The Kidsâ€™ Cancer Project.
Annual Report Financial Year 2011/2012.
Col Reynolds OAM Chairman & Founder
“Over the years I’ve made the same promise again and again to countless parents of children with cancer: I’ve vowed with my heart that I will never give up on my mission until a cure is found.”
Contents Report from the Chief Executive Officer
Board of Directors
Research Advisory Committee
Cancer Gene Therapy Project
Drug Discovery Project
Muscle Stem Cell Project
Childhood Cancer Cytoskeleton Consortium (C4)
- Targeting the cytoskeleton in leukaemia
- Tissue organisation and cell-to-cell communication
- Regulation of metastasis by the cytoskeleton
- Developing new drugs to treat childhood cancers
- Modelling childhood brain tumours in the fly
- The role of LIMK2 in sensitivity to chemotherapeutic drugs in neuroblastoma
- Potential side effects of targeting tropomyosins to treat childhood cancer
- Controlling the cytoskeleton in neuroblastoma
2011-2012 Research Publications
Research Publications to Date
Report from the Chief Executive Officer Looking back over the last 18 months since my appointment, I am proud of what we have achieved.
survival. We are very hopeful for the success of the trial as similar work overseas in adults has yielded very promising results.
This has been a big year for The Kids’ Cancer Project. First of all, because we have changed our name, and our brand from the Oncology Children’s Foundation to The Kids’ Cancer Project. Despite our mission remains very much the same: to cure kids’ cancer. A project is something that by definition, works towards a specific goal and has an end date. The change has come as part of an overall strategy to ensure that we can continue to support the very best researchers and continue to make progress towards a cure.
The Drug Discovery Program is also progressing and we expect Phase 1 clinical trials to begin in the coming year. In order to move to clinical trials quickly, trials will first be conducted in adults, however documentation is being prepared to ensure that the drug is translated to children.
This year also marks a significant research milestone for the charity. The Cancer Gene Therapy Project launched Phase 1 clinical trials of a never before used treatment regime for childhood brain tumours. In an Australian first, the children participating in the trial will have a gene added to their bone marrow to protect it from the harmful effects of chemotherapy. Being able to offer this sort of protection of one of the most vulnerable parts of a child in treatment’s body, will allow doctors to use more aggressive treatments to hopefully give these children a chance at
Our overall research strategy is to ensure that Australian children receive the best frontline care available in the world today. We are achieving this by focusing on three main pillars of research; basic cell research, building capacity through collaboration and resources and investing in translational research, research that we can move from the laboratory into hospitals quickly. We can’t achieve such a great task on our own. We rely on our supporters, and we are working closely with governing bodies and building relationships with children’s hospitals to make sure that our strategy is best aligned with our children’s needs. The great support we have received this year has enabled us to welcome aboard a new
research program from the Garvan Institute, led by Dr Alex Swarbrick. Dr Swarbrick is a highly awarded researcher in his field and he has applied his expertise to a preclinical trial for neuroblastoma. His new approach will target specific â€˜switchesâ€™ within a cancer cell that cause it to become more aggressive. This year, and certainly going forward, we are determined to become increasingly efficient so that our main beneficiaries, children with cancer continue to receive the best treatments. One of our priority areas is to look at ways that we can increase our revenue by increasing efficiencies and ultimately our research funding. Evidence that we are on track is in the continued support that you give us and the new support that we have welcomed this year. Sanofi, one of the leaders in global healthcare have committed to supporting The Kidsâ€™ Project. One of the very exciting aspects of this partnership is its depth. Sanofi itself has made a significant contribution and their staff have also been engaged in fundraising and volunteering activities for us, as their chosen charity. In closing, I would like to thank every single
one of our supporters. Individuals, groups, organisations alike. Your support has been instrumental to our ability to continue to fund vital childhood cancer research. I would like to thank our Board, Research Advisory Committee, our ambassadors and our dedicated employees and volunteers. Each person on our team takes us one step closer to the day when 100% of children survive cancer.
Board of Directors Colin Reynolds OAM Founder & Chairman
Peter Neilson Chief Executive Officer
As the founder of The Kids’ Cancer Project, Col Reynolds’ outstanding contribution to the lives of children with cancer was officially recognised when he was honoured with an Order of Australia award in 2000. In 2010, Col was again recognised for his contribution to the lives of children with a Golden Harold Award. It was from unlikely beginnings that Col’s passion for helping children with cancer was first kindled.
Peter Neilson is a Certified Practising Accountant with 18 years of work experience, 11 of those years in senior management. Holding senior roles he has demonstrated strong leadership skill and commercial acumen. He specialises in finance, analysis, planning, strategy, quality, training, business growth and adding value.
Col had worked as a Tour Coach operator for more than 30 years. During this time he had looked after many high profile clients, managing the Secret Service convoy for both George Bush and Bill Clinton, and the Papal visit of Pope John Paul II.
One day, driving his empty coach past the old Camperdown Children’s Hospital, Col stopped to let two young children with bald heads cross the road. In that instant, Col resolved to do everything in his power to assist children with cancer. This single event changed the trajectory of his life, and planted the seeds for what in 1993 was to become The Kids’ Cancer Project.
Adrian is currently a partner at KPMG. He has over 20 years experience in the professional and financial services industries and his clients have included some of the largest property and financial services companies on the ASX. Adrian holds a Masters of Economics and is a member of the Institute of Chartered Accountants. Adrian became involved with The Kids’ Cancer Project after his son was diagnosed with a brain tumour at the age of five.
As a founding member of the Board of The Kids’ Cancer Project, Philip has a long standing history with the charity. When the doors of The Kids’ Cancer Project first opened, he held the position of CEO and worked closely with Col Reynolds fundraising to build and develop the charity to where it stands today.
Scott has been the National General Manager, Human Resources for Australia and New Zealand at Jardine Lloyd Thompson Pty Ltd since 2009. Prior to this, Scott has held senior HR positions with Telstra Corporation and The Seven Network. Previous employers include Thomas Cook, Century Yuasa Batteries and National Australia Bank.
Philip has extensive experience in the not-forprofit sector at the committee level, having worked closely with sporting associations in cricket, rugby league and soccer. These ties later assisted him in building successful relationships between The Kids’ Cancer Project and particular sporting bodies.
Lyndall Stoyles Lyndall is the Senior Legal Counsel for Patrick Container Ports, with particular experience in corporation and competition law. She is presently completing her Masters in Law.
Scott holds a Bachelor of Business, and is a certified professional of the Australian Institute of Human Resources (CAHRI). Scott has previously held a position as the Seven Network management representative on the Children’s Medical Research Institute (CMRI) fundraising committee for Jeans for Genes.
Ken Moroney OAM
Caroline has more than two decadesâ€™ experience in publishing, journalism, digital media and knowledge management. She has held senior positions in magazine production and at local and major metropolitan newspapers including as a regular weekly columnist.
Ken was the Commissioner of The New South Wales Police Force from 2002 to 2007. He has occupied a range of Executive positions as well as resided on 11 key Boards and Committees.
Currently, Caroline is the Company Secretary of a privately owned consultancy specialising in workflow applications and web enablement for local government. Her responsibilities cover business process analysis, application development, marketing and administration.
Simmone Reynolds Simmone has a Bachelor of Commerce from the University of New South Wales majoring in Marketing and Hospitality Management. Simmone is now a Captain in the Australian Army and is currently serving overseas. The Board have granted Simmone leave from her Directorship while she is serving with the Australian Defence Forces.
Ken was awarded the Order of Australia in 2006 and has received numerous medals such as The Australian Police Medal and the National Medal. Ken has also been awarded three New South Wales Commissionerâ€™s Commendations for Service and has an Honorary Doctorate from Charles Stuart University.
Supporting the brightest minds from the best research centres. Research Advisory Committee By supporting The Kids’ Cancer Project you’re supporting the best, most promising research. Rather than supporting one research team or research centre we search out and support the brightest minds and the most accomplished researchers from the best research centres. The projects we support are driven by three key goals: • Increasing the knowledge and understanding of childhood cancer • Building capacity to support childhood cancer research • The pursuit of innovation in treatment We are committed to making kids’ cancer history. We have appointed some of the world’s most experienced childhood cancer researchers to ensure that we invest your donations wisely. This eminent group forms our Research Advisory Committee, which annually reviews the milestones of our research programs.
Our Research Partners
Cancer Gene Therapy Project Dr Geoff McCowage (Oncology Unit) Dr Belinda Kramer (Children’s Cancer Research Unit) The Children’s Hospital at Westmead, NSW
Brain tumours are the second most common childhood cancer. These tumours can be extremely difficult to treat, and more deaths result from brain tumours than from any other childhood cancer. In June 2012, the Cancer Gene Therapy Project at The Children’s Hospital at Westmead launched a Phase 1 clinical trial aimed at improving survival for childhood brain tumours. The trial is testing the safety and feasibility of a gene therapy strategy to treat childhood brain tumours. In particular, the trial aims to provide the greatest benefit to children with highly malignant tumours that have recurred following standard treatments. The most significant dose limiting side effect in treating these children is that the drugs used also destroy bone marrow, resulting in their immune system being unable to fight off even the common cold. In an Australian first, a DNA repair protein, called MGMT, will be introduced into a child’s own bone marrow. Genetically modifying bone marrow in this way will make it drug resistant. This strategy may then allow increased doses of chemotherapy to be delivered to better target the child’s brain tumour without the harmful side effects for their bone marrow. The trial will also use a chemotherapy regimen not used previously in Australia. The key drug especially for use in the trial for the Cancer Gene Therapy team has been formulated in Australia. The newly opened Gene Therapy Trial represents the culmination of many years work by the team, and will run for three years.
Drug Discovery Project Professor Peter Gunning University of New South Wales, NSW The Drug Discovery Project is developing new chemotherapeutics for the treatment of childhood cancer. Drawing on 30 years of work, researchers have developed a new understanding of the structure of our cells and the way that they are put together. As a result, they have discovered that cancer cells use only a small number of building blocks within their architecture as compared with other cells in the body. By targeting one or more of the building blocks associated with cancer, they have developed a drug that is able to selectively destroy neuroblastoma cells. Neuroblastoma is the most common childhood cancer in children under the age of five. It also has one of the poorest outcomes. Survival rates remain around 50% and relapse rates are high. The longer-term effects of treatments are significant due to the high toxicity of treatment that is used on very young children whose bodies are still developing. The Drug Discovery Project is broken into two main areas. 1. Target Validation: Researchers have been able to show in the last year that the cancer drug target, called Tm5NM1, is directly involved in the growth of cells. Researchers have also been able to show that Tm5NM1 controls a cell proliferation pathway. Using a combination of research approaches the Drug Discovery Project has now identified where the target influences this pathway. This will be important information to provide to regulatory agencies moving forward to clinical trials since it is important to understand how anti-cancer drugs work.
2. Drug Development: Researchers have focussed on two major issues in the last year. The first is to more fully characterise the five drug candidates to understand the ability of these drugs to eliminate cancer cell growth. It is now clear that these drugs will have high efficacy against all neuroblastoma cells. The Drug Discovery Project has identified two drugs which may be the best to take forward. Researchers are currently having a test developed to follow the metabolism of these drugs in the body. The second issue is the development of different classes of drugs. Researchers have developed a new class that compromises a second part of the target. These drugs show promise and will be developed as â€˜second-in-classâ€™. Researchers have also developed a high throughput screen to identify drug candidates in large-scale screens of chemical libraries. This will allow chemicals to be identified which could not be predicted from computer modelling. This should allow development of a range of additional, unrelated drug candidates. The Drug Discovery Project expects to enter Phase 1 clinical trials in 2013.
Tumour Bank Dr Daniel Catchpoole The Children’s Hospital at Westmead, NSW Successful translational research depends on biobanking. The Tumour Bank is more than a storage facility. When treating physicians collect tumour samples for diagnosis, the Tumour Bank seeks permission from the patient to collect any excess tissue from the sample that is not required for diagnosis. The samples are linked with clinical data about the patient’s disease, their treatment and longerterm data relating to their outcome. It uses a highly specialised storage system that keeps samples at a constant -80C along with other specialised technologies for tissue handling. The Tumour Bank ensures that the maximum knowledge is gained from, sometimes the smallest specimen of tissue. It is the most
tangible resource available to researchers, providing direct access to patient samples and information without the need to instigate a full clinical trial, which is costly. Funding by The Kids’ Cancer Project has enabled the Tumour Bank at The Children’s Hospital at Westmead to be recognised as one of the premier examples of biobanking in Australia. The Tumour Bank has supported six national and international research investigations in the last 12 months and have agreed to support a further four studies.
Muscle Stem Cell Project Professor Edna Hardeman University of New South Wales, NSW The Muscle Stem Cell Project is addressing problems associated with the treatment of cancer in children using body irradiation. It has been known for some time that children treated with total body irradiation become highly susceptible to type II diabetes and secondary cancers. One mechanism which may account for this is the impact of the irradiation on muscle stem cells which over time will replace the muscle fibres in the body. Researchers are investigating the impact of irradiation on the chemical modification of muscle stem cell chromosomes.
Childhood Cancer Cytoskeleton Consortium (C4) The aim of the Childhood Cancer Cytoskeleton Consortium (C4) is to enhance research into the cytoskeleton of cancer cells to improve outcomes for children with cancer through collaboration, innovation and research support. C4 has been effectively achieving this goal through fostering collaborative research throughout Australia. Ultimately, C4 will lead to the generation of novel diagnostics and therapeutics toward the treatment of childhood cancers. By the end of December 2012, The Kidsâ€™ Cancer Project will have invested more than $2 million in C4 projects. This has resulted in identification of over a dozen new research collaborations and most of the eight C4 Post Doctoral researchers have spent time as guests in their peersâ€™ labs sharing resources and skills.
Targeting the cytoskeleton in leukaemia Professor Maria Kavallaris Childrenâ€™s Cancer Institute Australia, NSW Resistance to chemotherapy can be a major problem for the successful treatment of leukaemia. Recently, researchers have discovered that drug resistance can be caused by changes in proteins of the cytoskeleton of leukaemia cells. As part of C4, Professor Kavallaris has identified a particular protein, gamma actin, that when lost, leads to resistance to key drugs used in the treatment of leukaemia and other cancers. Future directions for this project include identifying the ways that gamma actin causes resistance so that better drug treatments can be developed.
Tissue organisation and cell-to-cell communication
Professor Alpha Yap University of Queensland, Qld The cells in our bodies are organised by their interactions with their neighbouring cells through receptors called cadherins. Cell interactions are commonly disturbed in childhood cancers, leading to metastasis or invasion of other tissues. The cytoskeleton plays an important role in the way that our cells communicate with each other through cadherins. In fact, cadherins are regulators for part of the cytoskeleton. Professor Yap is investigating the way that
cells stop recognising their neighbours, causing them to move away and metastasise. With the support of The Kidsâ€™ Cancer Project, this group has recently discovered new mechanisms that control the signals that cells send at junctions; importantly, these mechanisms involve genes implicated in cancer.
Regulation of metastasis by the cytoskeleton Associate Professor Geraldine O’Neill The Children’s Hospital at Westmead, NSW Most cells in our bodies have anchors holding them in the correct place. Neuroblastoma cells are able to pull up their anchors, enabling them to invade and metastasise to other parts of the body. Associate Professor O’Neill is focussed on understanding how the cytoskeleton regulates a cell’s anchors, allowing cancer cells to move and spread away from the primary tumour. Her team is investigates cancer cell movement using 3-dimensional systems that mimic the environment that confronts migrating cancer cells in the body.
Developing new drugs for the treatment of childhood cancers Professor Peter Gunning University of New South Wales, NSW
Professor Gunning’s lab has shown that tropomyosins are an integral component of the cytoskeleton and that tumour cells have only a specific subset of tropomyosins. This project is characterising the way that drugs targeting tropomyosins in cancer cells disrupt the cytoskeleton and causes the cell to die. In the last twelve months Professor Gunning’s group have focused on understanding how these drugs cause cancer cell death. Results
indicate that the drugs cause childhood cancer cells to undergo a process known as ‘programmed cell death’. They have compared this to the way other anti-cancer drugs do this and have found that their drugs may be able to short-circuit the pathway to ‘death’. This is particularly exciting and suggests that their drugs may be more efficient in killing cancer cells than other currently used chemotherapeutics. They also have evidence that a specific tropomyosin may be responsible for regulating a specific type of cell death pathway.
Modelling childhood brain tumours in the fly Associate Professor Helena Richardson Peter MacCallum Cancer Centre, Vic The vinegar fly, known also by its scientific name Drosophila, is an excellent animal system for modelling human cancer because they have the same key cancer-causing genes as humans. Associate Professor Richardson is looking for new regulators of the cytoskeleton in childhood brain tumours as therapeutic targets or possible tools for diagnosis.
The role of LIMK2 in sensitivity to chemotherapeutic drugs in neuroblastoma Dr Ora Bernard St Vincentâ€™s Institute, Vic The protein, LIMK2 is a key regulator of the actin cytoskeleton and it correlates with resistance to anticancer drugs, suggesting that LIMK2 might be a possible target to overcome drug resistance in neuroblastoma. Dr Bernard is investigating the possibility of combining LIMK2 inhibitors with chemotherapeutic drugs in the treatment of multi-drug resistant neuroblastoma and potentially other cancers.
Potential side effects of targeting tropomyosins to treat childhood cancer
Professor Edna Hardeman University of New South Wales, NSW Changes to the cytoskeleton are a characteristic feature of cancer cells and are critical for metastasis to occur. A particular protein, called tropomyosin, that is present in normal cells is enriched in cancer cells, particularly neuroblastoma. This has recently led to the development of drugs that target this protein.
Professor Hardemanâ€™s group are taking two approaches to this issue. On the one hand, they have identified a role for this tropomyosin in regulating the growth of some tissues in the mouse. Their work suggests that fat, brain and kidney are the most likely tissues to respond to the drug in terms of growth.
Professor Hardeman is investigating whether drugs that target tropomyosins in the cytoskeleton have a function in normal cells. This study is important in assessing whether anti-tropomyosin drugs will have unwanted side effects on normal cells.
The second approach is to measure the impact of the drug on the function of other body tissues. This is being done to identify which tissues may be most affected by drug treatment.
Controlling the cytoskeleton in neuroblastoma Professor Gregory Goodall Centre for Cancer Biology, SA The degree of metastasis is part of the process of neuroblastoma staging. The greater the metastasis, the more progressed a childâ€™s disease and the less promising their prognosis. Professor Goodall is investigating factors that limit metastasis. MicroRNAs are like small switches that turn off genes all over the body. A particular type of RNA, miR-200, appears in very low levels in neuroblastoma compared to other types of cells. Professor Goodall has showed that increased levels of miR-200 causes significant rearrangement of the cytoskeleton. He is investigating whether or not increasing levels of miR-200 can be used to limit metastasis in neuroblastoma.
Financials Balance Sheet as at 30 June 2012 2012
Non current assets
Non current liabilites
Profit & Loss Statement for the year ended 30 June 2012 2012
Surplus / (deficit) for the year
Research / Charitable Performance Expenditure
Donation per $ into Research Raffles - $0.23 Merchandise - $0.69 Donations - $0.82
2011-12 Research Publications 1. Bradbury P, Mahmassani, Zhong J, Turner K, Paul A, Verrills NM and O’Neill GM. PP2A phosphatase suppresses function of the mesenchymal invasion regulator NEDD9. BBA Mol. Cell Res. (2012) 1823(2):290-297. 2. de Bock CE, Ardjmand A, Molloy TJ, Bone SM, Johnstone D, Campbell DM, Shipman KL, Yeadon TM, Holst J, Spanevello MD, Nelmes G, Catchpoole DR, Lincz LF, Boyd AW, Burns GF, Thorne RF. The Fat1 cadherin is over expressed and an independent prognostic factor for survival in paired diagnosis-relapse samples of precursor B-cell acute lymphoblastic leukemia. Leukaemia (2012) 26(5):918-26. 3. Creed SJ, Desouza M, Bamburg JR, Gunning P, Stehn J. Tropomyosin isoform 3 promotes the formation of filopodia by regulating the recruitment of actin-binding proteins to actin filaments. Exp Cell Res. (2011) 317: 249-61. 4. Failes TW, Mitic G, Abdel-Halim H, Po’uha ST, Liu M, Hibbs DE, Kavallaris M. Evolution of resistance to Aurora kinase B inhibitors in leukaemia cells. PLoS ONE (2012) 7(2);e30734.
5. Gallant C, Appel S, Graceffa P, Leavis P, Lin JJ, Gunning PW, Schevzov G, Chaponnier C, DeGnore J, Lehman W, Morgan KG. Tropomyosin variants describe distinct functional subcellular domains in differentiated vascular smooth muscle cells. Am J Physiol Cell Physiol. (2011) 300: C1356-65. 6. Gomez GA, McLachlan RW, Yap AS. Productive tension: force-sensing and homeostasis of cell-cell junctions. Trends in Cell Biology (2011) 21, 499-505. 7. Guven K, Gunning P, Fath T. TPM3 and TPM4 gene products segregate to the postsynaptic region of central nervous system synapses. Bioarchitecture. (2011) 1: 284-289. 8. Hook J, Lemckert F, Schevzov G, Fath T, Gunning P. Functional identity of the gamma tropomyosin gene: Implications for embryonic development, reproduction and cell viability. Bioarchitecture. (2011) 1: 49-59. 9. Kopecki Z, O’Neill GM, Arkell R and Cowin AJ. Regulation of focal adhesions by flightless 1 involves inhibition of paxillin phosphorylation via a Rac1-dependent pathway. J. Invest. Dermatol. (2011), 131(7): 1450-1459.
10. Lees JG, Bach CT, Bradbury P, Paul A, Gunning PW, O’Neill GM. The actin-associating protein Tm5NM1 blocks mesenchymal motility without transition to amoeboid motility. Oncogene. (2011)30: 1241-51.
15. Tojkander S, Gateva G, Schevzov G, Hotulainen P, Naumanen P, Martin C, Gunning PW, Lappalainen P. A molecular pathway for myosin II recruitment to stress fibers. Curr Biol. (2011) 21: 539-50.
11. Nakano M, Saldanha R, Gobel A, Kavallaris M, Packer NH. Identification of glycan structure alterations on cell membrane proteins in desoxyepothilone B resistant leukemia cells. Molecular and Cellular Proteomics, 10(11):M111.009001. Epub 22 August 2011.
16. Wolf S, Huynh T, Bryce N, Hambley T, Wakelin LPG, Stewart BW, Catchpoole DR. Intracellular trafficking as a determinant of AS-DACA cytotoxicity in rhabdomyosarcoma cells. BMC Cell Biology (2011) 12:36.
12. Ratheesh A, Gomez GA, Priya R, Verma S, Kovacs EM, Jiang K, Brown NH, Akhmanova A, Stehbens SJ, Yap AS. Centralspindlin and -catenin regulate Rho signalling at the epithelial zonula adherens. Nature Cell Biology (Published on-line, July 1, 2012). 13. Schevzov G, Whittaker SP, Fath T, Lin JJ, Gunning PW. Tropomyosin isoforms and reagents. Bioarchitecture. (2011) 1: 135-164. 14. Shum MS, Pasquier E, Po’uha ST, O’Neill GM, Chaponnier C, Gunning PW, Kavallaris M. γ-Actin regulates cell migration and modulates the ROCK signalling pathway. FASEB J. (2011) 25: 4423-33.
17. Wolf SJ, Wakelin LPG, Catchpoole DR. Considerations for Treatment Development in Rhabdomyosarcoma: In Vitro Assessment of Novel DNA Binding Drugs. In Soft Tissue Tumors, Fethi Derbel (Ed.), ISBN: 978-953-307862-5, InTech Publishers, (2011). 18. Xiang Guo, Qing-Rong Chen, Young K Song, Jun S Wei, Javed Khan. Exon array analysis reveals neuroblastoma tumors have distinct alternative splicing patterns according to stage and MYCN amplification status. BMC Medical Genomics, 4:35, 2011. 19. Zhong J, Baquiran JB, Bonakdar N, Lees J, Ching YW, Pugacheva E, Fabry B and O’Neill GM. NEDD9 stabilizes focal adhesions, increases binding to the extra-cellular matrix and differentially affects 2D versus 3D cell migration. PLoS ONE (2012) 7(4):e35058.
Research Publications to date 20. Alagaratnam S, Hardy JR, Lothe RA, Skotheim RI, Byrne JA. TPD52, a candidate gene from genomic studies, is overexpressed in testicular germ cell tumours. Mol Cell Endocrinol. (2009) 306(1-2):75-80.
24. Bach CTT, Schevzov G, Bryce NS, Gunning PW, O’Neill GM. Tropomyosin isoform modulation of focal adhesion structure and cell migration. Cell Adhesion and Migration. (2010) 4(2):226-34.
21. Al-Oqaily A, Kennedy PJ, Catchpoole DR, Simoff SJ. Comparison of Visualization Methods of Genome-wide SNP Profiles in Childhood Acute Lymphoblastic Leukaemia. In Proc. Seventh Australasian Data Mining Conference (AusDM 2008), Glenelg, South Australia. Conference in Research and Practice in Information Technology, 87. Roddick JF, Li J, Christen P, Kennedy PJ, Eds ACS. 111-121.
25. Bach CTT, Creed S, Zhong J, Mahmassani M, Schevzov G, Stehn J, Cowell LN, Naumanen P, Lappalainen P, Gunning PW, O’Neill GM. Tropomyosin isoform expression regulates the transition of adhesions to determine cell speed and direction. Molecular and Cellular Biology. (2009) 29(6):1506-14.
22. Ashworth SL, Wean SE, Campos SB, Temm-Grove CJ, Southgate EL, Vrhovski B, Gunning P, Weinberger RP, Molitoris BA. Renal ischemia induces tropomyosin dissociationdestabilizing microvilli microfilaments. Am J Physiol Renal Physiol. (2004) 286(5):F988-96. 23. Astuti D, Latif F, Wagner K, Gentle D, Cooper WN, Catchpoole D, Grundy R, FergusonSmith AC, Maher ER. Epigenetic alteration at the DLK1-GTL2 imprinted domain in human neoplasia: analysis of neuroblastoma, phaeochromocytoma and Wilms’ tumour. Br J Cancer. (2005) 92(8):1574-80.
26. Barbaric D, Byth K, Dalla-Pozza L, Byrne JA. Expression of tumor protein D52-like genes in childhood leukemia at diagnosis: clinical and sample considerations. Leuk Res. (2006) 30(11):1355-63. 27. Barbaric D, Dalla-Pozza L, Byrne JA. A reliable method for total RNA extraction from frozen human bone marrow samples taken at diagnosis of acute leukaemia. J Clin Pathol. (2002) 55(11):865-7. 28. Bargon SD, Gunning PW, O’Neill GM. The Cas family docking protein, HEF1, promotes the formation of neurite-like membrane extensions. Biochim Biophys Acta. (2005) 1746(2):143-54.
29. Bilke S, Chen QR, Westerman F, Schwab M, Catchpoole D, Khan J. Inferring a tumor progression model for neuroblastoma from genomic data. J Clin Oncol. (2005) 23(29):7322-31. 30. Bonello TT, Stehn J, Gunning PW. New approaches to targeting the actin cytoskeleton for chemotherapy., Future Medicinal Chemistry (2009) 1311-1331. 31. Boutros R, Byrne JA. D53 (TPD52L1) is a cell cycle-regulated protein maximally expressed at the G2-M transition in breast cancer cells. Exp Cell Res. (2005) 310(1):152-65. 32. Boutros R, Fanayan S, Shehata M, and Byrne JA. The Tumor Protein D52 family: many pieces, many puzzles. BiochemBiophys Res Comm. (2004) 325: 1115-1121.
35. Byrne JA, Balleine RL, Schoenberg Fejzo M, Mercieca J, Chiew YE, Livnat Y, St Heaps L, Peters GB, Byth K, Karlan BY, Slamon DJ, Harnett P, Defazio A. Tumor protein D52 (TPD52) is overexpressed and a gene amplification target in ovarian cancer. Int J Cancer. (2005) 117(6):1049-54. 36. Catchpoole D, Mackie N, McIver S, Chetcuti A, Henwood A, Graf N, Arbuckle S. Tape transfer sectioning of tissue microarrays introduces nonspecific immunohistochemical staining artifacts. Biotech Histochem. (2011) 86(6):421-428. 37. Catchpoole DR, Kennedy P, Skillicorn DB, Simoff S. The curse of dimensionality: a blessing to personalized medicine. J Clin Oncol. (2010) 28(34):e723-4.
33. Boutros R, Bailey AM, Wilson SH, Byrne JA. Alternative splicing as a mechanism for regulating 14-3-3 binding: interactions between hD53 (TPD52L1) and 14-3-3 proteins. J Mol Biol. (2003) 332(3):675-87.
38. Catchpoole D, Guo D, Jiang H, Biesheuvel C. Predicting outcome in childhood acute lymphoblastic leukemia using gene expression profiling: prognostication or protocol selection? Blood. (2008) 111(4):2486-7; author reply 7-8.
34. Bryce NS, Schevzov G, Ferguson V, Percival JM, Lin JJ, Matsumura F, Bamburg JR, Jeffrey PL, Hardeman EC, Gunning P, Weinberger RP. Specification of actin filament function and molecular composition by tropomyosin isoforms. Mol Biol Cell. (2003) 14(3):1002-16.
39. Catchpoole D, Defazio A, Devereux L, Fleming M, Hof M, Schmidt C, Thorne H, Zeps N. The importance of biorepository networks: The Australian Biospecimen Network Oncology. Australian Journal for Medical Science. (2007) 28(1):16-20.
40. Catchpoole D, Lail A, Guo D, Chen QR, Khan J. Gene expression profiles that segregate patients with childhood acute lymphoblastic leukaemia: an independent validation study identifies that endoglin associates with patient outcome. Leuk Res. (2007) 31(12):1741-7. 41. Chang AC, Hook J, Lemckert FA, McDonald MM, Nguyen MA, Hardeman EC, Little DG, Gunning PW, Reddel RR. The murine stanniocalcin 2 gene is a negative regulator of postnatal growth. Endocrinology. (2008) 149(5):2403-10. 42. Chetcuti A, Aktas S, Mackie N, Ulger C, Toruner G, Alkan M, Catchpoole D. Expression profiling reveals MSX1 and EphB2 expression correlates with the invasion capacity of Wilms tumors. Pediatr Blood Cancer. (2011) 57(56):950-957. 43. Corbett MA, Akkari PA, Domazetovska A, Cooper ST, North KN, Laing NG, Gunning PW, Hardeman EC. An alphaTropomyosin mutation alters dimer preference in nemaline myopathy. Ann Neurol. (2005) 57(1):42-49. 44. Creed SJ, Desouza M, Bamburg JR, Gunning P, Stehn J. Tropomyosin isoform 3 promotes the formation of filopodia by regulating the recruitment of actin-binding proteins to actin filaments. Experimental Cell Research (2011) 317:249-261. 45. Creed SJ, Bryce N, Naumanen P, Weinberger R, Lappalainen P, Stehn J, Gunning P. Tropomyosin isoforms define distinct microfilament populations with different drug
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