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As in previous years NDLR 2010 has invited a wealth of talent both from
Australia and Internationally as well. Delegates can look forward to
listening to the best that Australia has to offer as well as the latest
research from our international guests.
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Oregon
Health & Science University Cancer Institute, OR, USA
Michael Deininger is currently an
Associate Professor at the Center for Hematologic Malignancies, Oregon Health
& Science University.
He graduated in 1990 from Wuerzburg University Medical
School (Germany),
and obtained an MD from Wuerzburg University in 1994 (Bone marrow histology in MDS),
followed by a PhD from Imperial College, London,
UK in 2000
entitled "Evaluation of imatinib in preclinical and molecular studies". Dr.
Deininger's clinical training continued in Hematology/Oncology and bone marrow
transplantation at Nuremberg General Hospital, from 1992-1995 and the
Department of Hematology, University of Leipzig, Germany, from 1999-2002. Since
2002 he has been the Scientific Director of the CML basic research program in
the laboratory of Brian Druker at Oregon
Health & Science University. His awards and professional
achievements include: Scholar of the
Mildred Scheel Foundation for Cancer Research (1995-1997), Scholar of the
American Society of Hematology (2004), Member of the East German Study Group Hematology/Oncology
(OSHO) (1999), Chronic Leukemia Working Party (CLWP) of the European Blood and
Marrow Transplantation Group (EBMT) (2000), American Society of Hematology
(ASH) (2000). He is also a peer reviewer
for Blood, Nature Genetics, The Lancet, Cancer Research and other journals.
Signal transduction in BCR-ABL-positive cells, resistance to
BCR-ABL-targeted therapy and novel ABL kinase inhibitors in CML, as well as
targeted therapy for other tyrosine kinase-driven malignancies, including acute
myeloid leukemia, pathogenesis of BCR-ABL-negative myeloproliferative diseases.
For further information on Michael please visit the following site:-
Oregan Health & Science University
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Dr.
Gary Gilliland joined Merck in March, 2009 and leads the implementation of Merck's
oncology research strategy. He's a member of MRL's Research Management
Committee and is responsible for the alignment of the Oncology research
franchise with Merck's Global Human Health organization.
Dr.
Gilliland comes to Merck after nearly 20 years on the faculty at Harvard, where
he served as Professor of Medicine at Harvard
Medical School,
and Professor of Stem Cell and Regenerative Biology at Harvard University.
He was also an Investigator of the Howard Hughes Medical Institute, Director of
the Leukemia Program at the Dana-Farber/Harvard Cancer Center, and Director of
the Cancer Stem Cell Program of the Harvard Stem Cell Institute.
An
oncology investigator, Dr. Gilliland made seminal discoveries that have
identified the genetic basis of leukemia and other cancers that affect the
blood and bone marrow. He has spearheaded the application of these findings
into the development of new investigational cancer treatments, including
molecularly targeted therapies, and has advanced this research into all phases
of clinical development.
His
work has earned him numerous honors including the William Dameshek Prize from
the American Society of Hematology, the Emil J. Freireich Award from the MD
Anderson Cancer Center, and the Stanley J. Korsmeyer Award from the American
Society for Clinical Investigation.
Dr.
Gilliland received his Ph.D. in Microbiology from the University
of California, Los
Angeles, and his M.D. from the University
of California, San Francisco. He completed his internship
and residency, including serving as Chief Medical Resident, at Brigham and
Women's Hospital, Harvard
Medical School.
He completed his Hematology and Medical Oncology training at the Brigham and
Women's Hospital and the Dana-Farber Cancer Institute, respectively.
Dr.
Gilliland is an elected member of the American Society for Clinical
Investigation and the Association of American Physicians.
For further information on Gary please visit the following sites;
Howard Hughes Medical Institute
Harvard University
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University of Cambridge, Cambridge, UK.
Tony
Green is Head of the University of Cambridge Department of Haematology and
Chairman of Addenbrooke's NHS Trust Department of Haematology.
He
trained in medicine at the University of Cambridge (1974-77) and University College
Hospital London
(1977-80) subsequently completing his haematology training at the Royal Free Hospital and the University Hospital of Wales, Cardiff. His scientific training in molecular biology
and haematopoiesis was gained at the Imperial Cancer Research Fund, London (1984-87) and the Walter and Eliza Hall Institute, Melbourne (1989-91), the
latter as a Hamilton-Fairley Travelling Fellow.
He moved to Cambridge
in 1991 as a Welcome Trust Senior Fellow and was elected to the Chair of
Haemato-Oncology there in 1999.
His
research interests focus on two aspects of haematopoietic stem cell biology:
the molecular pathogenesis of myeloid malignancies (Leukaemia Research Fund
programme) and the transcriptional regulation of haematopoietic stem cells
(Welcome Trust programme). Clinical
research activities are mainly in the area of the myeloproliferative disorders.
For further information on Tony please visit the following site;
University of Cambridge
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The research carried out in our laboratory focuses on the molecular mechanisms
and the genetics underlying the pathogenesis of human cancer as well as in
modeling cancer in vivo in model systems such as the mouse. Throughout the years
we have identified and functionally characterized major novel proto-oncogenes
and tumor suppressors (e.g. PTEN, p53, PML and POKEMON). The elucidation of the
molecular basis underlying tumor initiation, progression and metastasis has led
to the development of novel and effective therapeutic concepts that are
currently been utilized and tested in clinical trials.
For more information about Pier, please visit this website:-
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Charles Mullighan is Assistant Member in
the Department of Pathology of St Jude Children's Research Hospital, Memphis,
Tennessee. He trained in medicine at the University of Adelaide (1987-1992),
and did doctoral studies in the immunogenetics of transplantation and complex
diseases in the Transplantation Immunology Laboratory of the Nuffield
Department of Surgery, University of Oxford (1994-1997). He returned to
Adelaide to train in internal medicine (1998-2000), hematology and
hematopathology (2000-2004). He joined Jim Downing's laboratory at St Jude in
2004 as an NH&MRC CJ Martin Fellow to study the genomics of acute leukemia.
He joined the faculty of St Jude in 2008.
He has received American Society of
Hematology Scholar, Merit and Joanne Levy Outstanding Achievement Awards, and
was named a Pew Scholar in the Biomedical Sciences in 2009.
His research interests include the genomic
interrogation of cancer genomes to identify genetic and epigenetic alterations
contributing to leukemogenesis and treatment responsiveness, and the
experimental modeling of genetic alterations. These approaches include
microarray analysis of structural genetic alterations, transcriptional
profiling and methylation, and second generation sequencing approaches. His
work has led to a number of key findings that have transformed our
understanding of the genetic basis of acute lymphoblastic leukemia, chronic
myeloid leukemia, and related disorders.
For further information about Dr
Mullighan's research, please visit
For more information about Charles, please visit St Jude's Children's Research Hospital
and St Jude Children's Hospital Research @ st.jude
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The Rajewsky Lab uses computational and experimental methods to
dissect, systems-wide, function and evolution of gene regulation in
metazoans. One major focus is to understand more about gene regulation
by small RNAs, in particular microRNAs. To probe general mechanisms in
gene regulation of microRNAs, the lab works with cell lines. We are
also investigating the function of small RNAs during very early
development of C. elegans. Furthermore, the lab has
established planaria as a model system within the lab. These freshwater
flatworms are famous for their almost unlimited ability to regenerate
any tissue via pluripotent, adult stem cells. The lab is studying the
role of small RNAs in planarian regeneration.
For further information on Nikolaus please visit the following site:-
Max Delbruck for Molecular Medicine (MDC) Berlin-Buch
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Our research involves identifying
novel targets involved in the pathophysiology of acute leukemia and
myelodysplastic syndrome. Inhibition of the FLT3 tyrosine kinase, for example,
may offer benefits in AML patients - especially those whose blasts have an
activating mutation in the enzyme - similar to the success of imatinib in the
treatment of patients with chronic myeloid leukemia (CML). After conducting
several trials with FLT3 inhibitors as single agents in myeloid malignancies,
we are now focusing on combining these drugs with chemotherapeutic agents. Our
laboratory continues to explore the mechanism of leukemic transformation via
mutated FLT3, especially regarding activation of downstream pathways such as
protein kinase A or AKT, which may be involved in key aspects of leukemogenesis
such as prevention of apoptosis and promotion of self-renewal.
Other areas of clinical research include targeted therapy in T cell ALL, based
on inhibition of NOTCH activation, a common survival mechanism in such cells;
application of intensive "pediatric-type" strategies in adults with
ALL; novel abl inhibitors in imatinib-resistant CML; clinical-translational
research with gefitnib in AML; and antiangiogenic therapy in MDS.
For more information on Richard, please visit this website:-
Dana-Farber / Harvard Cancer Center
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Harvard Medical School,
Boston, MA, USA
National University of Singapore
Dr.
Tenen's laboratory focuses on transcription factors and gene regulation, and
their relationship to differentiation. The laboratory has characterized
transcription factors which play a role in the differentiation of hematopoietic
stem cells into different specific lineages, with particular focus on myeloid
(granulocyte and monocyte) differentiation in normal and leukemic cells.
Current efforts in the laboratory focus on understanding regulation, signal
transduction pathways, and interacting partners of PU.1 and C/EBP alpha, and
their role in stem cells. We have now identified mutations and specific
abnormalities in expression and function of C/EBP alpha and PU.1 in specific
subtypes of myeloid leukemias, and a major effort in our laboratory is now
focused on further characterization of the role of C/EBP alpha and PU.1 in
leukemogenesis, as well as developing drugs and other therapies specifically
aimed at C/EBP alpha and PU.1.
Other projects directed at leukemogenic
mechanisms include models of murine leukemia using inducible expression of
translocation fusion proteins, such as the Bcr-Abl protein. Our long term goals
are to understand the abnormalities seen in acute myelogenous leukemia (AML),
in which differentiation of myeloid blasts is blocked, and to use these myeloid
promoters as tools to drive lineage and stage specific expression of
heterologous genes in recipient ES cells and transgenic mice, as a step toward
gene therapy applications.
For more information about Daniel, please visit this site:-
Harvard Stem Cell Institute
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Our laboratory studies
transformation and leukemogenesis by tyrosine kinases, with a particular focus
on the ABL family.
Bcr-Abl is the product of the t(9;22) Philadelphia chromosome translocation and is
found in patients with chronic myeloid leukemia (CML) as well as acute
B-lymphoblastic leukemia. A central tool in our approach to understanding the
molecular pathogenesis of these leukemias is the ability to express the Bcr-Abl
gene in the bone marrow of laboratory mice, a model system we developed over a
decade ago that is now widely used in the study of leukemia and other blood
cell disorders. Mice that receive a transplant of bone marrow transduced with a
retrovirus expressing Bcr-Abl develop a fatal myeloproliferative syndrome that
closely resembles human CML. We are currently using this system to analyze the
critical signaling pathways necessary for development of leukemia and to test
molecularly targeted drugs directed against these pathways.
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