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Peter Mac Research Report 2007 PETER MACCALLUM CANCER CENTRE PETER MACCALLUM RESEARCH REPORT JANUARY–DECEMBER 2007 JANUARY–DECEMBER www.petermac-research.org PETER MACALLUM CANCER CENTRE RESEARCH REPORT JANUARY–DECEMBER 2007 WWW.PETERMAC-RESEARCH.ORG CONTENTS Director’s REPORT 2 CHIEF EXECUTIVE Officer’s OVERVIEW 4 ORGANISATIONAL STRUCTURE 6 RESEARCH DIVISION PROGRAMS TRANSLATIONAL RESEARCH ETHICAL CONDUCT OF Cancer Immunology Program 8 PROGRAM 66 RESEARCH 121 Translational Research 68 Cancer Cell Death 10 COMMERCIALISATION 124 Cellular Immunity 13 Molecular Imaging 70 CORE TECHNOLOGIES 128 Gene Regulation 16 Centre for Blood Cell Therapies 72 Tissue Bank 130 Immune Signalling 18 Haematology Immunology Translational Research 75 Microscopy 131 Immunotherapy 20 Microarray 132 CLINICAL AND ASSOCIATED Cancer Genomics Program 22 RESEARCH 78 Flow Cytometry 133 VBCRC Cancer Genetics 24 Advanced Cancer Imaging 80 Media and Laboratory Services 134 Cancer Genetics and Genomics 27 Familial Cancer Centre 82 Bioinformatics 135 Surgical Oncology 30 Molecular Pathology 84 Sarcoma Genomics and Genetics 32 EDUCATION AND LEARNING 136 OnTrac@PeterMac 86 kConFab 34 PUBLICATIONS AND PATENTS 146 Nursing and Supportive Care Research 88 kConFab Follow-up Project 36 Infectious Diseases 91 Growth Control and Pharmacy 92 Differentiation Program 38 Psycho-oncology Research Unit 93 Protein Chemistry 40 Growth Control 42 CLINICAL TRIALS AND Molecular Oncology 44 MULTIDISCIPLINARY CARE 94 Haematology 96 Cancer Cell Biology Program 46 Breast 99 Cancer Biology 48 Head and Neck 102 Differentiation and Transcription 51 Lung 104 Cell Growth and Proliferation 54 Gastrointestinal 106 Cell Cycle and Cancer Genetics 56 Sarcoma 108 Epithelial Stem Cell Biology 58 Skin and Melanoma 110 DNA Repair 60 Uro-oncology 112 Molecular Radiation Biology 62 Gynae-oncology 114 Cell Cycle and Development 64 Paediatric and Late Effects 116 Neuro-oncology 117 Centre for Biostatistics and Clinical Trials (BaCT) 118 Clinical Trials Unit 120 DIRECtor’s REPORT CANCER IS A SOFTWARE PROBLEM Just as a computer requires an operating system, so do our cells. However, our cells are controlled not by a binary code of 0s and 1s but by multidimensional information encoded in DNA that regulates cell growth, number and function. In the same way that the software of a computer can be corrupted, so can the code in our cells. Damage to DNA by carcinogens, such as UV light or cigarette smoke, corrupt the cellular code in the individual’s cells, and mutations in the germline lead to inherited errors. Most of the time this damage is inconsequential; however, if a critical gene is hit, then cancer can result in the exposed individual or their children. In essence, then, cancer is a software problem. To make progress in curing cancer, we need to understand the software that controls normal cells and how it goes awry in cancer cells. Peter Mac’s research is geared towards understanding the fundamental processes that control the development and growth of cancer cells. Armed with this information, we seek to develop new therapies and diagnostic and imaging procedures to treat cancer patients more effectively. OUR RESEARCH PROGRAM Peter Mac houses Australia’s largest cancer research group, uniquely integrating a large laboratory complex within a specialist cancer hospital, with over 450 scientists, clinician–researchers, research nurses, support staff, and allied health professionals engaged in research. Fuelled by an annual research budget of over $35m, mostly generated from peer- reviewed national and international research grants, we generally publish about 300 peer-reviewed research papers a year in topics spanning basic, translational and clinical research. In 2007, Peter Mac was ranked third among the 30-plus medical research institutes in Australia for the impact of its publications and was one of the most successful sites for competitive National Health and Medical Research (NHMRC) funding, with the awarding in 2007 of twenty new project grants (≈$9m) and a special collaborative program grant (≈$3m), in addition to collaborating in a further four project grants and one program grant awarded through other institutes (≈$7m). Our research program is underpinned at all levels by a belief in the importance of developing a deep understanding of the processes that control cancer cells and employing this knowledge in the clinic to develop rational, evidence-based protocols that improve cancer outcomes. The close physical location of the laboratories and the clinic makes for a dynamic interplay whereby each informs the research program of the other. Professor David Bowtell Figure 1: The role of polarity proteins in controlling cell fate. Figure 2. Tissue regeneration of early differentiating keratinocytes. This image demonstrates tissue reconstitution six weeks Images of a T cell dividing (grey arrows) while still attached to an antigen-presenting cell (white arrows). Polarisation of the attached T cell after transplantation. means that the two daughter cells inherit different molecules and so go on to adopt different fates. [Source: Dr Pritinder Kaur, Epithelial Stem Cell Biology Laboratory, [Source: Dr Sarah Russell, Immune Signalling Laboratory, pp. 18–19. Reference: Chang et al., (2007) Science 315: 1687–91; publication pp. 58–9. Reference: Gangatirkar et al., (2007) Nature Protocols number 28.] 2(1): 178–86; publication number 93.] HIGHLIGHTS OF 2007 Research 67(23): 11428–11437). The Cancer The concept of personalised medicine continues to Genomics and Genetics, Cell Biology, and Growth be rapidly developed as our understanding grows of The work highlighted below outlines areas of strength Control programs seek to understand the genetic and the molecular changes occurring in human cancers. and achievement throughout 2007. Some of this work biochemical control of normal and cancerous cells. We have an active program in defining the action was conducted solely by Peter Mac researchers, but These programs defined the role of critical genes in of novel anticancer agents (Proc Natl Acad Sci much of it involved external collaboration, where colon cell growth (PNAS, 104(10): 3829–3834), U S A 104(19): 8071–6) and made an important Peter Mac researchers either contributed to work led described the development of novel techniques to contribution to international trials of targeted by others or where they took the lead role themselves. manipulate epithelial cells (Nature Protocols 2(1): therapy in colon cancer (N Engl J Med 357(20): About half of our publications involve authors 178–186, see Fig. 2) and identified how cellular 2040–48), multiple myeloma (New England Journal external to Peter Mac, reflecting our belief in the microenvironment can influence the outgrowth of of Medicine 357(21): 2123–2132), melanoma (Clin importance of collaboration to address major tumour cells (Cell 129(6): 1097–1110; American Cancer Res 13(12): 3630–36; Journal of Clinical questions, quickly and effectively. Journal of Pathology 170(6): 2135–2148 see Fig. Oncology 25(28): 4493–4494) and chronic myeloid The Cancer Immunology program seeks to understand 4). Understanding inherited and somatic change in leukaemia (Clinical Cancer Research 13(23): 7080– how immune cells recognise and kill cancer cells. cancer is critical to defining key driver mutations. 7085), and in defining the role of PET imaging head Important insights were gained during 2007 in Peter Mac researchers contributed to a worldwide and neck cancer (Head and Neck 29(11): 986–995; immune surveillance in the control of cancer (Nature, effort to map new genes associated with breast see Fig. 3). We have a vibrant program in allied 2007, 450 903–7), the role of polarity proteins in cancer risk, leading to some of the most significant health and supportive care research, which seeks controlling cell fate (Science 315(5819): 1687–91; findings in this area in the last decade (Cancer Res to develop evidence-based approaches to patient see Fig. 1) and structural properties of the cytotoxic 67(7): 3027–35; Nature 447(7148): 1087–93; Nat support and survival (European Journal of Cancer granule protein, perforin (Science 317(5844): 1548– Genet 39(3): 352–8). Key insights and technology Care (Engl) 16(5): 417– 423; Journal of Clinical 51). The Cancer Immunology program has a major development also occurred in defining changes in Oncology 25(9): e13–14). focus on enhancing immune responses to cancer DNA copy number for key genes involved in breast cells by increasing their ability to recognise and kill and ovarian cancer (Cancer Res 67(6): 2544 –51; these cells (Nature Biotechnology 25(2): 192–193; Clinical Cancer Research 13(16): 4731– 4739). Cancer Research 67(15): 7495–7504; Cancer Figure 3. Defining the role of PET imaging head and neck cancer. This research investigated the clinical impact and prognostic stratification of F-18 FDG PET/CT in head and neck mucosal squamous cell carcinoma. PET/CT indentified uptake at the previously ‘not suspicious’ neck node (arrow), leading to improved identification of disease state. [Source: Connell CA, et al., (2007) Head and Neck, 29 (11), 986–95. Copyright 2007 Wiley Periodicals, Inc. See pages 102–3, and publication number 40.] 3 Figure 4. The function of laminins (LMs) during This was another year of solid achievement metastatic progression in breast cancer. for research at Peter Mac, with considerable These images show sections of normal (left column) grant success and an emphasis on strategic and malignant (right column) human breast tissue collaborations, as well as on planning for stained with an antibody specific for the human our future. LMα5 subunit (a and b) or a control isotype- matched ID4.5 antibody (c and d). Results We were very pleased when, in mid-September indicated that high tumour cell expression of 2007, the Premier of Victoria, the Hon. John LM-511 is specifically associated with spontaneous Brumby MP, announced that $5 million would breast cancer metastasis, supporting the role of be provided to fund the preparation of a LM-511 in breast cancer progression through business case for the establishment of a world- autocrine mechanisms.
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