Contact
d.dowhan"at"uq.edu.au
Ph. 07 3240 5285

Dr Dennis Dowhan

Biography
Dr Dennis Dowhan began his formal scientific education while studying for his BSc(Hons) degree at Griffith University. Dennis then went on to study retinoid nuclear receptors involved in muscle differentiation with Professor George Muscat at The University of Queensland. After finishing his PhD, Dennis decided to expand his knowledge in the field of hormonal regulation of gene expression by doing his postdoctoral training at one of the Mecca’s of nuclear/steroid receptor research, the Department of Molecular and Cellular Biology, Baylor College of Medicine, in Houston, Texas, USA. He studied the role of nuclear receptor cofactors in gene expression in the laboratory of Professor David D. Moore. Later, Dennis was promoted to Instructor and joined the laboratories of Professor Bert W. O’Malley and Professor Susan M. Berget to study the coupling of steroid hormone receptor mediated transcription and alternative splicing. In late 2004, Dennis returned to Australia to join the Diamantina Institute.

Research Interests
One form of gene regulation is by alternative splicing of nascent RNA to produce proteins with potentially different enzymatic or functional characteristics. There are an increasing number of genes that undergo alternative splicing and are associated with cellular processes that can lead to cancer, including apoptosis, cell cycle regulation, metastasis and angiogenesis. Accordingly, we are interested in testing the hypothesis that (I) multifunctional cofactor proteins play a significant role in gene activation and RNA processing; and (II) these cofactors facilitate important alternative splicing decisions that are involved in the ability of cancer cells to proliferate or differentiate.

Selected Publications
1. Drabsch Y, Hugo H, Zhang R, Dowhan DH, Miao YR, Gewirtz AM, Barry SC, Ramsay RG and Gonda TJ. (2007) “Mechanism of and requirement for estrogen-regulated MYB expression in estrogen-receptor-positive breast cancer cells.” Proc Natl Acad Sci USA. 104(34):13762-13767.
2. Dowhan DH, Hong EP, Auboeuf D, Dennis AP, Wilson MM, Berget SM and O'Malley BW. (2005) “Steroid hormone receptor coactivation and alternative RNA splicing by U2AF65-related proteins CAPERalpha and CAPERbeta.” Molecular Cell. 17(3):429-439.
3. Auboeuf D, Dowhan DH, Kang YK, Larkin K, Lee JW, Berget SM and O'Malley BW. (2004) “Differential recruitment of nuclear receptor coactivators may determine alternative RNA splice site choice in target genes.” Proc Natl Acad Sci USA. 101(8):2270-2274.

Contact
briang“at”uq.edu.au
Ph. 07 3240 7129

Associate Professor Brian Gabrielli

Biography
Associate Professor Gabrielli completed his undergraduate education at James Cook University in Townsville and PhD at La Trobe University in Melbourne. After two postdoctoral positions in the USA in the emerging field of cell cycle regulation, he was recruited to establish his own independent research at the Queensland Institute of Medical Research, and then recruited to the Diamantina Institute in 2002. He is currently an NHMRC Senior Research Fellow.

Research Interests
Mechanisms that regulate cell division, particularly progression into mitosis. These mechanisms are often mutated in cancers and are likely to be major contributors to cancer development. Identifying the genetic mutations that disrupt normal progression and particularly mechanisms, known as checkpoints, provides diagnostic and prognostic opportunities. It also provides potential new targets for chemotherapeutics as drugs targeting defective checkpoints have tumour selective cytotoxic potential.

Selected Publications
1. Gabrielli BG, Roy LM and Maller JL. (1993) “Requirement for Cdk2 in Cytostatic Factor-Mediated Metaphase II Arrest.” Science 259:1766-1769.
2. Gabrielli BG, De Souza CPC, Tonks ID, Clark JM, Hayward NK and Ellem KAO (1996) “Cytoplasmic accumulation of cdc25B phosphatase in mitosis triggers centrosomal microtubule nucleation in HeLa cells.” J. Cell Sci. 109:1081-1093.
3. Pavey S, Conroy S, Russell T and Gabrielli B. (1999) “Ultraviolet radiation induces p16CDKN2A expression in human skin.” Cancer Res. 59:4185-4189.
4. Qui L, Burgess A, Fairlie DP, Parsons PG and Gabrielli BG. (2000) “Histone deacetylase inhibitors trigger a G2 checkpoint in normal cells that is defective in tumour cells.” Mol. Biol. Cell 11:2069-2083.
5. Warrener R, Beamish H, Burgess A, Waterhouse N, Giles N, Fairlie D and Gabrielli B. (2003) “Histone deacetylase inhibitors derive their specific cytotoxicity by targeting cell cycle checkpoints.” FASEB J. 17:1550-1552.

Contact
t.gonda“at”uq.edu.au
Ph. 07 3240 2524

Professor Tom Gonda

Biography
Professor Tom Gonda carried out postdoctoral research from 1979-81 at the University of California, San Francisco in the laboratory of Nobel Laureate Professor J Michael Bishop. This position started Professor Gonda’s continuing interest in leukaemia and the myb oncogene. He returned to Australia in 1982 as a Research Fellow at the Ludwig Institute for Cancer Research, Melbourne, where he expanded his research to include retroviral vectors, cytokines and leukaemia. He returned to Adelaide in 1990 as an NHMRC Research Fellow at the Hanson Centre for Cancer Research. In 2001 he tried his hand at biotechnology as Chief Scientist, Bionomics Ltd, Adelaide, where he directed the company’s research and development programs. In 2003 he returned to academia in his current position at the Diamantina Institute. He has been a member of ARC and NHMRC grant review panels and involved in the organisation of a number of scientific conferences.

Research Interests
Professor Gonda’s major research interest is in identifying and characterising oncogenes involved in major human cancers – particularly leukaemia and breast cancer. His work has a particular focus on the MYB oncogene, which is a key player in normal haemopoiesis and leukaemia. He has also been extensively involved in work on cytokines and their receptors. The other main focus of Professor Gonda’s work has been the development and application of functional gene discovery using retroviral vectors. His work has a long-term goal not only to enhance understanding of cancer but also to apply the results to developing novel cancer therapeutics.

Selected Publications
1. Gonda TJ and Metcalf D. (1984) “Expression of c-myb, c-myc and c-fos during the differentiation of a murine myeloid leukemia.” Nature 310:249-251.
2. Lang RA, Metcalf D, Gough NM, Dunn AR and Gonda TJ. (1985) “Expression of a hemopoietic growth factor cDNA in a factor-dependent cell line results in autonomous growth and tumorigenicity.” Cell 43:531-542.
3. Gonda TJ, Buckmaster C and Ramsay RG. (1989) “Activation of c-myb by carboxy-terminal truncation: relationship to transformation of murine hemopoietic cells in vitro.” EMBO J 8:1777-1783. 
4. Kanei-Ishii C, Macmillan EM, Nomura T, Sarai A, Ramsay, RG, Aimoto, S, Ishii S and Gonda TJ. (1992) “Transactivation and transformation by Myb are negatively regulated by a leucine zipper structure.” Proc. Natl. Acad. Sci. USA 89:3088-3092.
5. Rayner JR and Gonda TJ. (1994) “A simple and efficient procedure for generating stable expression libraries by cDNA cloning in a retroviral vector.” Mol. Cell. Biol. 14:880-887.
6. Jenkins BJ, D'Andrea R and Gonda TJ. (1995) “Activating point mutations in the common beta subunit of the human GM-CSF, IL-3 and IL-5 receptors suggest the involvement of beta subunit dimerisation and cell type-specific molecules in signalling.” EMBO J. 14:4276-4287.
7. McCormack MP and Gonda TJ. (1999) “Myeloproliferative disorder and leukaemia induced in mice by different classes of constitutive mutants of the human IL-3/IL-5/GM-CSF receptor common beta subunit.” Oncogene 18:7190-7199.
8. Brown AL, Peters M, D’Andrea RJ and Gonda TJ. (2004) “Constitutive mutants of the GM-CSF receptor reveal multiple pathways leading to myeloid cell survival, proliferation and granulocyte-macrophage differentiation.” Blood 103:507-16.
9. Drabsch Y, Hugo H, Zhang R, Dowhan D, Miao YR, Gewirtz AM, Barry SC, Ramsay RG, and Gonda TJ (2007). “Mechanism of and Requirement for Estrogen-Regulated MYB Expression in Estrogen Receptor-Positive Breast Cancer Cells.” Proc Natl Acad Sci USA 104:13762-13767.
10. Ramsay RG and Gonda TJ (2008). “MYB function in normal and cancer cells.” Nature Reviews Cancer 8:523-534.

Contact
w.gu"at"uq.edu.au
Ph. 07 3240 5834

Dr Wenyi Gu

Biography
Dr Gu was trained as a vet in XinJiang, China. After three years teaching at the same university in microbiology and immunology, he undertook his Masters in immunology and immuno-pathology in Harbin, China. He migrated to Canberra in 1996 and pursued his PhD study in biochemistry & molecular biology at the Australian National University (ANU). After a short period of work at John Curtin Medical School, he moved to Brisbane in 2001 for his postdoc at The University of Queensland and is currently a senior research officer at the Diamantina Institute.

Research Interests
Research interests include investigating the strategy and mechanism of enhancing immunity to viral or tumour antigens via RNAi. Other interests include studying the roles of viral miRNA of HPV in pathogenesis and tumourigenic and miRNA biological function in cancer or cancer stem cells.

Selected Publications

1.Gu W, Cochrane M, Leggatt G, Payne E, Choyce A, Zhou F, Tindle R and McMillan NA. (2009) "Both treated and untreated tumors are eliminated by short hairpin RNA-based induction of target-specific immune responses." Proc. Natl. Acad. Sci. USA, 106 (20), 8314-9.
2. Gu W, Putral L and McMillan NAJ. (2008) "SiRNA and shRNA as anti-cancer agents in a cervical cancer model." in RNAi: Design and Application, Methods in Molecular Biology 442, Humana Press Inc. p159-172.
3. Gu W, Ding J, Fang N-X, de Kluyver RL, Frazer IH and Zhao K-N. (2007) "Generalised substitution of isoencoding codons shortens the duration of papillomavirus L1 protein expression in transiently gene-transfected keratinocytes due to cell differentiation." Nucleic Acids Research, 35(14):4820-32.
4. Gu W, Li M, Zhao WM, Fang N-X, Bu S, Frazer IH, and Zhao K-N. (2004) " tRNAser (CGA) differentially regulates expression of wild-type and codon modified papillimavirus L1 genes." Nucleic Acids Research, 32 (15), 4448-61.
5. Zhao K-N, Gu W, Fang N-X, Saunders N and Frazer IH. (2005) "Gene codon composition determines differentiation-dependent expression of a viral capsid gene in keratinocytes in vitro and in vivo." Mol.Cell Biol. 25:8643-55.
6. Putral L, Bywater M, Gu W, Saunders N, Leggatt G and McMillan N. (2005) "RNAi against HPV oncogenes results in senescence of cervical cancer cells and increased sensitivity to cisplatin." Mol Pharmcol. 68:1311-9.
7. Gu W, Holland M, Janssens P, Seamark R and Kerr P. (2004) "Immune response in rabbit ovaries to the infection of a recombinant myxoma virus expressing a rabbit zona pellucida protein B." Virology 318(2); 516-523.
8. Gu W, Putral L, Hengst K, Minto K, Saunders N, Leggatt G and McMillan N. (2006) "Lentiviral delivery of short hairpin RNAs against the human papillomvirus type 18 E6 gene inhibits cervical tumour cell growth both in vitro and in vivo." Cancer Gene Therapy, 13:1023-1032.
9. Gu W, Holland M, Janssens P and Kerr P. (2003) "Immune response in the female rabbit reproductive tract to influenza virus HA encoded by a recombinant myxoma virus." Virology 313:285-295.
10. Jonsson J, Gu W, Vanags D, Bishop A, McCaughan G, Fawcett J, Lynch S, Balderson G, Powell E and Clouston A. (2004) "Increased mononuclear cell activation and apoptosis early after human liver transplantation is associated with a reduced frequency of acute rejection." Liver Transplantation, 10:397-403.

Contact
n.mcmillan“at”uq.edu.au
Ph. 07 3240 5392

Associate Professor Nigel McMillan

Biography
Associate Professor McMillan completed his PhD in molecular virology in 1991 at the University of Otago, New Zealand before undertaking postdoctoral studies at the Hospital for Sick Children, Toronto, Canada and the Cleveland Clinic, USA in the laboratory of Dr Bryan Williams. He set up the Molecular Virology Laboratory in 1995. The laboratory studies the role that viruses play in cancer formation and the use of gene silencing technology as a cancer therapy.

Research Interests
The McMillan Lab's interests are centred around the human papillomavirus (HPV) and RNA interference (RNAi). For HPV we are interested in its role in other cancers and have, for example, found HPV on normal skin and in breast and prostate tumours. These findings suggest a potential role for HPV in other cancers and have implications for future therapies, including vaccine-based treatments. The lab also works on RNAi-based therapies for cancers and use cancers caused by HPV as a model system. We want to know how we can deliver RNAi better and make it more potent. Finally, we are interested in the role of RNAi in the activation of the immune response.

Selected Publications
1. Hii SI, Crough T, Payne EJ, Grimmett K, Gill D and McMillan NAJ (2004) “Loss of PKR activity in chronic lymphocytic leukaemia cells.” International Journal of Cancer 109:329-335.
2. Clarke DT, Irving AT, Lambley E, Payne E, and McMillan NAJ (2004) “A Novel Method for Screening Viral Interferon-Resistance Genes.” Journal of Interferon and Cytokine Research 24(8):32-39.
3. Endo-Munoz L,Warby T, Harrich D and McMillan NAJ (2005) “Phosphorylation of HIV Tat by PKR increases interaction with TAR RNA and enhances transcription.” Virology Journal 2:17.
4. Putral LN, Bywater MJ, Gu W, Saunders NA, Gabrielli BG, Leggatt GR and McMillan NAJ. (2005) “RNAi against HPV oncogenes in cervical cancer cells results in increased sensitivity to cisplatin.” Molecular Pharmacology 68(5):1311-9.
5. Harrich D, McMillan NAJ, Munoz L, Apolloni A, Meredith L. (2006) “Will diverse Tat interactions lead to novel antiretroviral drug targets?” Current Drug Targets 7(12):1595-606.
6. Antonsson A, Payne E, Hengst K and McMillan NAJ. (2006) “The human papillomavirus E7 protein binds human Interferon regulatory factors via a novel PEST domain.” Journal of Interferon and Cytokine Research 26(7):455-61.
7. Putral L, Gu W and McMillan NAJ. (2006) “Cancer Therapies based on RNA interference.” Drug News and Perspectives 19(6):317-24.
8. Gu W, Putral L, Saunders N, Legatt G and McMillan NAJ. (2006) “Inhibition of cervical cancer cell growth in vitro and in vivo with lentiviral-vector delivered short hairpin RNA targeting human papillomavirus E6 and E7 oncogenes.” Cancer Gene Therapy 13:1023-1032.
9. Fothergill T and McMillan NAJ. (2006) “Papillomavirus virus-like particles activate the PI3-kinase pathway via alpha-6 beta-4 integrin upon binding.” Virology 352:319-328.
10. Gu W, Putral LN, Irving A and McMillan NAJ. (2007) “Development and Future of oligo-based therapies for Cervical Cancer.” Current Opinion In Molecular Therapeutics 9(2):126-131.

Contact
a.naderi"at"uq.edu.au
Ph. 07 3240 5285

Dr Ali Naderi

Biography
Dr Ali Naderi completed his medical school training in Tehran and his Internal Medicine training in the USA. He carried out his Medical Oncology Fellowship at Mayo Clinic and during this time he developed a research interest in breast cancer. Dr Naderi subsequently moved to Cambridge, UK and completed a postdoctoral research fellowship at Hutchison/MRC Research Centre from 2002 to 2006. He next worked as a Clinician-Scientist with a focus on breast cancer at University of Cambridge until December 2007. Dr Naderi immigrated to Brisbane in December 2007 and currently holds a position as Research Fellow and Medical Oncologist at the Diamantina Institute and Princess Alexandra Hospital with a focus on breast cancer. Dr Naderi has certifications from the American Boards of Internal Medicine and Medical Oncology as well as a specialist qualification in medical oncology (CCST) by the Medical Royal Colleges, UK. He also holds the Fellowship of American College of Physicians.

Research Interests
Dr Naderi’s research is focused in identification of novel molecular markers and therapeutic targets in breast cancer. As a clinician-scientist and breast cancer oncologist, he is interested in translating his laboratory findings to patient care. This involves establishing early-phase clinical trials to test novel findings in the management of breast cancer patients.

Selected Publications
1. Naderi A and Hughes-Davies L. (2009) "Nerve Growth Factor/Nuclear Factor-кB pathway as a therapeutic target in Breast Cancer." Journal of Cancer Research and Clinical Oncology 135 (2):211-6.
2. Naderi A and Hughes-Davies L. (2008) “A Functionally Significant Cross-Talk between Androgen Receptor and ErbB2 pathways in Estrogen Receptor negative Breast Cancer.” Neoplasia 10(6):542-548.
3. Cariati M, Naderi A, Brown JP, et al. (2008) “Alpha-6 integrin is necessary for the tumourigenicity of a stem cell-like sub-population within the MCF7 breast cancer cell line.” International Journal of Cancer 122(2):298-304.
4. Naderi A, Teschendorff AE, Biegel J, et al. (2007) “BEX2 is overexpressed in a subset of primary breast cancers and mediates Nerve Growth Factor /Nuclear Factor-κB inhibition of apoptosis in breast cancer cell lines.” Cancer Research 67(14):6725-36.
5.Naderi A, Teschendorff AE, Barbosa-Morais NL, et al. (2007) “A gene-signature to predict survival in breast cancer across independent data sets.” Oncogene 26(10):1507-16.
6. Chin SF, Wang Y, Thorne N, Teschendorff A, Pinder S, Vias M, Naderi A, et al. (2007) “Using array-comparative genomic hybridizations to define molecular portraits of primary breast cancers.” Oncogene 26(13):1959-70.
7. Teschendorff AE, Naderi A, Barbosa-Morais NL, et al.(2006) “A consensus prognostic gene expression classifier for ER positive breast cancer.” Genome Biology 7(10):R101.
8. Teschendorff AE, Naderi A, et al. (2006) “PACK: Profile Analysis using Clustering and Kurtosis to find molecular classifiers in cancer.” Bioinformatics 22(18):2269-75.
9. Naderi A, Ahmed AA, Wang Y., et al. (2005) “Optimal amounts of fluorescent dye improve expression microarray results in tumor specimens.” Molecular Biotechnology 30(2):151-154.
10. Naderi A, Ahmed AA, Barbosa-Morais NL, et al. (2004) “Expression microarray reproducibility is improved by optimizing purification steps in RNA amplification and labelling.” BMC Genomics 5(1):9.

Contact
nsaunders"at"uq.edu.au

Associate Professor Nicholas Saunders

Biography
Associate Professor Nicholas Saunders trained as a pharmacologist at the University of Western Australia under the supervision of Professor Rodney Minchin and Professor Ken Illett. Dr Saunders was then awarded a Fogarty Visiting Fellowship to pursue postdoctoral studies at the National Institute of Environmental Health Sciences in the USA under the supervision of Professor Anton Jetten. In 1993, Dr Saunders was approached by Professor Ian Frazer to return to Australia and set up the Epithelial Pathobiology Group. Since establishing his research group, Dr Saunders has attracted more than $10 million in competitive research funding and has been the recipient of a Lions Medical Research Foundation Senior Research Fellowship and a Garnett Passe and Rodney Williams Memorial Foundation Principal Research Fellowship. Dr Saunders is also Head of the Translational Research Unit at the Princess Alexandra Hospital and is an Adjunct Associate Professor with the School of Biomedical Sciences at The University of Queensland.

Research Interests
The lab's research interests are focused on translating advances in the biological sciences to improved patient outcomes. In particular, we have interest in the molecular basis for the control of squamous differentiation and how it is perturbed during cutaneous or head and neck squamous cell carcinoma formation. To date, our research has included basic molecular biology of squamous differentiation through to the completion of a clinical trial on a new anti-cancer strategy in head and neck cancer patients. More recently we have developed an interest in the molecular basis for the development of lung metastases in patients with the primary bone malignancy, osteosarcoma. We are particularly interested in the molecular basis of lung metastasis and how we may target this therapeutically.

Selected Publications
1. Saunders NA, Dicker AJ, Jones SJ and Dahler AL. (1998) “E2F1 mRNA is destabilised in response to growth inhibitors in normal human keratinocytes but not in a squamous carcinoma cell line.” Cancer Res. 58:1646-1649.
2. Saunders NA, Dicker AJ, Popa C, Jones S J and Dahler AL. (1999) “Histone deacetylase inhibitors as potential anti-skin cancer agents.” Cancer Res. 59:399-404.
3. Dicker AJ, Popa C, Dahler AL, Serewko MM, Hilditch-Maguire PA, Frazer IH and Saunders NA. (2000) “E2F-1 induces proliferation-specific genes and suppresses squamous differentiation-specific genes in human epidermal keratinocytes.” Oncogene, 19:2887-2894.
4. Brinkmann H, Dahler AL, Popa C, Serewko MM, Parsons PG, Gabrielli BG, Burgess AJ and Saunders NA. (2001) “Histone hyperacetylation induced by histone deacetylase inhibitors is not sufficient to cause growth inhibition in human dermal fibroblasts.” J. Biol. Chem. 276:22491-22499.
5. Serewko MM, Popa C, Dahler AL, Smith L, Strutton GM, Coman W, Dicker AJ and Saunders NA. (2002) “Alterations in gene expression and activity during squamous cell carcinoma development.” Cancer Res. 62:3759-3765.
6. Wong CF, Barnes LM, Dahler AL, Smith L, Serewko-Auret MM, Popa C, Jabbar IA and Saunders NA. (2003) “A role for E2F in the modulation of keratinocyte squamous differentiation: implications for the use of an E2F inhibitor in squamous cell carcinoma.” J. Biol. Chem. 278(31):28516-28522.
7. Wong CF, Barnes LM, Dahler AL, Smith L, Popa C, Serewko-Auret MM, and Saunders NA. (2005) “Sp1 is a downstream effector of E2F-mediated suppression of squamous differentiation.” Oncogene, 24:3525-3534.
8. Walshe J, Serewko-Auret MM, Teakle N, Cameron S, Minto K, Smith L, Burcham PC, Russell CT, Strutton G, Griffin A, Chu FF, Esworthy S, Reeve VE and Saunders NA. (2007) “Inactivation of glutathione peroxidise activity contributes to UV-induced squamous cell carcinoma formation.” Cancer Res. 67:4751-4758.
9. Dahler AL, Rickwood D, Guminski A, Teakle N and Saunders NA. (2007) “Indole-3-carbinol – induced growth inhibition can be converted to a cytotoxic response in the presence of TPA + Ca2+ in squamous cell carcinoma cell lines.” FEBS Letters, 581(20):3839-3847.
10. Erlich RB, Rickwood D, Coman W, Saunders NA and Guminski A. “Valproic acid as a therapeutic agent for head and neck squamous.” Cancer Chemotherapy and Pharmacology. In Press.