozygous for risk haplotypes compared to 14% of controls� Whole genome sequencing is underway to identify causative variants is in the region� Identification of a heritable genetic aberration will influence breeding decisions to reduce the frequency of the disease in the population�

P24 Gadolinium as a novel nano-probe to enhance image-guided targeted x-ray therapyHilary Byrne, P. Spence, W. S. Price, A. Gupta, L. M. Rendina, Z. Kuncic


Heavy metal nanoparticles have attracted widespread interest for their potential use as radiosensitising agents that can enhance the therapeutic effect of both targeted x–ray and heavy-ion beams in radiotherapy applications� Nanoparticle enhanced radiotherapy is highly suited to targeted therapies for difficult to treat cancers such as resistant glioblastoma and paediatric cancers� The ability of high-Z atoms to generate more secondary electrons than normal tissue following irradiation leads to a higher absorbed dose in the treated region through a chain of physical interactions (including Auger electron cascades) that can produce large numbers of ionisations in the surrounding molecules� Where the nanoparticles can be located in the cell nucleus, complex damage may be caused in the DNA primarily mediated by radical oxygen species caused by ionisation of water molecules� However, high-Z nanoparticles are often observed to locate outside the cell nucleus yet the cells still exhibit radiosensitisation responses, implying that the radioenhancement in these cases may be mediated indirectly by cell death signalling pathways� While much attention to date has been paid to gold nanoparticle radiosensitisation, recent studies have begun to focus on gadolinium because of its additional advantage as a contrast agent for magnetic resonance imaging (MRI), allowing the exciting possibility of diagnostic imaging and enhanced radiotherapy treatment delivered by the same nanoparticle� Indeed, there is the possibility of developing new gadolinium-based nanotheranostic paradigms for emerging MR image-guided radiotherapies, including with the integrated MRI-linac technology now available� We have conducted Monte Carlo radiation transport simulations to model the relevant physical processes involved in irradiation of high-Z nanoparticles, including gold and gadolinium, with x-rays� Our simulation results reveal that atomic de-excitation by both Auger electron emission and fluorescence (mainly K-alpha) photon emission both contribute to radiosensitisation� We also present preliminary results on a novel gadolinium (GdIII) complex that exhibits excellent preferential uptake into the mitochondria of tumour cells and radiosensitivity to synchrotron x-ray irradiation� NMR relaxivity measurements and imaging confirm its enhanced MRI contrast capability� We aim to carry out the first study of this nano-complex for image-guided radiotherapy using an integrated MRI-linac system�

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P25 BRAF mutations and response to BRAF inhibition in epithelial ovarian cancerTania Moujaber1,2,3,4, Dariush Etemadmoghadam5,6, Catherine Kennedy1,2,3,4, Rosemary L Balleine1,2,4,8, Catherine Saunders2,9, Gerard V Wain2,3,4, Alexander Dobrovic6,10,11, David D L Bowtell5,6,7,12,13, Paul R Harnett1,2,4, Anna DeFazio1,2,3,4

1Centre for Cancer Research, The Westmead Millennium Institute for Medical Research2The University of Sydney3Department of Gynaecological Oncology, Westmead Hospital4Crown Princess Mary Cancer Centre, Westmead Hospital5Peter MacCallum Cancer Centre6Department of Pathology, University of Melbourne7Sir Peter MacCallum Cancer Centre Department of Oncology, University of Melbourne8Pathology West ICPMR Westmead9Department of Nuclear Medicine, PET and Ultrasound, Westmead Hospital10Ludwig Institute for Cancer Research, Olivia Newton John Cancer and Wellness Centre11La Trobe University12Ovarian Cancer Action Research Centre, Department of Surgery and Cancer, Imperial College, London13Department of Biochemistry and Molecular Biology, University of Melbourne

Background: Low-grade serous carcinomas (LGSC) are a subtype of epithelial ovarian cancer that tends to occur in younger woman and are generally resistant to chemotherapy� LGSC are characterised by somatic RAS-MAPK pathway mutations, including mutations in KRAS, BRAF and NRAS, and a number of drugs targeting this pathway have been developed� However, it is not yet known which pathway-targeted drugs, or combination of drugs, will be effective in the treatment of LGSC�

Aim: To characterise BRAF mutations in LGSC and to determine whether BRAF inhibitors could demonstrate a clinical benefit in ovarian cancer patients�

Methods: Patients with LGSC were identified through the Australian Ovarian Cancer Study and the Westmead GynBiobank� Tumour mutations were assessed using targeted and exome sequencing, and gene copy number was measured by whole genome SNP arrays� Tumour expression of BRAFV600E protein was also assessed by immunohistochemistry� The BRAF inhibitor, dabrafenib, was trialled in a patient with a somatic BRAFV600E mutation and progress was monitored clinically, biochemically using CA125 tumour marker levels and radiologically with PET imaging�

Results: In a cohort of LGSC, molecular characterisation revealed 6/47 (12�8%) to have a BRAF mutation, most of which were the common V600E variant� A heavily pre-treated patient with chemoresistant LGSC known to harbour a BRAFV600E mutation received dabrafenib monotherapy for 11 months� The patient demonstrated a complete biochemical response, with her CA125 level normalising for the first time since diagnosis, accompanied by a substantial clinical and radiological response�

Conclusion: The response to dabrafenib suggests that BRAF inhibition represents a potential therapeutic option for LGSC patients with somatic BRAFV600E mutations� These results demonstrate that molecular analysis of LGSC can provide effective treatment options and highlights the need for ongoing research and novel clinical trials in this understudied tumour-type�

P26 Sourcing novel anticancer drugs by the enzymatic fragmentation of natural productsTomas Richardson-Sanchez, William Tieu, Rachel Codd

Discipline of Pharmacology, The University of Sydney

Background: Enzymatic fragmentation of structurally complex natural products can allow access to small building blocks in yields that could be difficult to achieve by chemical synthesis� This method could provide a new route to drug leads� Desferrioxamine B (DFOB) is a large bacterially-produced iron chelator� The enzymatic fragmentation of DFOB by A� irakense established the production of monomeric hydroxamic acid fragments such as N-5-aminopentyl-N-(hydroxy)-acetamide (APHA)� Monomeric hydroxamic acids can act as anticancer agents, such as histone deacetylase (HDAC) inhibitors scriptaid and M344 or 5-lipoxygenase (5-LO) inhibitor BWA4C� This project aimed to generate, purify and test the parent compound DFOB, the APHA fragment and semi-synthetic derivatives of APHA for inhibition of HDAC and 5-LO� Methods: APHA was chemically modified by the addition of large hydrophobic motifs at the amine tail to create structural analogues of commercially available drugs scriptaid, M344 and BWA4C� DFOB, APHA, the commercially available drugs and all semi-synthetic derivatives of APHA were then tested for in vitro inhibition of HeLa nuclear extract (rich in HDAC isoforms), HDAC1, HDAC11 and 5-LO� Results: The scriptaid analogue showed inhibition of HeLa nuclear extract (IC50 = 77�68 μM, 95% CI [40�31, 149�7]), 40% inhibition of HDAC11 at 500 μM, 70% inhibition of HDAC1 at 200 μM and complete inhibition of 5-LO at 300 μM� The M344 analogue showed 50% inhibition of HDAC11 at 500 μM� The BWA4C analogue showed 40% inhibition of 5-LO at 300 μM�

Conclusions: Desferrioxamine B was enzymatically fragmented to generate the APHA fragment, which was chemically modified to give three novel drug leads� Scriptaid analogue in particular showed the most promise of these, both as a HDAC1 inhibitor and as an inhibitor of 5-LO� These data have shown a new platform for the discovery of drug leads for the treatment of cancer and other conditions�

P27 Development of novel anti-cancer metastasis agents derived from omega-3 fatty acid metabolitesNooshin Koolaji


Epidemiological and experimental studies show that omega-3 polyunsaturated fatty acids (ω-3 PUFAs) such as eicosapentaenoic acid (EPA), that are found in oily fish produce significant health benefits by inhibiting the development and spread of breast cancer� Recent evidence suggests that the anticancer effects of EPA are due to the formation in the body of an active metabolite, ω-3-epoxy-EPA, that inhibits cell proliferation� As ω-3 PUFAs are blood brain barrier (BBB) permeable the ω-3 PUFA epoxide structure offers a novel template for the development of drugs to treat primary breast cancers and secondary tumours in the brain� Previously drug design strategies for preparing ω-3-epoxy-EPA analogues have produced agents that display extremely potent inhibition of breast cancer cell proliferation� The CENTRAL AIM of this project to develop ω-3-epoxy-EPA analogues as novel growth inhibitors of primary breast and secondary brain cancers� The HYPOTHESIS underlying this project is that analogues of ω-3-epoxy-EPA may be developed as novel anticancer drugs capable of penetrating the BBB� The MAJOR SIGNIFICANT OUTCOME is that these new agents would represent a completely new class of anticancer drugs with the potential to treat metastatic brain cancers that are resistant to current chemotherapeutics� The SPECIFIC AIMS of this project are to: 1� To develop ω-3-epoxy-EPA analogues with structural characteristics for optimal anti-proliferative activity, BBB permeability and metabolic stability� 2� To determine the molecular mechanisms by which the optimal analogues inhibit cancer cell proliferation and penetrate into brain in an animal model�

P28 Glucose conjugation for targeted delivery of metal based anticancer agentsAlexandra Glenister, Michela Simone, Trevor Hambley

School of Chemistry, The University of Sydney

To improve the efficacy of anticancer chemotherapy it is necessary to develop targeted treatments, which can be achieved by exploiting differences between healthy and cancerous cells� The avid consumption of glucose by cancerous tissue compared with healthy cells has been known for almost a century� Today elevated levels of glucose uptake is one of the hallmarks of malignant cells� Deregulation of the expression of glucose transporters (GLUTs) has been identified in many tumour types, and results in overexpression of these sugar transporters in cancer cells�[2] Exploiting these differences to increase uptake of anticancer agents by tumours is being explored as a method of increasing selective delivery, and thereby lowering required dosage and minimising side effects� We have synthesised a glucose analogue, designed to be a substrate for glucose transporters and hexokinase, to target the increased glucose consumption of cancer cells� This targeting group has been designed to be attached to various metal complexes, with the potential to enable increased tumour selective delivery and uptake of the anticancer prodrugs or imaging agents� To determine the effectiveness of our targeting strategy we will assess uptake of cobalt(III) and platinum(IV) complexes with this targeting group by cancer cell lines� This will be achieved through cytotoxicity and accumulation studies and fluorescence imaging�

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P29 The design of stabilised platinum(iv) complexes for targeted drug deliveryCatherine Chen, Trevor Hambley

School of Chemistry, The University of Sydney

Platinum(II) anticancer drugs are considered the most successful chemotherapy agents� Cisplatin, carboplatin and oxaliplatin, have worldwide clinical approval and are used to treat up to 50% of patients undergoing chemotherapy� Despite their clinical success, platinum(II) anticancer drugs are often associated with toxic side effects as the result of its lack of specificity and binding irreversibly to biomolecules in blood plasma and cells resulting in its deactivation before reaching the tumour site� Platinum(IV) complexes are a promising class of pro-drugs which may bypass the problems associated with their platinum(II) counterparts� We have recently reported a class of platinum(IV) complexes that exhibit resistance to reduction by endogenous reductants� In this study, we investigate the relationship between the structure and stability of the overall complex using various spectroscopic techniques in biological models, as well as employing various synthetic targeting strategies� Preliminary results show that this class of platinum(IV) complex appears to be stable in the extracellular environment, but is reduced rapidly once they are within cancer cells�

P30 Biological speciation of the anticancer rh(iii)-dimethylsulfoxide complexes via x-ray absorption spectroscopyJun Liang1, Aviva Levina1, Barry Lai2, Stefan Vogt2, Peter Lay1

1School of Chemistry, The University of Sydney2X-ray Science Division, Argonne National Laboratory, Argonne, USA

Background: Recent progress on metal-based chemotherapeutics suggested that precious metals other than Pt and Ru might also possess antitumor activities� Although a number of Rh(III) coordination and organometallic complexes have been identified to exhibit promising anticancer properties, their clinical application was hampered by insufficient understanding on the mechanisms of action�

Methods: The cytotoxic and anti-metastatic properties of a series of Rh(III)-dimethylsulfoxide complexes have been studied in various cell biology assays and live cell imaging analysis� The degradation of these compounds in biological media under physiologically-relevant conditions has been followed using X-ray absorption near edge structure (XANES) spectroscopy, and their sub-cellular localization has been visualised via X-ray fluorescence microscopy (XFM)�

Results: The complexes having labile ligands undergo rapid aquation in aqueous media and interact extensively with serum proteins and the extracellular matrix, possess anti-metastatic properties comparable to the Ru anti-metastatic drug, NAMI-A� The complexes bearing bulky hydrophobic ligands were rapidly taken up by cancer cells and exhibit promising cytotoxicity against a Pt-resistant tumour cell line� The XFM images revealed that Rh accumulates primarily on the surface of the cells treated with anti-metastatic compounds, while the treatment with cytotoxic compounds resulted in the Rh accumulation within the perinuclear region of cytoplasm�

Conclusion: The present study revealed that a number of Rh complexes are potential anticancer agents with promising cytotoxicity and anti-metastatic properties comparable to established Pt and Ru counterparts, and also demonstrated the advantages of using synchrotron light source to provide valuable biochemical information on the physiological transformation and speciation of metal-based anticancer compounds that otherwise difficult to acquire by conventional spectroscopic methods�

Salman AlbesshanMedical Radiation Sciences, The University of Sydney

− salb5075@uni�sydney�edu�au

Marina AliWestmead Hospital, The University of Sydney

− marina�ali@sydney�edu�au

Ghazal Alipour TaleshStorr Liver Unit, Westmead Millennium Institute, The University of Sydney

− ghazaal�alipour@gmail�com

Ahmed AlmansourSydney Nursing School, The University of Sydney

− aalm1832@uni�sydney�edu�au

Juliana AndriciNorthern Clinical School, The University of Sydney

− juliana�andrici@gmail�com

Ali AzimiDepartment of Dermatology, The University of Sydney

− aazi9158@uni�sydney�edu�au

Dong-Hun BaeDiscipline of Pathology, The University of Sydney

− dbae5413@uni�sydney�edu�au

Hilary ByrneThe University of Sydney

− h�byrne@physics�usyd�edu�au

Aritrick ChatterjeeFaculty of Health Sciences, The University of Sydney

− acha5275@uni�sydney�edu�au

Yongjuan ChenThe University of Sydney

− yong�chen@sydney�edu�au

Catherine ChenThe University of Sydney

− catherine�chen@sydney�edu�au

Rebecca DaggThe Children’s Hospital at Westmead

− rebecca�dagg@health�nsw�gov�au

Anna deFazioThe University of Sydney and Westmead Millennium Institute

− anna�defazio@sydney�edu�au

Ernest EkpoFaculty of Health Sciences, The University of Sydney

− eekp9437@uni�sydney�edu�au

Sarah FrostSydney Medical School, The University of Sydney

− sfro5957@uni�sydney�edu�au

Jorge GaleanoThe University of Sydney

− jgal6417@uni�sydney�edu�au

Jorge Luis Galeano NinñoCentenary Institute of Cancer Medicine and Cell Biology

− j�galeano@centenary�org�au

Shila GhazanfarThe University of Sydney

− s�ghazanfar@maths�usyd�edu�au

Alexandra GlenisterSchool of Chemistry, The University of Sydney

− alexandra�glenister@sydney�edu�au

Anthony GloverNorthern Clinical School, Kolling Institute of Medical Research

− antglover@gmail�com

Mark GorrellCentenary Institute

− mark�gorrell@sydney�edu�au

Anjali GowripalanSchool of Molecular Bioscience, The University of Sydney

− agow7978@uni�sydney�edu�au

Fadi GurgisDiscipline of Pharmacology, The University of Sydney

− fgur9639@uni�sydney�edu�au

Nunki HassanPhD Student

− nunkihassan@gmail�com

James HendersonThe University of Sydney

− j�henderson@centenary�org�au

Merilyn HeuschkelCancer Research Network, The University of Sydney

− merilyn�heuschkel@sydney�edu�au

Monira HoqueFaculty of Pharmacy, The University of Sydney

− mhoq4913@uni�sydney�edu�au

Shelley Ji Eun HwangWestmead Hosptial, The University of Sydney

− shelley�hwang@hotmail�com

Stephanie JohnsonThe University of Sydney

− stephanie�johnson@sydney�edu�au

Lauren JooKolling Institute of Medical Research, The University of Sydney

− jjoo5893@uni�sydney�edu�au

Candice Kielly-CarrollResearch in Implementation Science and eHealth

− candice�kielly-carroll @sydney�edu�au

Hannah KimFaculty of Pharmacy, The University of Sydney

− hkim0212@uni�sydney�edu�au

Nooshin KoolajiThe University of Sydney

− n�koolaji@gmail�com

Attendee list

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Elisabeth KrupkaCancer Council NSW

− ekrupka@hotmail�com

Grace KwokKolling Institute of Medical Research

− kwok0027@gmail�com

Michael LeeChildren’s Medical Research Institute

− mlee@cmri�org�au

Joanne LewisThe University of Sydney

− jo�lewis@sydney�edu�au

Tong LiMedical Image Optimisation and Perception Group, The University of Sydney

− toli7326@uni�sydney�edu�au

Jun LiangSchool of Chemistry, The University of Sydney

− jlia1517@uni�sydney�edu�au

Siew Kee (Amanda) LowFaculty of Pharmacy, The University of Sydney

− siewkee�low@sydney�edu�au

Cristina MapaguCentre for Cancer Research, Westmead Millennium Institute, The University of Sydney

− cristina�mapagu@sydney�edu�au

Mark McEnteeFaculty of Health Sciences, The University of Sydney

− mark�mcentee@sydney�edu�au

Rebecca Mercieca-BebberThe University of Sydney

− rebecca�mercieca@sydney�edu�au

David MeredithThe University of Sydney

− david�meredith@sydney�edu�au

Sally MortlockFaculty of Veterinary Science, The University of Sydney

− smor5136@uni�sydney�edu�au

Tania MoujaberWestmead Millennium Institution, The University of Sydney

− tania�moujaber@sydney�edu�au

Timothy NewsomeThe University of Sydney

− tim�newsome@sydney�edu�au

Brooke NickelSchool of Public Health, The University of Sydney

− brooke�nickel@sydney�edu�au

Rosita PangBosch Institute, The University of Sydney

− tpan2483@uni�sydney�edu�au

Michael PapadimitriousANZAC Research Institute

− michael�papadimitrious @sydney�edu�au

Nadi SadrThe University of Sydney

− nadi�sadr@sydney�edu�au

Tomas Richardson-SanchezDiscipline of Pharmacology, The University of Sydney

− tric3775@uni�sydney�edu�au

Steven SchlichtemeierRoyal North Shore Hospital

− sschlich@gmp�usyd�edu�au

Balakrishnan ShammugasamyThe University of Sydney

− bsha6187@uni�sydney�edu�au

Tim ShawThe University of Sydney

− tim�shaw@sydney�edu�au

Freddy SitasSchool of Public Health

− frederick�sitas@sydney�edu�au

Megan SmithThe University of Sydney

− megan�smith@nswcc�org�au

Rachael StenhouseThe University of Sydney

− rste0498@uni�sydney�edu�au

Elisabeth TondlSchool of Chemistry, The University of Sydney

− elisabeth�tondl@sydney�edu�au

Parth UpadhyayThe University of Sydney

− pupa6081@uni�sydney�edu�au

Stephanie WhiteThe University of Sydney

− swhi8396@uni�sydney�edu�au

Sile Fiona YangChildren’s Medical Research Institute

− syan6494@uni�sydney�edu�au

Alison YoungThe University of Sydney

− ayou1666@uni�sydney�edu�au

Madiha YunusThe University of Sydney

− myun8191@uni�sydney�edu�au

Amgad ZakyThe University of Sydney

− amgadadolf@hotmail�com

Hui ZhangCentenary Institute

− e�zhang@centenary�org�au

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Cancer Research Network Officesydney�edu�au/cancer-research/+61 2 8627 1532cancer-research@med�usyd�edu�au

The Cancer Research Network links cancer researchers at the University of Sydney and its teaching hospitals and affiliated research institutes to build high quality cancer research capacity and achieve international cancer research excellence in areas of strength�

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2015_Postgraduate_Symposium_booklet