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The Kids’ Cancer Project.

Annual ReportFinancial Year2011/2012.

thekidscancerproject.org.au

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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.”

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Contents

Report from the Chief Executive Officer 4

Board of Directors 6

Research Advisory Committee 9

Cancer Gene Therapy Project 11

Drug Discovery Project 12

Tumour Bank 14

Muscle Stem Cell Project 15

Childhood Cancer Cytoskeleton Consortium (C4) 16

- Targeting the cytoskeleton in leukaemia 17

- Tissue organisation and cell-to-cell communication 18

- Regulation of metastasis by the cytoskeleton 19

- Developing new drugs to treat childhood cancers 20

- Modelling childhood brain tumours in the fly 21

- The role of LIMK2 in sensitivity to chemotherapeutic drugs in neuroblastoma 22

- Potential side effects of targeting tropomyosins to treat childhood cancer 23

- Controlling the cytoskeleton in neuroblastoma 24

Financials 26

2011-2012 Research Publications 28

Research Publications to Date 30

Thank you 39

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Report from the Chief Executive Officer

Looking back over the last 18 months since my appointment, I am proud of what we have achieved.

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.

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

survival. We are very hopeful for the success of the trial as similar work overseas in adults has yielded very promising results.

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.

Our overall research strategy is to ensure that Australian children receive the best front-line 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

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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 ‘switches’ 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 Kids’ 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.

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Board of Directors

Colin Reynolds OAM Founder & Chairman

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.

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.

Peter Neilson Chief Executive Officer

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.

Adrian Fisk

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.

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Phillip Belford

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.

Philip has extensive experience in the not-for-profit 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 Blakeman

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.

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.

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Caroline Pierce

Caroline has more than two decades’ 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.

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 Moroney OAM

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.

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 Commissioner’s Commendations for Service and has an Honorary Doctorate from Charles Stuart University.

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Supporting the brightest minds from the best research centres.Research Advisory Committee

Our Research Partners

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.

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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.

Cancer Gene Therapy ProjectDr Geoff McCowage (Oncology Unit) Dr Belinda Kramer (Children’s Cancer Research Unit) The Children’s Hospital at Westmead, NSW

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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.

Drug Discovery ProjectProfessor Peter Gunning University of New South Wales, NSW

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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 ‘second-in-class’. 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.

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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 longer-term 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.

Tumour BankDr Daniel Catchpoole The Children’s Hospital at Westmead, NSW

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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.

Muscle Stem Cell ProjectProfessor Edna Hardeman University of New South Wales, NSW

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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 Kids’ 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 peers’ labs sharing resources and skills.

Childhood Cancer Cytoskeleton Consortium (C4)

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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.

Targeting the cytoskeleton in leukaemiaProfessor Maria Kavallaris Children’s Cancer Institute Australia, NSW

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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

Tissue organisation and cell-to-cell communication

cells stop recognising their neighbours, causing them to move away and metastasise. With the support of The Kids’ 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.

Professor Alpha Yap University of Queensland, Qld

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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.

Regulation of metastasis by the cytoskeletonAssociate Professor Geraldine O’Neill The Children’s Hospital at Westmead, NSW

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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

Developing new drugs for the treatment of childhood cancersProfessor Peter Gunning University of New South Wales, NSW

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.

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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.

Modelling childhood brain tumours in the flyAssociate Professor Helena Richardson Peter MacCallum Cancer Centre, Vic

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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.

The role of LIMK2 in sensitivity to chemotherapeutic drugs in neuroblastomaDr Ora Bernard St Vincent’s Institute, Vic

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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 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.

Potential side effects of targeting tropomyosins to treat childhood cancer

Professor Hardeman’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.

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.

Professor Edna Hardeman University of New South Wales, NSW

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The degree of metastasis is part of the process of neuroblastoma staging. The greater the metastasis, the more progressed a child’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.

Controlling the cytoskeleton in neuroblastoma

Professor Gregory Goodall Centre for Cancer Biology, SA

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Financials

2012 2011

Current assets 2,822,203 3,153,942

Non current assets 205,977 97,261

Total assets 3,028,180 3,251,203

Current liabilites 1,887,659 2,204,960

Non current liabilites 20,990 2,595

Total liabilities 1,908,649 2,207,555

Net assets 1,119,531 1,043,648

Accumulated funds 1,119,531 1,043,648

2012 2011

Fundraising income 11,846,738 10,797,486

Other income 241,146 149,351

Total income 12,087,884 10,946,837

Fundraising expenses 6,966,676 6,691,065

Research expenses 2,775,634 2,445,000

Other expenses 2,269,691 1,827,452

Total expenses 12,012,001 10,963,517

Surplus / (deficit) for the year 75,883 (16,680)

Balance Sheet as at 30 June 2012

Profit & Loss Statement for the year ended 30 June 2012

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Research / Charitable Performance Expenditure

Donation per $ into Research

Benevolent Activities 620,539

Research 3,264,389

Awareness Raising 935,705

4,820,633

Raffles - $0.23Merchandise - $0.69Donations - $0.82

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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.

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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.

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.

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. -Actin regulates cell migration and modulates the ROCK signalling pathway. FASEB J. (2011) 25: 4423-33.

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.

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.

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: 978-953-307-862-5, 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.

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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.

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.

22. Ashworth SL, Wean SE, Campos SB, Temm-Grove CJ, Southgate EL, Vrhovski B, Gunning P, Weinberger RP, Molitoris BA. Renal ischemia induces tropomyosin dissociation-destabilizing 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, Ferguson-Smith 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.

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.

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.

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.

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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.

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.

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.

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.

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.

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.

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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

susceptibility. Eur J Cell Biol. (2008) 87(8-9):709-20.

46. Dalby-Payne JR, O’Loughlin EV, Gunning P. Polarization of specific tropomyosin isoforms in gastrointestinal epithelial cells and their impact on CFTR at the apical surface. Mol Biol Cell. (2003) 14(11):4365-75.

47. Dallas PB, Gottardo NG, Firth MJ, Beesley AH, Hoffmann K, Terry PA, Freitas JR, Boag JM, Cummings AJ, Kees UR. Gene expression levels assessed by oligonucleotide microarray analysis and quantitative real-time RT-PCR -- how well do they correlate? BMC Genomics. (2005) 6:59.

48. Domazetovska A, Ilkovski B, Cooper ST, Ghoddusi M, Hardeman EC, Minamide LS, Gunning PW, Bamburg JR, North KN. Mechanisms underlying intranuclear rod formation. Brain. (2007) 130(Pt 12):3275-3284.

49. Dunwell T, Hesson L, Rauch TA, Wang L, Clark RE, Dallol A, Gentle D, Catchpoole D, Maher ER, Pfeifer GP, Latif F. A genome-wide screen identifies frequently methylated genes in haematological and epithelial cancers. Mol Cancer. (2010) 9:44.

50. Dunwell TL, Dickinson RE, Stankovic T, Dallol A, Weston V, Austen B, Catchpoole D, Maher ER, Latif F. Frequent epigenetic inactivation of the SLIT2 gene in chronic and acute lymphocytic leukemia. Epigenetics. (2009) 4(4):265-269.

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51. Dunwell TL, Hesson LB, Pavlova T, Zabarovska V, Kashuba V, Catchpoole D, Chiaramonte R, Brini AT, Griffiths M, Maher ER, Zabarovsky E, Latif F. Epigenetic analysis of childhood acute lymphoblastic leukemia. Epigenetics. (2009) 4(3):185-193.

52. Fanayan S, Shehata M, Agterof AP, McGuckin MA, Alonso MA, Byrne JA. Mucin 1 (MUC1) is a novel partner for MAL2 in breast carcinoma cells. BMC Cell Biol. (2009) 10:7.

53. Ghous H, Ho N, Catchpoole DR, Kennedy PJ. Comparing functional visualizations of genes. ECML-PKDD. 5th Workshop on Data Mining in Functional Genomics and Proteomics: Current Trends and Future Directions, Athens Greece. (2011).

54. Ghous H, Kennedy PJ, Catchpoole DR, Simoff SJ. Kernel-based Visualisation of Genes with the Gene Ontology. 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. 133-140.

55. Ginn SL, Liao SH, Dane AP, Hu M, Hyman J, Finnie JW, Zheng M, Cavazzana-Calvo M, Alexander SI, Thrasher AJ, Alexander IE. Lymphomagenesis in SCID-X1 mice following lentivirus-mediated phenotype correction independent of insertional mutagenesis and gammac overexpression. Mol Ther. (2010) 18(5):965-76

56. Gomes L, Mackie N, Catchpoole D, Henwood T. Teach and Teach - In a fix about immunohistochemistry on 60 year old tissue blocks? Journal of Histotechnology. (2008) 31:183-4.

57. Gunning P. Emerging issues for tropomyosin structure, regulation, function and pathology. Adv Exp Med Biol. (2008) 644:293-8.

58. Gunning P. Introduction and historical perspective. Adv Exp Med Biol. (2008) 644:1-5.

59. Gunning P, O’Neill G, Hardeman E. Tropomyosin-based regulation of the actin cytoskeleton in time and space. Physiol Rev. (2008) 88(1):1-35.

60. Gunning PW, Schevzov G, Kee AJ, Hardeman EC. Tropomyosin isoforms: divining rods for actin cytoskeleton function. Trends Cell Biol. (2005) 15(6):333-41.

61. Henson JD, Hannay JA, McCarthy SW, Royds JA, Yeager TR, Robinson RA, Wharton SB, Jellinek DA, Arbuckle SM, Yoo J, Robinson BG, Learoyd DL, Stalley PD, Bonar SF, Yu D, Pollock RE, Reddel RR. A robust assay for alternative lengthening of telomeres in tumors shows the significance of alternative lengthening of telomeres in sarcomas and astrocytomas. Clin Cancer Res. (2005) 11(1):217-25.

62. Hesson LB, Dunwell TL, Cooper WN, Catchpoole D, Brini AT, Chiaramonte R, Griffiths M, Chalmers AD, Maher ER, Latif F. The novel RASSF6 and RASSF10 candidate tumour suppressor genes are frequently epigenetically inactivated in childhood leukaemias. Mol Cancer. (2009) 8:42.

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63. Hill VK, Dunwell TL, Catchpoole D, Krex D, Brini AT, Griffiths M, Craddock C, Maher ER, Latif F. Frequent epigenetic inactivation of KIBRA, an upstream member of the Salvador/Warts/Hippo (SWH) tumor suppressor network, is associated with specific genetic event in B-cell acute lymphocytic leukemia. Epigenetics. (2011) 6(3):326-32.

64. Hook J, Lemckert F, Schevzov G, Fath T, Gunning P. Functional identity of the gamma tropomyosin gene. BioArchitecture (2011) 1:1-11.

65. Hughes JA, Cooke-Yarborough CM, Chadwick NC, Schevzov G, Arbuckle SM, Gunning P, Weinberger RP. High-molecular-weight tropomyosins localize to the contractile rings of dividing CNS cells but are absent from malignant pediatric and adult CNS tumors. Glia. (2003) 42(1):25-35.

66. Kadupitige SR, Leung KC, Sellmeier J, Sivieng J, Catchpoole DR, Bain ME, Gaeta BA. MINER: exploratory analysis of gene interaction networks by machine learning from expression data. BMC Genomics. (2009) 10 Suppl 3:S17.

67. Kennedy PJ, Simoff SJ, Catchpoole DR, Skillicorn DB, Ubaudi F, Al Oqaily A. Integrative visual data mining to biomedical data: Investigating cases in Chronic Fatigue Syndrome and Acute Lymphoblastic Leukaemia. (Eds: Simoff SJ, Böhlen M, Mazeika A), in Lecture Notes in Computer Science, Volume 4404, Visual Data Mining: Theory, Techniques and Tools for Visual Analytics. 367-388, Springer, Heidelberg, (2008).

68. Kennedy PJ, Simoff SJ, Catchpoole DR, Ubaudi F, Al-Oquaily A, Yildiz S, Du Y, Skillicorn DB. Does CFS have a biological basis? – A constructionist approach. Critical Assessment of Microarray Data Analysis, Duke University, North Carolina, USA, (2006).

69. Kennedy PJ, Simoff SJ, Skillicorn D, Catchpoole DR. Extracting and explaining biological knowledge in microarray data. In Lecture Notes in Artificial Intelligence, Volume 3056 Advances in Knowledge Discovery and Data Mining: 8th Pacific-Asia Conference, PAKDD 2004.Proceedings.(Eds: Dai, Srikant, Zhang), 699-703, Springer (2004), (ISBN 3-540-22064-X).

70. Kramer BA, Lemckert FA, Alexander IE, Gunning PW, McCowage GB. Characterisation of a P140K mutant O6-methylguanine-DNA-methyltransferase (MGMT)-expressing transgenic mouse line with drug-selectable bone marrow. J Gene Med. (2006) 8(9):1071-85.

71. Lee AS, Kahatapitiya P, Kramer B, Joya JE, Hook J, Liu R, Schevzov G, Alexander IE, McCowage G, Montarras D, Gunning PW, Hardeman EC. Methylguanine DNA methyltransferase-mediated drug resistance-based selective enrichment and engraftment of transplanted stem cells in skeletal muscle. Stem Cells. (2009) 27(5):1098-1108.

72. 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(10):1241-51.

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73. Lindblom A, Bhadri V, Soderhall S, Ohrmalm L, Wong M, Norbeck O, Lindau C, Rotzen-Ostlund M, Allander T, Catchpoole D, Dalla-Pozza L, Broliden K, Tolfvenstam T. Respiratory viruses, a common microbiological finding in neutropenic children with fever. J Clin Virol. (2010) 47(3):234-7.

74. Lloyd C, Gunning P. beta- and gamma-actin genes differ in their mechanisms of down-regulation during myogenesis. J Cell Biochem. (2002) 84(2):335-42.

75. MacArthur DG, Seto JT, Chan S, Quinlan KG, Raftery JM, Turner N, Nicholson MD, Kee AJ, Hardeman EC, Gunning PW, Cooney GJ, Head SI, Yang N, North KN. An Actn3 knockout mouse provides mechanistic insights into the association between alpha-actinin-3 deficiency and human athletic performance. Hum Mol Genet. (2008) 17(8):1076-86.

76. MacArthur DG, Seto JT, Raftery JM, Quinlan KG, Huttley GA, Hook JW, Lemckert FA, Kee AJ, Edwards MR, Berman Y, Hardeman EC, Gunning PW, Easteal S, Yang N, North KN. Loss of ACTN3 gene function alters mouse muscle metabolism and shows evidence of positive selection in humans. Nat Genet. (2007) 39(10):1261-5.

77. Margetts CD, Morris M, Astuti D, Gentle DC, Cascon A, McRonald FE, Catchpoole D, Robledo M, Neumann HP, Latif F, Maher ER. Evaluation of a functional epigenetic approach to identify promoter region methylation in phaeochromocytoma and neuroblastoma. Endocr Relat Cancer. (2008) 15(3):777-86.

78. Margetts CD, Astuti D, Gentle DC, Cooper WN, Cascon A, Catchpoole D, Robledo M, Neumann HP, Latif F, Maher ER. Epigenetic analysis of HIC1, CASP8, FLIP, TSP1, DCR1, DCR2, DR4, DR5, KvDMR1, H19 and preferential 11p15.5 maternal-allele loss in von Hippel-Lindau and sporadic phaeochromocytomas. Endocr Relat Cancer. (2005) 12(1):161-72.

79. Martin C, Schevzov G, Gunning P. Alternatively spliced N-terminal exons in tropomyosin isoforms do not act as autonomous targeting signals, J Struct Biol (2010) 170:286-293.

80. Martin C, Gunning P. Isoform sorting of tropomyosins. Adv Exp Med Biol. (2008) 644:187-200.

81. Mitchell SA, Brown KM, Henry MM, Mintz M, Catchpoole D, LaFleur B, Stephan DA. Inter-platform comparability of microarrays in acute lymphoblastic leukemia. BMC Genomics. (2004) 5:71.

82. Natrajan R, Little SE, Sodha N, Reis-Filho JS, Mackay A, Fenwick K, Ashworth A, Perlman EJ, Dome JS, Grundy PE, Pritchard-Jones K, Jones C. Analysis by array CGH of genomic changes associated with the progression or relapse of Wilms’ tumour. J Pathol. (2007) 211(1):52-9.

83. Natrajan R, Little SE, Reis-Filho JS, Hing L, Messahel B, Grundy PE, Dome JS, Schneider T, Vujanic GM, Pritchard-Jones K, Jones C. Amplification and overexpression of CACNA1E correlates with relapse in favorable histology Wilms’ tumors. Clin Cancer Res. (2006) 12(24):7284-93.

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84. Natrajan R, Reis-Filho JS, Little SE, Messahel B, Brundler MA, Dome JS, Grundy PE, Vujanic GM, Pritchard-Jones K, Jones C. Blastemal expression of type I insulin-like growth factor receptor in Wilms’ tumors is driven by increased copy number and correlates with relapse. Cancer Res. (2006) 66(23):11148-55.

85. Natrajan R, Williams RD, Hing SN, Mackay A, Reis-Filho JS, Fenwick K, Iravani M, Valgeirsson H, Grigoriadis A, Langford CF, Dovey O, Gregory SG, Weber BL, Ashworth A, Grundy PE, Pritchard-Jones K, Jones C. Array CGH profiling of favourable histology Wilms tumours reveals novel gains and losses associated with relapse. J Pathol. (2006) 210(1):49-58.

86. Nguyen QV, Simoff S, Catchpoole DR. Interactive visualization with user perspective for biological data analysis. Health Informatics Society of Australia. (2011) 168:125-132.

87. O’Neill GM, Zhong J, Paul A, Kellie SJ. Mesenchymal migration as a therapeutic target in glioblastoma. Journal of Oncology. (2010).

88. O’Neill GM, Stehn J, Gunning PW. Tropomyosins as interpreters of the signalling environment to regulate the local cytoskeleton. Seminars in Cancer Biology. (2008) 18(1):35-44.

89. O’Sullivan M, Stone G, Catchpoole D, Wood G. Comparison of cDNA and Affymetrix microarray data for paediatric acute lymphoblastic leukaemia. International

Workshop on Statistics Modelling, Bondi, Australia, (2005).

90. Percival JM, Hughes JA, Brown DL, Schevzov G, Heimann K, Vrhovski B, Bryce N, Stow JL, Gunning PW. Targeting of a tropomyosin isoform to short microfilaments associated with the Golgi complex. Mol Biol Cell. (2004) 15(1):268-80.

91. Sarmah CK, Samarasinghe S, Kulasari D, Catchpoole D. A Simple Affymetrix ratio-transformation methods yields comparable expression level quantifications with cDNA data. World Academy of Sciences, Engineering and Technology. (2010) (61):78-83.

92. Sathasivam P, Bailey AM, Crossley M, Byrne JA. The role of the coiled-coil motif in interactions mediated by TPD52. Biochem Biophys Res Commun. (2001) 288(1):56-61.

93. Schevzov G, Fath T, Vrhovski B, Vlahovich N, Rajan S, Hook J, Joya JE, Lemckert F, Puttur F, Lin JJ, Hardeman EC, Wieczorek DF, O’Neill GM, Gunning PW. Divergent regulation of the sarcomere and the cytoskeleton. J Biol Chem. (2008) 283(1):275-83.

94. Schevzov G, O’Neill G. Tropomyosin Gene Expression in Vivo and in Vitro, In Tropomyosin (Gunning, P., Ed.), pp 43-59, Springer New York (2008).

95. Schevzov G, Vrhovski B, Bryce NS, Elmir S, Qiu MR, O’Neill GM, Yang N, Verrills NM, Kavallaris M, Gunning PW. Tissue-specific tropomyosin isoform composition. Journal of Histochemistry and Cytochemistry. (2005) 53(5):557-70.

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96. Schevzov G, Bryce NS, Almonte-Baldonado R, Joya J, Lin JJ, Hardeman E, Weinberger R, Gunning P. Specific features of neuronal size and shape are regulated by tropomyosin isoforms. Mol Biol Cell. (2005) 16(7):3425-37.

97. Shehata M, Bieche I, Boutros R, Weidenhofer J, Fanayan S, Spalding L, Zeps N, Byth K, Bright RK, Lidereau R, Byrne JA. Nonredundant functions for tumor protein D52-like proteins support specific targeting of TPD52. Clin Cancer Res. (2008) 14(16):5050-60.

98. Shehata M, Weidenhofer J, Thamotharampillai K, Hardy JR, and Byrne JA.Tumor protein D52 overexpression and gene amplification in cancer- from a mosaic of microarrays. Crit. Rev. Oncogenesis. (2008) 14: 33-55.

99. Skillicorn DB, Simoff S, Kennedy P, Catchpoole DR. Strategies for winnowing microarray data. Proceedings of the Workshop on Scientific Data Mining at the Society for Industrial and Applied Mathematics Data Mining Conference, (2004).

100. Stallings RL, Nair P, Maris JM, Catchpoole D, McDermott M, O’Meara A, Breatnach F. High-resolution analysis of chromosomal breakpoints and genomic instability identifies PTPRD as a candidate tumor suppressor gene in neuroblastoma. Cancer Res. (2006) 66(7):3673-80.

101. Stehn JR, Schevzov G, O’Neill GM, Gunning PW. Specialisation of the tropomyosin composition of actin filaments provides new potential targets for chemotherapy. Current Cancer Drug Targets. (2006) 6(3):245-56.

102. Tay ES, Guven KL, Subramaniam N, Polly P, Issa LL, Gunning PW, Hardeman EC. Regulation of alternative splicing of Gtf2ird1 and its impact on slow muscle promoter activity. Biochem J. (2003) 374(Pt 2):359-67.

103. Taylor JGt, Cheuk AT, Tsang PS, Chung JY, Song YK, Desai K, Yu Y, Chen QR, Shah K, Youngblood V, Fang J, Kim SY, Yeung C, Helman LJ, Mendoza A, Ngo V, Staudt LM, Wei JS, Khanna C, Catchpoole D, Qualman SJ, Hewitt SM, Merlino G, Chanock SJ, Khan J. Identification of FGFR4-activating mutations in human rhabdomyosarcomas that promote metastasis in xenotransplanted models. J Clin Invest. (2009) 119(11):3395-407.

104. Tojkander S, Gateva G, Schevzov G, Hotulainen P, Naumanen P, Martin C, Gunning P, Lappalainen P. A molecular pathway for myosin II recruitment to stress fibres. Current Biology (2011) 21(7), 539-550.

105. Ubaudi F, Catchpoole DR, Guo D, Simoff SJ, Kennedy PJ. Microarray data mining: selecting trustworthy genes with Gene Feature Ranking. In Data Mining For Business Applications (Eds: Longbing Cao, Philip S. Yu, Chengqi Zhang, Huaifeng Zhang), Springer. (2009) 11:159–168.

106. Verrills NM, Po’uha ST, Liu ML, Liaw TY, Larsen MR, Ivery MT, Marshall GM, Gunning PW, Kavallaris M. Alterations in gamma-actin and tubulin-targeted drug resistance in childhood leukemia. J Natl Cancer Inst. (2006) 98(19):1363-74.

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107. Vlahovich N, Kee A J, Van der Poel C, Kettle E, Hernandez-Deviez D, Lucas C, Lynch G S, Parton RG, Gunning PW, Hardeman EC. Cytoskeletal tropomyosin Tm5NM1 is required for normal excitation-contraction coupling in skeletal muscle, Mol Biol Cell (2009) 20:400-409.

108. Vlahovich N, Schevzov G, Nair-Shaliker V, Ilkovski B, Artap ST, Joya JE, Kee AJ, North KN, Gunning PW, Hardeman EC. Tropomyosin 4 defines novel filaments in skeletal muscle associated with muscle remodelling/regeneration in normal and diseased muscle. Cell Motil Cytoskeleton. (2008) 65(1):73-85.

109. Vrhovski B, McKay K, Schevzov G, Gunning PW, Weinberger RP. Smooth muscle-specific alpha tropomyosin is a marker of fully differentiated smooth muscle in lung. J Histochem Cytochem. (2005) 53(7):875-83.

110. Vrhovski B, Lemckert F, Gunning P. Modification of the tropomyosin isoform composition of actin filaments in the brain by deletion of an alternatively spliced exon. Neuropharmacology. (2004) 47(5):684-93.

111. Vrhovski B, Schevzov G, Dingle S, Lessard JL, Gunning P, Weinberger RP. Tropomyosin isoforms from the gamma gene differing at the C-terminus are spatially and developmentally regulated in the brain. J Neurosci Res. (2003) 72(3):373-83.

112. Weidenhofer J and Byrne JA.Isolation of nucleic acids from hard tissues. In: Handbook of Nucleic Acid Purification. Liu D. (Ed.), Taylor & Francis CRC Press. (2009) pp. 427-448.

113. Whiteford CC, Bilke S, Greer BT, Chen Q, Braunschweig TA, Cenacchi N, Wei JS, Smith MA, Houghton P, Morton C, Reynolds CP, Lock R, Gorlick R, Khanna C, Thiele CJ, Takikita M, Catchpoole D, Hewitt SM, Khan J. Credentialing preclinical pediatric xenograft models using gene expression and tissue microarray analysis. Cancer Res. (2007) 67(1):32-40.

114. Wilson SH, Bailey AM, Nourse CR, Mattei MG, Byrne JA. Identification of MAL2, a novel member of the mal proteolipid family, though interactions with TPD52-like proteins in the yeast two-hybrid system. Genomics. (2001) 76(1-3):81-8.

115. Wolf S, Wakelin LPG, Catchpoole DR. Considerations for Treatment Development in Rhabdomyosarcoma: In Vitro Assessment of Novel DNA Binding Drugs. In “Soft Tissue Tumors”, Intech Publishers (Croatia). (2011) (ISBN 978-953-307-862-5.)

116. Wolf SJ, Wakelin LP, He Z, Stewart BW, Catchpoole DR. In vitro assessment of novel transcription inhibitors and topoisomerase poisons in rhabdomyosarcoma cell lines. Cancer Chemother Pharmacol. (2009) 64(6):1059-69.

117. Xiang H, Schevzov G, Gunning P, Williams HM, Silink M. A comparative study of growth-inhibitory effects of isoflavones and their metabolites on human breast and prostate cancer cell lines. Nutr Cancer. (2002) 42(2):224-32.

118. Zihlif M, Catchpoole DR, Stewart BW, Wakelin LP. Effects of DNA threading bis(9-aminoacridine-4-carboxamides) on global gene expression. Cancer Genomics Proteomics. (2009) 6(6):317-23.

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