CSC Rhon Postgrad Book

CENTRE FOR
STEM CELL RESEARCH

Honours, Masters and PhD Projects
POSTGRADUATE RESEARCH OPPORTUNITIES
STUDENT PROJECT BOOKLET FOR 2015
CENTRE FOR STEM CELL RESEARCH HONOURS AND POSTGRADUATE OPPORTUNITIES 2015
Human nerve and glial cells | Wai Khay, PhD student
2
CONTENTS
INTRODUCTION 1
MESSAGE FROM THE DIRECTORS
THE 4 STEPS TO ENROLMENT
ABOUT THE CENTRE
HONOURS PROGRAMS
POSTGRADUATE PROGRAMS
SCHOLARSHIPS 7
PROFESSIONAL DEVELOPMENT
INTERNATIONAL STUDENTS
2015 PROJECTS
NOTES 40
STEM CELL
RESEARCH
OPPORTUNITIES
2015 HONOURS, MASTERS AND PHD STUDENTS
The University of Adelaides Centre for Stem Cell Research is a
collaborative initiative comprising 19 research groups based at various
locations and organisations across Adelaide. The members of the
Centre for Stem Cell Research undertake internationally-recognised
research in bone marrow, neural, periodontal, ovarian and cord
blood stem cells. With applications in areas such as stroke, cardiac
and tissue repair, cystic fibrosis and leukaemia, the Centre is at the
forefront of stem cell research in Australia.
A MESSAGE FROM
THE DIRECTORS
Dear Student,
Welcome to the 2015 Honours and
Postgraduate Opportunities booklet for
the Centre for Stem Cell Research at the
University of Adelaide.
The focus of our Centre is on translating
basic research into clinical and commercial
outcomes via collaboration between our
members and with external partners.
The Centre is committed to conducting world
class research and providing excellent higher
degrees and research training opportunities.
We look forward to meeting you and
discussing the many exciting projects on offer
at the Centre.
A/Prof Mark Nottle & Prof Stan Gronthos

Directors
Centre for Stem Cell Research
2
THE 4 STEPS TO
ENROLMENT
The process to undertake Honours or a higher degree by research with the
Centre for Stem Cell Research is simple:
1
2
3
BROWSE this booklet to determine a group or project

that interests you
REFER to the blue panel on each of the research group

pages for all the necessary details for supervisors and
faculty/school/discipline enrolment contacts
CONTACT a specific supervisor directly to discuss a

place in their group in 2015 or ATTEND the Honours
and Postgraduate Information Day for the Centre for
Stem Cell Research on 15 August 2014 to meet the
supervisors
WHEN the supervisor agrees to take you on as an

Honours or postgraduate student and any other
necessary criteria are fulfilled, CONTACT the Honours
or postgraduate coordinator from the relevant School to
verify eligibility and arrange enrolment
ABOUT THE CENTRE

The Centre for Stem Cell Research was officially launched by the Vice- Chancellor of the University
of Adelaide, Professor James McWha, in September 2008. With a vision of strengthening its
reputation as one of Australias most research-intensive universities, The University of Adelaide laid
the foundation for a South Australian based initiative that could carry out stem cell research with
international impact.
The Centre for Stem Cell Research is made up of 16 primary research groups and 3 affiliate groups.
Groups are based at various locations across Adelaide, at the University of Adelaide, Womens and
Childrens Hospital, Institute of Medical and Veterinary Sciences, the Royal Adelaide Hospital, the
Queen Elizabeth Hospital, the Hanson Institute and the South Australian Research and Development
Institute. The research programs focus on the potential applications of bone marrow, neural,
periodontal, ovarian and cord blood stem cells. Areas of application include stroke repair, cardiac
repair, tissue repair (dental, muscle, cartilage), cystic fibrosis, lysosomal storage and other inherited
disorders, transplantation medicine, developmental biology, immune diseases and leukaemia.
A/Prof Simon Koblar with Peter Couche of the Peter Couche Foundation
4
HONOURS
The Honours program at the Centre for Stem Cell Research equips participants with
tangible experience in analytical thinking, written and verbal communication and
working as a team member. These qualifications are highly sought by employers in
all fields. Honours at the Centre for Stem Cell Research leads to the awards of BSc
(Hons), BMedSci (Hons), BHSc (Hons) or BDS (Hons).
Lauren Sandeman,
Honours student, 2010
What are the entry requirements?
What is involved in Honours?
Assessment
The Centre does not have subject

prerequisites for entry into Honours. In
past years, students with backgrounds
in Physiology, Biochemistry,
Microbiology and Immunology, Health
Sciences, Genetics, Animal Sciences,
Anatomy, Pharmacology, Psychology,
Public Health, Medicine, Nutrition and
others have been successful in the
Honours program.
The Honours program varies depending

on the faculty & school. Largely, it
consists of one academic year of
original research and structured
training, primarily in an interactive
relationship with one or two specific
supervisors (which may be from one
or more groups). This culminates
in the candidates preparation and
presentation of a thesis outlining the
research project. The thesis is marked
by two examiners with specific expertise
in the research area and a general
examiner from the Centre.
Assessment of the Honours year will

vary between faculties and schools. The
following is an example assessment
schedule from the School of Paediatrics
and Reproductive Health:
Some Honours programs also include

participation in a series of tutorials on
contemporary knowledge of physiology,
methodology and philosophy in areas
of research. Student knowledge of
these principles is assessed by written
examination.
How to apply?
A critical assessment of relevant

literature and research plan is usually
submitted at the end of May.
If the supervisor agrees to take you

on as an Honours student and your
academic record is acceptable to the
Centre and corresponding School, you
will be invited to enrol in the program.
Students from any University who have

completed a Bachelor of Science,
Health Science, Biomedical Science,
Arts or Agricultural Science degrees, or
three years of the MBBS and BDS (or
others as negotiated) are eligible for the
course.
In general, students should have an
aggregate credit level or higher in third
year subjects, particularly in those
subjects relevant to the proposed
research area. However, students who
have not achieved this level but are
highly motivated to become involved in
research are encouraged to discuss this
with their proposed supervisor.
Throughout the year candidates are

likely to present at up to three seminars,
following a form similar to the following:
Critical literature review: 15%

Tutorial contribution: 5%
Written Examination: 15%
Thesis: 50%
Final Seminar: 15%
Total: 100%
If you have decided that you would

like to undertake Honours in 2014 you
should firstly identify a project or project
area in this booklet that interests you,
then arrange to meet with the supervisor
to discuss the details of the project.
1. Introduction/research proposal
2. Progress seminar
3. Final seminar, after thesis submission
MASTERS | PHD
Entry requirements for Masters & PhD Programs
In order to gain admission to most postgraduate research programs in the University
of Adelaide, it is necessary to have qualified for a four-year Australian university
Honours degree (first or second class, division A Honours) or the equivalent from
an approved overseas university. Some faculties may require students to enrol as a
candidate for a Masters degree in the first instance, with the possibility of upgrading
to a PhD at a later date if progress is deemed to be satisfactory.
Jared Campbell
PhD student,
The Masters Program
The PhD Program
How to apply?
A Masters degree involves one to

two years of research for a full-time
candidate and is similar in nature to a
PhD, but does not necessarily require
candidates to make a significant original
contribution to research. Examiners
of a Masters degree will be seeking
evidence that the candidate has:
A PhD is the basic qualification for a

research career or academic position.
It involves two to four years of research
for a full-time candidate. Candidates
develop the capacity to conduct
research independently, that is original
and of high quality and makes a
significant contribution to knowledge in
their chosen discipline.
The decision to undertake Masters

or a PhD should involve interest
in a proposed project or area and
then considerable discussion with a
proposed supervisor.
a thorough understanding of
the relevant techniques and
methodologies in the field as
demonstrated by a thorough critical
review of the literature
demonstrated competence in the
chosen field through judicious
selection and application of
appropriate methodology to yield
meaningful results
A PhD thesis may comprise a

conventional written narrative presented
as typescript or other forms such as
publications, text in manuscripts, a
book, or visual work(s). Examiners will
be looking for a candidate to:
produce a clearly, accurately and
cogently written thesis that is suitably
illustrated and documented;
demonstrated the capacity to evaluate

critically these results
demonstrate a deep knowledge of the

research topic;
presented a clear and well-written

thesis.
relate the research topic to the

broader framework of the discipline
within which it falls;
Whilst a number of Masters degrees

include an advanced course work
component, the focus is on research.
demonstrate an independence of
thought and approach; and
make a significant and original
contribution to knowledge by
the discovery of new facts, the
formulation of theories, or the
innovative reinterpretation of known
data and established ideas.
6
If the supervisor agrees to take you

on as postgraduate student and your
academic record is acceptable to the
Centre and corresponding School, you
will be invited to enrol in the program.
To apply for your Masters or PhD
position you must fill out an application
form available from the Adelaide
Graduate Centre website:
www.adelaide.edu.au/graduatecentre/
scholarships/postgrad/pgforms.html
Alternatively, a hard copy of this form
can be obtained from the Centre for
Stem Cell Research:
P: 08 8313 4482
E: stemcell@adelaide.edu.au
W: www.adelaide.edu.au/stemcell
SCHOLARSHIPS
PROFESSIONAL DEVELOPMENT
INTERNATIONAL STUDENTS
Scholarship Information
Postgraduate Scholarships
Information for Future Students
The University offers a range of Honours

and postgraduate scholarships each
year. There are scholarship opportunities
for both local and international students.
Information on scholarships and
application procedures is regularly
updated on the universitys website:
The University of Adelaide scholarships

site provides a list of both full and
supplementary and top-up scholarships
for postgraduate students:
Visit www.adelaide.edu.au/student/future
for information for students looking at
studying at the University of Adelaide.
www.adelaide.edu.au/graduatecentre/
scholarships/postgrad/
International Students
www.adelaide.edu.au/scholarships/
Professional Development
More information on scholarships is also

available from:
There are a number of professional

development opportunities for students
undertaking Honours or postgraduate
research to improve their research skills,
including reviewing literature, working
with statistics and scientific writing.
Student Centre, level 4, Wills Building

P: +61 8 8313 5208
E: student.centre@adelaide.edu.au
Honours Scholarships
Honours scholarships are available from
various Faculties, Schools and Groups
associated with the Centre for Stem
Cell Research as well as from external
sources. A comprehensive list can be
found at the University of Adelaides
Honours scholarships site:
www.adelaide.edu.au/scholarships/
honours/
University of Adelaides Research

Education & Development (RED)
workshops
Information for International Students

who are interested in Honours, PhD
and Masters study at the University of
Adelaide is available on the Universitys
International Students web site:
www.international.adelaide.edu.au
This website also provides relevant
information on application procedures
and forms, visa procedures, University
contacts and overseas representatives
and scholarships.
The candidates school or discipline

may offer opportunities
The Robinson Institute offers a
mentoring program and a number
of professional and scientific skills
building courses
Marketing & Strategic Communications Office - The University of Adelaide
Vascular Biology and Cellular Recruitment Laboratory
8
2015 PROJECTS
CENTRE FOR STEM CELL RESEARCH
10
LIST OF PROJECTS
ACUTE LEUKAEMIA - Prof Richard DAndrea & Dr Ian Lewis
12
Project 1: -catenin activation and target gene identification in Acute Myeloid Leukaemia (AML)
Project 2: Transcriptional regulation of the KLF5 transcription factor
Project 3: Post-translational modification of transcription factors in AML
Project 4: Regulation of Gadd45a in AML
Project 5: Screening for compounds that induce differentiation or cell death of AML cells
Project 6: Molecular characterisation of Polycythemia Vera
NEUROVASCULAR RESEARCH - Dr Quenten Schwarz
15
Project 1: Investigating the molecular control of neural crest stem cell (NCSC) development
Project 2: Identifying the embryonic origin of the childhood cancer Neuroblastoma
Project 3: How does VEGF control development of the Cardiac outflow tract?
Project 4: Investigating the role of 14-3-3 in schizophrenia
GENE THERAPY FOR CYSTIC FIBROSIS - A/Prof David Parsons
16
Project 1: Investigating the differentiating and self proliferating potential of endogenous respiratory stem cells lacking the CFTR protein
Project 2: Increasing the level of therapeutic CFTR transduction in a CF mouse model
Project 3: Effects of LPC airway pre-treatment on airway and lung health
MESENCHYMAL STEM CELLS - Prof Stan Gronthos
17
Project 1: Mesenchymal stem cells in skeletal tissue regeneration

Project 2: The role of MSC in the maintenance and support of haematopoiesis and modulation of immune responses
Project 3: Dental mesenchymal stem cells for tissue regeneration
MOLECULAR IMMUNOLOGY - A/Prof Simon Barry
20
Project 1: Molecular identification of Regulatory T cells

Project 2: Cord Blood Stem cell differentiation in to regulatory T cells
Project 3: Lentiviral vectors for gene delivery and gene ablation
Project 4: Is there a role for FOXP3 in breast cancer?
ANIMAL REPRODUCTION - Prof Paul Verma
23
Project 1: Generation and characterization of pluripotent stem cells from large animals
Project 2: Genome editing of pluripotent livestock stem cells
MYELOMA RESEARCH PROGRAM - Prof Andrew Zannettino
Project 1: Identification of genetic factors which trigger the progression from asymptomatic MGUS to overt malignant MM
Project 2: Defining the role of the bone marrow microenvironment in the development MM
24
Project 3: Determining the effects of myeloma plasma cells on mesenchymal stem cell (MSC) differentiation
Project 4: Identifying the role of the mTOR pathway in mesenchymal stem cell biology and bone formation
LYSOSOMAL DISEASE - Dr Kim Hensley
27
Project: Elucidating the basis of cognitive dysfunction in a murine model of a paediatric neurodegenerative disorder
OVARIAN DEVELOPMENTAL BIOLOGY - Prof Ray Rodgers
28
Project 1: Granulosa Stem Cells

Project 2: Regulation of GREL Cell Lineages
Project 3: Thecal Stem Cells
DEVELOPMENTAL GENETICS - Prof Paul Thomas
30
Project 1: Identifying SOX3 target genes

PERIODONTAL REPAIR - Prof Mark Bartold
31
Project 1: Dental mesenchymal stem cells for tissue regeneration

Project 2: Induced Pluripotent Stem Cells to regenerate Periodontal Tissue
Project 3: Induction of Neural Crest Cell Differentation from Periodontla iPS cells Characterization and Utilization of iPS cells for Dental Regeneration
REPRODUCTIVE BIOTECHNOLOGY - A/Prof Mark Nottle
32
Project 1: Making embryos for research

Project 2: Saving endangered species
Project 3: Reducing early embryonic loss
Project 4: Isolation and characterisation of embryonic stem cells
STROKE RESEARCH - A/Prof Simon Koblar
34
Project 1: Stem cell therapy in stroke

Project 2: Investigating the neurogentic potential of DPSC
Project 3: Mechanisms through which DPSC improve functional outcome after stroke
TRANSPLANTATION RESEARCH - A/Prof Toby Coates
36
Project 1: Enhancing pancreatic islet transplantation for Type 1 Diabetes

Project 2: Cellular therapy to treat kidney disease and kidney repair after transplantation and injury
Project 3: Dendritic cell therapy to improve kidney transplantation
VASCULAR BIOLOGY AND CELLULAR RECRUITMENT - Dr Claudine Bonder
38
Project 1: Endothelial progenitor cells (EPCs) in disease

Project 2: EPCs in islet transplantation
Project 3: Vasculogenic mimicry in cancer
11
12
ACUTE
LEUKAEMIA
ACUTE LEUKAEMIA
LABORATORY
CONTACT DETAILS
FACULTY: Sciences
SCHOOL: Molecular & Biomedical Science
DISCIPLINE: Genetics
SUPERVISORS
Prof Richard DAndrea
Our major focus is to understand the

mechanisms underlying normal blood
cell growth and differentiation, and
the changes associated with myeloid
diseases, in particular acute myeloid
leukaemia (AML) and myeloproliferative
neoplasms (MPN). We have used a
number of molecular and biochemical
approaches to investigate in detail
growth factor receptor signaling
responses and downstream events
occurring during normal myelopoiesis,
and associated with the aberrant growth
and survival of disease cells.
A significant research effort concerns
analysis of receptor signaling
mechanisms that control stem and
progenitor cell responses to a number
of key haemopoietic growth factors,
and which are commonly mutated
or up-regulated in acute myeloid
leukaemia. These receptor-activated

pathways link to key transcriptional
regulators involved in control of selfrenewal and myeloid differentiation
and we are investigating the role of
a number of established and novel
transcription factors in myeloid growth
and differentiation and haemopoietic
disorders.
Finally we are using a number of genetic
approaches to identify new genes and
mutations that contribute to myeloid
disease. These include studies of
families with inherited predisposition to
hematological disease, microarray gene
expression profiling and fine resolution
analysis of DNA from blood cells of
patients with myeloproliferative disease.
We have identified a number of genes
of interest that are the subject of current
studies.
Below: Professor Richard DAndrea
+61 8 8222 3636

Richard.dandrea@health.sa.gov.au
Dr Ian Lewis
Dr Anna Brown
Ms Carolyn Butcher
Dr Michelle Perugini
Dr Sarah Bray
HONOURS COORDINATOR
Prof Jeremy Timmis
Jeremy.timmis@adelaide.edu.au
+61 8 8313 4661
POSTGRADUATE COORDINATOR
A/Prof Frank Grutzner
frank.grutzner@adelaide.edu.au
+61 8 8313 4812
Project 1: -catenin activation and

target gene identification in Acute
Myeloid Leukaemia (AML)
-catenin is a central regulator of
growth and self-renewal in multiple
cell types, and mutations that cause
activation of -catenin activity have
been found in many solid tumours
(e.g. colorectal, lung, ovarian, breast).
Self-renewal is a critical property of
cancer stem cells that contributes to
disease relapse and targeting selfrenewal regulators is an important new
approach in cancer treatment. -catenin
is a transcriptional co-activator that is
central to transmission of canonical
Wnt signalling. Over the past several
years evidence has been emerging
that -catenin protein stabilisation,
which is essential for its transcriptional
regulatory activity, has important roles
in self-renewal of normal haemopoietic
stem cells as well as leukaemic stem
cells. The mechanism associated with
-catenin stabilisation in haemopoietic
cells is not well understood. We have
shown -catenin regulation downstream
of receptor signalling in AML and we
will use several approaches to dissect
the pathways associated with this.
The transcription factor DNA-binding
partners and direct target genes of
-catenin are also poorly defined. We
hypothesise that the action of -catenin
in myeloid cells may not be solely
through TCF/LEF family members (DNA
binding members of the canonical Wnt
signalling pathway) and propose here to
analyse specific gene targets identified
by chromatin immunoprecipitation
and high-throughput sequencing
(ChIP-seq) using -catenin antibodies.
This will characterise the function of
the direct target genes and partner
binding proteins for -catenin in myeloid
leukaemia.
Project 2: Transcriptional regulation
of the KLF5 transcription factor
KLF5 is a member of the Kruppel-likefactor family of transcription factors that
have important roles in cell proliferation,
differentiation and carcinogenesis. We
have identified that KLF5 is a potential
tumour suppressor gene in AML and
that it is subject to modification by
DNA methylation. Projects are available
to further study the mechanism by
which DNA methylation may regulate
KLF5 transcription. This would involve
characterising the contribution of
particular transcription factor binding
sites in the KLF5 promoter and

regulatory regions that affects its
transcription. The techniques used
would include reporter assays and
chromatin immunoprecipitation.
or translocations involving the MLL

gene; and 4) the ability of Gadd45a
to induce DNA demethylation and
activation of tumour suppressor genes
in AML cells.
Project 3: Post-translational
modification of transcription factors
in AML
Project 5: Screening for compounds

that induce differentiation or cell
death of AML cells.
Transcription factors (TFs) are a class

of genes that are frequently affected
in AML. Their activity can be modified
at the genetic level through several
mechanisms including chromosomal
translocation, DNA methylation and
direct mutation. More recently it has
been recognized that post-translational
modification of TF proteins can have
major effects on their target gene
selection and transcriptional activity.
However in AML this field of research
is in its infancy with modifications of
many key TF proteins and the upstream
signaling pathways that cause these
modifications still to be identified. In
AML, mutations in the FLT3 tyrosine
kinase receptor (FLT3-ITD) often lead
to constitutive signaling which results
in the modification of TF proteins. We
have projects looking at the modification
of several TFs downstream of FLT3-ITD
and also projects aimed at identifying
novel proteins modified by FLT3-ITD
using mass spectrometry.
AML is associated with a number of

chromosome translocations which
produce transcription factor fusion
proteins that disrupt the normal myeloid
differentiation program. The most
frequent chromosome translocations
are t(15;17) PML-RARa, t(8;21) AMLETO, inv(16) CBF-MYH11 and the
der(11q23) MLL-fusions. The presence
of these readily identifiable karyotypic
abnormalities may define features of
the AML that will provide for selective
therapy. This is clearly the case with
AML carrying the t(15:17) translocation
which can be successfully treated with
ATRA. We have used a novel approach
to better understand the contribution of
the aberrant fusion-products involved in
AML pathogenesis and identify selective
therapies. To identify unique features
associated with particular translocations
and to define overlapping pathways
involved in AML we examined gene
expression signatures associated
with the major PML-RARa, AML-ETO,
CBF-MYH11 and MLL gene fusions.
We compared the gene expression
patterns of 76 AML patients (N Engl J
Med. 350:1617-28) with translocation
events categorized as t(15;17), t(8;21),
inv(16) or der(11q23) and determined
the gene expression changes, relative
to normal bone marrow. We generated
translocation-specific gene signatures,
which were used to query drug gene
expression profiles via the Connectivity
Map identifying small molecules or
FDA-approved drugs associated
with reversal of the signature. This
has suggested a number of potential
treatments selective for these sub-types
of AML. Projects are available to test
the effectiveness of these candidate
therapies on AML cell lines, patient
samples and using in vivo models.
Project 4: Regulation of Gadd45a in

AML
Gadd45a is a member of the Growth
Arrest and DNA Damage Inducible
gene family and has been implicated
as a tumour suppressor in many
cancers. Gadd45a down-regulation
is an important marker of tumour
progression, and we observe Gadd45a
down-regulation in several classes of
AML and in association with common
receptor mutations in AML. We have a
number of ongoing projects to establish
the mechanisms of down-regulation
of Gadd45a and its role in AML.
Specifically, these include; 1) studying
epigenetic modification at the Gadd45a
locus, in particular CpG methylation
of the Gadd45a promoter in AML; 2)
characterisation of the mechanism
associated with down-regulation of
Gadd45a in AML with mutations in
the FLT3 receptor; 3) using in vitro
and in vivo models to characterise
the co-operation of loss of Gadd45a
with other oncogenic lesions such as
activating mutations in FLT3 receptors
Project 6: Molecular characterisation

of Polycythemia Vera
Myeloproliferative neoplasms (MPN)
are haemopoietic stem cell disorders
associated with somatic mutations
of JAK2 and although murine in vivo
studies indicate that their acquisition
13
14
is sufficient for development of MPN,

it is evident from human studies that
additional genes are involved. We
have shown acquisition of RUNX1 and
JAK2 mutations in divergent clones
in a PV patient who developed acute
leukemia, consistent with a model for
MPN involving a pre-clinical unstable
hematopoietic phenotype. A number
of genes have now been identified
with a role in disease progression
however the nature of a pre-JAK2
event remains undetermined. We have
used a number of genetic approaches
with our MPN patient cohort to identify
changes associated with disease
initiation. These include candidategene sequencing from granulocyte and
BFU-e DNA, exon capture followed by
Next-gen sequencing and genome-wide
paired SNP-array analysis (Affymetrix
Genome-Wide Human array 6.0) of
granulocyte samples and corresponding
germ-line DNA to identify genomic
regions of acquired LOH and copy
number variation. These analyses have
highlighted a number of novel genes for
further study with a focus on identifying
initiating molecular lesions in MPN.
References :
1. Estey E, Dhner H. Acute myeloid
leukaemia. Lancet. 2006
368(9550):1894-907.
2. Levine RL, Gilliland DG.
Myeloproliferative disorders. Blood
2008 112(6):2190-8.
3. Butcher CM, Hahn U, To LB, Gecz J,
Wilkins EJ, Scott HS, Bardy PG,
DAndrea RJ Two novel JAK2 exon
12 mutations in JAK2V617F-negative
polycythaemia vera patients.
Leukemia. 2008 22(4):870-3.
4. Butcher CM, Hutton JF, Hahn U, To
LB, Bardy P, Lewis I, DAndrea
RJ. Cellular origin and lineage
specificity of the JAK2(V617F) allele
in polycythemia vera. Blood. 2007
109(1):386-7.
5. Perugini M, Kok CH, Brown AL,
Wilkinson CR, Salerno DG, Young
SM, Diakiw SM, Lewis ID, Gonda
TJ, DAndrea RJ. Repression of
Gadd45alpha by activated FLT3
and GM-CSF receptor mutants
contributes to growth, survival and
blocked differentiation. Leukemia.
2009 23(4):729-38
Project 7: Molecular Characterisation

of Diamond Blackfan Anemia
Diamond Blackfan Anemia (DBA)
is a bone marrow failure syndrome
characterised by haploinsufficiency
for a number of ribosomal proteins
associated with abnormal haemopoietic
stem cell proliferation and differentiation
leading to specific red cell and skeletal
defects. The mechanism of tissue
specificity in this disease remains
unclear. We aim to understand how
loss of these ubiquitously expressed
ribosomal proteins translates to defective
erythropoisis, causing a distinct erythroid
phenotype. To achieve this we aim to
identify key proteins in erthythroblasts
that are produced at reduced levels in
cells with mutant ribosomal proteins
(RPS/RPL), and contribute to the disease
phenotype. For this we will make use of
proteomic technologies which allow us
to compare the complement of proteins
produced in cells with and without
the ribosomal protein defect. These
proteins will subsequently be tested
in established experimental models to
assess their contribution to the defective
erythropoiesis.
NEUROVASCULAR
RESEARCH
NEUROVASCULAR
RESEARCH
CONTACT DETAILS
FACULTY: Health Sciences
SCHOOL: Paediatrics & Reproductive Health
DISCIPLINE: Obstetrics and Gynaecology
SUPERVISOR
Dr Quenten Schwarz
Project 1: Investigating the molecular

control of neural crest stem cell
(NCSC) development
NCSCs are a transient population of
stem cells that give rise to all cells types
in the peripheral nervous system. We
have recently identified a novel role for
the Neuropilin (Nrp) family of receptors
in NCSC migration. To understand how
these receptors function we are now
undertaking experiments to characterize
the intracellular signaling pathways that
control neuronal migration.
Project 2: Identifying the embryonic

origin of the childhood cancer
Neuroblastoma
Neuroblastoma is the most prevalent
extracranial solid tumour in childhood and
arises from incorrect NCSC differentiation.
We have recently shown that the Nrp1
receptor is expressed in a subset of
NCSCs that from neuroblastoma. This now
gives us the unique tools to dissect the
aberrant genetic programs initiating tumour
formation.
Project 3: Title: How does VEGF

control development of the cardiac
outflow tract?
Cardiac outflow tract defects represent the
most prevalent birth defect in humans. A
major component of these defects arise
from defects in NCSC development. We
have recently shown that the Nrp1 receptor
and its ligand VEGF are essential for
NCSC development and now addressing
their role in cardiac development.
mice appear small but outwardly normal

and display various patterning defects
in brain development and neuronal
migration. Our preliminary findings
suggest that these mice have behavioural
issues akin to schizophrenia. We are now
analysing the development of cerebral
and hippocampal neurons in mouse
models of 14-3-3 .
+61 8 8222 3714

quenten.schwarz@adelaide.edu.au
HONOURS COORDINATOR
Dr Kathy Gatford
+61 8 8313 4158
Kathy.gatford@adelaide.edu.au
References:
A/Prof David Kennaway
1. Q.P. Schwarz, C. Maden, J.M. Vieira

and C. Ruhrberg. Neuropilin 1
signalling guides neural crest cells
to coordinate pathway choice with
cell specification. Proceedings of
the National Academy of Science,
USA, 106(15), pp6164-9 (2009).
+61 8 8313 4093 / +61 8 8313 4090
2. Q.P. Schwarz, C. Maden, K. Davidson

and C. Ruhrberg. Neuropilin-mediated
neural crest cell guidance is essential
to organize sensory neurons into
segmented dorsal root ganglia.
Development, 136(11), pp1785-9
(2009).
3. C. Ruhrberg and Q.P. Schwarz. In the
beginning: Generating neural crest
cell diversity. Cell Adhesion and
Migration, 4(4), epub ahead of print
(2010).
David.kennaway@adelaide.edu.au
Neuropilin 1 and neuropilin 2 control

cranial gangliogenesis and axon
guidance through neural crest cells.
Development, 135(9), pp1605-13
(2008).
5. PS. Cheah, H. Ramshaw, P. Thomas, K.
Toyo-oka, X. Xu, S. Martin, P. Coyle,
M. Guthridge, F. Stomski, M. van den
Buuse, A. Wynshaw-Boris, A. Lopez
& Q. Schwarz. Neurodevelopmental
and neuropsychiatric behaviour
defects arise from 14-3-3 deficiency.
Molecular Psychiatry, 17, pp 451-66
(2012).
4. Q. P. Schwarz, B. Howard, J. M. Vieira,

B. J. Eickholt and C. Ruhrberg.
Below: Doctor Quenten Schwarz
Project 4: Title: Investigating the role of

14-3-3 in schizophrenia
14-3-3 proteins are expressed abundantly in
the brain and are thought to control survival
and developmental pathways. We have
recently generated mice deficient in one
of the 14-3-3 isoforms, 14-3-3. These KO
15
GENE THERAPY
FOR
CYSTIC FIBROSIS
GENE THERAPY FOR

CYSTIC FIRBROSIS
LABORATORY
CONTACT DETAILS
SUPERVISORS
Development of gene
therapy for prevention
of treatment of cystic
fibrosis
Lung disease is the primary cause of
worsening health problems in young
people with CF. It greatly affects their
quality of life and is the overwhelming
cause of early death. Our group is
developing an effective treatment and
potentially a life-long correction for the
airway disease of Cystic Fibrosis (CF).
Our research utilises a lentiviral (LV)
vector delivery system to study how to
produce safe and effective gene delivery
into airway cells in animal models.
We use reporter genes such as LacZ,
luciferase, GFP and eYFP, as well as the
therapeutic CFTR gene.
Our work has included studies across
mice, sheep and marmoset animal

models, and we are planning to establish
a CF ferret colony in Adelaide to improve
the testing of our genetic treatments
for CF airway disease. Our approach
especially targets airway stem cells in
vivo, and in some mouse studies this
approach has already produced up to
lifetime gene expression after a single
dose event.
Our new state-of-the-art research
laboratory opened in 2012. Through the
enthusiastic initial work of the Cure4CF
Foundation Ltd (www.cure4cf.org), and
substantial completion funding provided
by the WCH Foundation, the Alan Scott
CF research laboratory is now in place
in the Gilbert Building at the WCH. This
laboratory is used for plasmid and viral
vector production, molecular assays
and histological processing, and a
range of bench and computer-based
development work for our gene therapy
and imaging studies.
A/Prof David Parsons

+61 8 8161 7004
david.parsons@health.sa.gov.au
Dr Martin Donnelley
Dr Patricia Cmielewski
Mr Nigel Farrow
HONOURS COORDINATOR
Dr Kathy Gatford
+61 8 8313 4158
+61 8 8313 4093 / +61 8 8313 4090
Below: Associate Professor David Parsons
16
Project 1: Investigating the

differentiating and self proliferating
potential of endogenous respiratory
stem cells lacking the CFTR protein
via transepithelial potential difference in

CF mouse models, and molecular and
histological analyses.
A recent study by our research team

has unveiled extensive stem cell
hyperplasia in cystic fibrosis (CF)
respiratory airways. It has also been
demonstrated that airway remodelling
of mucus secreting goblet cells as
both hyperplasic and hypertrophic
is present in the same region. It is
unclear if goblet cell remodelling is a
consequence of stem cell remodelling.
This exciting project will investigate
this further utilising flow cytometric cell
sorting to isolate respiratory airway
stem cells from both CF transgenic
and normal mice, and clonal assays
to evaluate the differentiating and self
proliferating potential of the respiratory
stem cell in absence of the membrane
bound CF channel. An additional CF
transgenic mouse group will be treated
with our well established gene therapy
technique to restore CF function in the
respiratory stem cells. This will allow us
to determine if any possible differences
in differentiating and/or self proliferating
potential can be corrected using our
gene therapy protocol.
Project 3: Effects of LPC airway pretreatment on airway and lung health
Project 2: Increasing the level of

therapeutic CFTR transduction in a
CF mouse model
Although most modern LV vectors are
gutted (i.e. most sequences, including
the tat gene, are removed to improve
vector safety), our LV vector delivery
system utilises a VSV-G pseudotyped
HIV-1 LV vector that does contain tat.
Our vector has been shown to produce
robust and extended reporter gene
transfer in normal mice, as well as
functional therapeutic CFTR correction
in CF knockout mice. Although other
groups have produced reporter gene
transfer using their tat-deficient vectors,
none have published reports of extended
therapeutic CFTR correction.
This project will compare our 5-plasmid
tat-containing vector against a 4-plasmid
tat-deficient vector of similar construction
to determine their relative effectiveness.
Initial comparisons will be made in
mouse airways through the use of
reporter genes. Their effectiveness as
a therapeutic gene vector will then be
assessed in CF mice using vectors
containing the CFTR gene. This
project will involve plasmid and vector
production, functional CFTR assessment
Our group has developed a proven gene

transfer method that involves a preconditioning of the airway surface using
the compound LPC, which is thought
to open tight junctions between cells
allowing vector access to the basolateral
membrane. Importantly, we have shown
that LPC use greatly enhances nasal
gene transduction. Although we have
never seen adverse effects from this
pre-treatment in healthy mouse lungs,
there is some concern that opening
tight junctions in a CF lung infected
with bacterial pathogens might increase
the risk of systemic infection. The aim
of this project is to test whether LPC
pre-treatment in a mouse model of lung
infection has positive, neutral or negative
effects on animal and lung health. This
project will involve plasmid and vector
production, Pseudomonas aeroginosa
agar bead production, animal handling
(including non-surgical intubation) and
molecular and histological analyses.
References:
1. Farrow, N., D. Miller, P. Cmielewski,
M. Donnelley, R. Bright and D.
W. Parsons (2013). Airway gene
transfer in a non-human primate:
Lentiviral gene expression in
marmoset lungs. Scientific Reports
3(1287).
2. Liu, C., E. Wong, D. Miller, G. Smith,
D. Anson and D. Parsons (2010).
Lentiviral airway gene transfer
in lungs of mice and sheep:
successes and challenges. J Gene
Med 12(8): 647-658.
3. Stocker, A. G., K. L. Kremer, R. Koldej,
D. S. Miller, D. S. Anson and D.
W. Parsons (2009). Single-dose
lentiviral gene transfer for lifetime
airway gene expression. J Gene
Med 11(10): 861-867.
4. Limberis, M., D. S. Anson, M.
Fuller and D. W. Parsons (2002).
Recovery of airway cystic fibrosis
transmembrane conductance
regulator function in mice with cystic
fibrosis after single-dose lentivirusmediated gene transfer. Hum Gene
Ther 13(16): 1961-1970.
Other Projects: The proposed projects

are only a small example of what is
available. We also have a range of other
projects related to the creation and
assessment of treatment of CF airway
disease that can be tailored to the
specific area of interest of the applicant.
LEFT: Strong lentiviral gene transfer (blue coloured cells) scattered throughout a
normal mouse nasal airway. This distribution of staining is thought to reflect how
the corrective CFTR gene would transduce in these airways in CF mice.
17
MESENCHYMAL
STEM CELLS
We have previously identified different
mesenchymal stem cell (MSC)
populations that live in adult bone
marrow, peripheral fat and dental pulp
tissue. These stem cells have the
capacity to differentiate into connective
tissue cell types and form the tissues
from which they were initially derived.
However, the precise molecular signals
responsible for maintaining these stem
cell pools or inducing differentiation
leading to the eventual formation of
bone, fat, muscle, cartilage or dentin
have yet to be determined.
We propose that primitive mesenchymal
stem cells express critical genes that
regulate maintenance of the stem cells
pool and their differentiation into bone,
cartilage and dentin.
We are currently analysing the gene
expression profiles of highly purified
mesenchymal stem cell populations
derived from bone marrow and dental

pulp tissue based on an isolation
protocol they have patented.The dental
work is conducted in collaboration
with the Periodontal Repair Group (P
24), led by Professor Mark Bartold at
the Colgate Australian Clinical Dental
Research Centre.
We are also working on identifying
genes uniquely expressed by these
stem cells that will yield important clues
for regulating cardiac, bone, fat muscle,
ligament and dentin development.
Our group is involved with several
animal pre clinical studies and human
clinical studies in Australia and the
USA examining the efficacy of MSC to
repair bone, cartilage, ligament and
cardiac defects in collaboration with
our commercial partners, Angioblast
Systems Inc., New York, NY, USA and
Mesoblast Ltd, Melbourne Vic Australia.
Below: Professor Stan Gronthos
18
MESENCHYMAL STEM
CELLS LABORATORY
CONTACT DETAILS
SCHOOL: Medicine
DISCIPLINE: Medicine
SUPERVISOR
Prof Stan Gronthos
+61 8 8222 3460
stan.gronthos@adelaide.edu.au
HONOURS COORDINATOR
A/Prof Chris Rayner
+61 8 8222 2916
chris.rayner@adelaide.edu.au
POSTGRADUATE COORDINATORS
Prof David Callen
+61 8 8222 3145
david.callen@adelaide.edu.au
Dr Lisa Butler
Lisa.butler@imvs.sa.gov.au
+61 8 8222 3270
Project 1: Mesenchymal stem cells in

skeletal tissue regeneration
This work investigates the molecular
mechanisms controlling maintenance of
osteo/chondrogenic precursor cells and
skeletal tissue regeneration. Projects will
focus on stem cell biology and the use
of microarray analysis and proteonomic
analysis for determining differences in the
gene expression profiles of normal and
genetically modified mesenchymal stem
cell populations. In particular the role of
transcription factors and epigenetic histone/
DNA modifying enzymes in postnatal MSC
maintenance and development will be
assessed in the context of diseases and
conditions that affect the skeleton including
bone fracture repair, osteoporosis and
osteoarthritis.
Project 2: The role of MSC in

the maintenance and support of
haematopoiesis and modulation of
immune responses
In addition to having tissue regenerative
properties, MSC have also been shown to
exhibit the potential to support and regulate
haematopoietic stem cells the precursors of
white cells, red cells and platelet producing
megakaryocytes. Furthermore, MSC are
capable of regulating immune cells through
direct contact or via secreted factors.
Projects will address the underlining
molecular mechanisms (soluble cytokine/
chemokine factors, extracellular matrix
components and cell surface bound
molecules) that mediate MSC and blood/
immune cell interactions. These projects will
focus on clinical models of haematopoiesis,
bone marrow transplantation, chronic
inflammatory diseases, autoimmune
diseases and organ transplantation.
Project 3: Dental mesenchymal stem

cells for tissue regeneration
These studies involve the identification
and characterization of human, rodent
and ovine periodontal ligament stem
cells (PDLSC) and dental pulp stem
cells (DPSC). Studies will determine the
efficacy of different stem cell preparations
and biomaterials to repair alveolar bone,
cementum, dentin and periodontal tissues
using both rodent and ovine models
representative of different dental defects or
following disease (periodontitis) or trauma.
Projects will investigate the underlining
molecular mechanisms (transcription
factors, epigenetic factors, cell adhesion
molecules, soluble factors extracellular
matrix components) that govern stem cell
maintenance, migration and differentiation

during the repair process.
References:
1. Gronthos S, Mankani M, Brahim J,
Gehron Robey P, Shi S (2000). PostNatal Human Dental Pulp Stem Cells
In vitro and In vivo. Proceedings of the
National Academy of Sciences (USA),
97 (25): 13625-13630.
2. Gronthos S., Zannettino ACW, Kortesidis
A, Shi S, Graves SE, Hay SJ, Simmons
PJ (2003). Molecular and cellular
characterisation of highly purified
human bone marrow stromal stem
cells. Journal of Cell Science 116:
1827-1835.
3. Shi S. and Gronthos S. (2003).
Perivascular Niche of Postnatal
Mesenchymal Stem Cells in Human
Bone Marrow and Dental Pulp. Journal
of Bone and Mineral Research, 18(4):
696-704.
4. Kortesidis A, Zannettino ACW, Isenmann
S, Shi S, Lapidot Tsvee L, and
Gronthos S (2005). Stromal derived
factor-1 promotes the growth, survival
and development of human bone
marrow stromal stem cells. BLOOD.
105(10):3793-3801.
5. Stokowski A, Shi S, Sun T, Bartold PM,
Koblar SA, S Gronthos S (2007).
EphB/ephrin-B interaction mediates
adult stem cell attachment, spreading
and migration: implications for dental
tissue repair. Stem Cells. 25:156-164.
6. Arthur A, Rychkov G, Shi S, Koblar SA,
Gronthos S. (2008). Adult Human
Dental Pulp Stem Cells Differentiate
Towards Functionally Active Neurons
Under Appropriate Environmental
Cues. Stem Cells, 26(7):1787-1795.
7. Isenmann S, Arthur A, Zannettino
AC, Turner JL, Shi S, Glackin CA,
Gronthos S (2009). TWIST family of
basic Helix-Loop-Helix Transcription
Factors Mediate Human Mesenchymal
Stromal/Stem Cell Growth and
Commitment. Stem Cells. 27(10):245768.
19
20
MOLECULAR
IMMUNOLOGY
MOLECULAR
IMMUNOLOGY LABORATORY
CONTACT DETAILS
DISCIPLINE: Paediatrics
SUPERVISORS
A/Prof Simon Barry
The Molecular Immunology Laboratory

is interested in how a healthy immune
system balances being ready to react
by swiftly fighting off pathogens, while
maintaining tolerance to harmless
challenges such as food and body
tissues. The cellular immune repertoire
in humans is broad, but this laboratory
is focussed on a T cell subset that
is shaped along with the immune
system from birth. These cells are
known as regulatory T cells, and they
are accepted as the policemen of the
immune system. There is increasing
evidence that in a wide number of
disease states including autoimmune
diseases such as Type 1 diabetes and
multiple Sclerosis, these cells fail to
regulate the immune system, and allow
inappropriate destruction of tissues
that are essential for life. In order to

understand how this breaks down in
disease one must first understand
what the basis of a healthy Treg is.
To do this, the Molecular Immunology
Laboratory focuses on human cells and
uses a number of state of the art gene
discovery tools such as microarrays
to identify and them confirm the key
genes in Treg function. As Treg play a
role in autoimmune disease, cancer and
transplantation tolerance, this groups
research findings have a wide clinical
application. The projects that this
laboratory can offer students are from
parts of this overall research program.
The Molecular Immunology Laboratory
currently has 11 members, who provide
lab and academic support for students.
+61 8 8161 6562

simon.barry@adelaide.edu.au
Dr Tim Sadlon
Dr Cheryl Brown
HONOURS COORDINATOR
Cheryl Shoubridge
+61 8 8161 8105
cheryl.shoubridge@adelaide.edu.au
A/Prof Simon Barry
+61 8 8161 6562
Below: Associate Professor Simon Barry
Project 1 Molecular identification of

Regulatory T cells
The recent identification of regulatory T
cells (Tregs) as a key mediator of central
and peripheral tolerance has led to an
increase in our understanding of the
cellular mechanisms by which humans
maintains the healthy state. This has
been confirmed by the identification of
a transcription factor named FOXP3 in
both mouse and human Tregs, which is
proven to be essential for formation and
function of the committed T cell subset
that has regulatory capacity. There is
however, very little known about the
molecular basis of this process. This
project aims to identify the genes directly
regulated by FOXP3 and to determine
their role in the regulatory phenotype.
We have used a number of direct and
indirect molecular approaches such as
Chromatin Immunoprecipitation and
microarray analysis to profile genes
regulated by FOXP3 (Fig 1),
H, Barry SC. Purification and

characterization of CD4+ CD25+
regulatory cells from Cord and
peripheral blood. J Immunuol
Methods 2007;327:53-62
Project 2: Cord Blood Stem cell
differentiation in to regulatory T cells
Fig 2: Comparative analysis of CD4

CD25+ natural Treg and Th17 in IBD
patients shows a defect in the ratio of
these cells
Techniques/skills/approach: Molecular
biology, RT PCR, microarray data
analysis, tissue culture lentiviral
production, gene silencing and over
expression, functional assay
Project type: Basic research project,
clinical /basic if patient sample analysis
References:
Fig 1: Comparative microarray analysis of

CD4 CD25+ natural Treg to identify the
key genes required for function
and we will validate their role in regulatory

function by direct assays and by over
expression or gene ablation studies.
The candidate genes identified in this
approach may lead to therapeutic
approaches for intervention in the
function of regulatory cells, and will also
have application for diagnostic analysis
of regulatory cell function. Analysis of
these and other T cells from disease
samples eg IBD (Fig 2) reveals the
clinical defect in numbers of Treg.
1. Beyer M, Thabet Y, Mller RU, Sadlon

T, Classen S, Lahl K, Basu S, Zhou
X, Bailey-Bucktrout SL, Krebs W,
Schnfeld EA, Bttcher J, Golovina
T, Mayer CT, Hofmann A, Sommer D,
Debey-Pascher S, Endl E, Limmer A,
Hippen KL, Blazar BR, Balderas R,
Quast T, Waha A, Mayer G, Famulok
M, Knolle PA, Wickenhauser C,
Kolanus W, Schermer B, Bluestone
JA, Barry SC, Sparwasser T, Riley
JL, Schultze JL. Repression of
the genome organizer SATB1 in
regulatory T cells is required for
suppressive function and inhibition
of effector differentiation. Nat
Immunol. 2011 Aug 14;12(9):898907.
2. Sadlon TS, Wilkinson BG, Pederson
S, Brown CY, Bresatz S, Gargett
T, Melville E, Peng K, Glonek G,
Goodall GJ, Zola H, Shannon
MF, Barry SC. Genome wide
identification of human FOXP3
target genes in natural regulatory T
cells. J Immunol. 2010 Jul 15;185
(2):1071-81.
3. Nicola Leung, Nicholas Mabarrack,
Angela Barbour , Adrian Cummins
and Simon Barry . Foxp3+
Regulatory T Cells, Th17 Effector
Cells and Cytokine Environment in
Inflammatory Bowel Disease. Clinical
Immunolgy 2010 Jan;30(1):80-9
The clinical application of regulatory

T cells is significantly hampered by
the limited cell numbers that can be
obtained from either cord or adult blood.
Attempts to expand these purified Treg
ex vivo have shown some promise,
but there is some evidence that after
extended culture ex vivo these cells
lose their suppressive capacity. An
alternative approach is to generate
large numbers of T cells de novo from
stem cells since these cells have the
capacity to differentiate into all cells
of the haemopoietic system. We have
established an ex vivo differentiation
assay that can expand cord blood stem
cells and induce their differentiation
along the lymphoid pathway using a
co-culture system giving notch signals
via the Notch ligand Delta like 1 (Fig 3).
In this system we robustly observe 5-600
fold expansion of cell numbers and the
generation of T cell subsets as defined
by CD4/CD8 staining.
Fig 3: Ex vivo differentiation and expansion

of cord blood stem cells on feeder cells
showing formation of CD4 CD25+ subsets
with similar characteristics to natural Treg
biology, RT PCR, tissue culture, lentiviral
expression, functional assay with cord
blood stem cells.
Project type: Basic research project
References:
1. Hutton JF, Gargett T, Sadlon TJ,
Bresatz S, Brown CY, Zola H,
Shannon MF, DAndrea RJ,
Barry SC: Development of
CD4+CD25+FOXP3+ Regulatory
T cells from Cord Blood
Haemopoietic Progenitor Cells.
Journal of Leukocyte Biology ePub
Dec 22 08.
4. Bresatz S Sadlon T, Millard D, Zola
21
22
Project 3: Lentiviral vectors for gene

delivery and gene ablation
Manipulation of primary cells has a
key limitation in that these cells are
refractory to standard transfection
protocols. Also, since they are often
of low mitotic index, they are only
infected at low efficiency by murine
retroviruses (RV), as these viruses
require cell division for integration.
The recent development of HIV1
based lentivectors (LV) provides an
attractive option for gene delivery into
T cell and stem cell populations, as
these viruses carry the necessary cis
elements to facilitate nuclear transport
and integration in the absence of cell
division. We have developed a suite of
lentiviral vectors for stable gene delivery
into primary cells both for gene therapy
and gene discovery applications,
and more recently for gene ablation
using RNA interference (Fig 4). This
technology relies on the expression of
a short hairpin RNA structure that is
complimentary to the gene target, and
that is processed by cellular machinery
to generate an RNA oligo that can bind
to and target the mRNA for destruction.
Goodall GJ: The microRNA-200

family and miR-205 regulate
epithelial-mesenchymal transition
by targeting the E-cadherin
repressors, ZEB1 and SIP1. Nature
Cell Biology2008 10 (5)593-601
3. Barry SC,Coates PT. Retroviral
escape using DC - thats what
Friends are for. Blood 2007
110(12)3819-3820
4. Drabsch Y, Hugo H, Zhang R,
Dowhan DH, Miao YR, Gewirtz AM,
Barry, SC, Ramsay RG and Gonda
TJ. Mechanism of and Requirement
for Estrogen-Regulated MYB
Expression in Estrogen ReceptorPositive Breast Cancer Cells. PNAS
2007;104(34):13762-7
5. Brzezinski M, Yanay O, Waldron L,
Barry SC and Osborne WRA.GCSF-lentivirus provided long-term
elevated neutrophil counts in rats
and sequential EPO-lentivirus
administration produced increased
hematocrits in both lentivirus
treated and nave rats. J Gene
Medicine 2007;9(7):571-8
6. Barry SC Brezinzki M, Yanay O,
Seppen, J Osborne WRA.
Sustained elevation of neutrophils
in rats induced by lentivirusmediated G-CSF delivery. J Gene
medicine 2005;7(12):1510-6.
Project 4: Is there a role for FOXP3
in Breast Cancer?
Fig 4: Lentiviral delivery of shRNAi

showing ablation of FoxP3 expression
that is inducible with doxicyclin and is
reversible
biology, RT PCR, Tissue culture,
lentiviral production, gene silencing and
over expression, functional assay, T cell
assays
Project type: Basic research project.
References:
1. Cheryl Y. Brown, Timothy Sadlon,
Tessa Gargett, Elizabeth Melville,
Rui Zhang, Yvette Drabsch, Craig
A. Strathdee, Thomas J. Gonda,
Simon C. Barry Robust, reversible
gene knockdown using a single
lentiviral shRNA vector Human
Gene Therapy 2010 30 1 80 - 89.
There is very recent evidence that

FOXP3 may also play a role in breast
cancer as a new tumour suppressor.
This means that its expression prevents
the transformation leading to cancer,
and in cells that have transformed it is
no longer correctly expressed. As we
have discovered a great many of the
genes that are directly regulated by
FOXP3 in Tregs, it is likely that some of
these are also required for prevention of
breast cancer. We have now confirmed
that FOXP3 is expressed in healthy
breast epithelial cells, and are testing a
number of genes for their role in either
the loss of normal FOXP3 expression, or
the progression to cancer.
2. Gregory PA, Bert AG, Paterson EL,

Barry SC, Tsykin A, Farshid G,
Vadas MA, Khew-Goodall Y and
Fig 5: When FOXP3 is over expressed

using a lentivirus in a breast cancer cell
line, we observe increased expression of
target micro RNAs.
This includes a number of micro

RNAs that are controlled by FOXP3
(quantitated by RT PCR in (Fig 5), one
of which (mir21) has been confirmed
to play a role on BC. We aim to
demonstrate that correction of the
FOXP3 expression defect can reverse
these transformation causing genes and
restore a healthy state.
biology, RT PCR, microarray data
analysis, tissue culture, lentiviral
expression, functional assay in breast
cancer cells.
Project type: Basic research project,
clinical /basic if patient sample analysis
References:
1. McInnes N, Sadlon TJ, Brown CY,
Pederson S, Beyer M, Schultze
JL, McColl S, Goodall GJ, Barry
SC FOXP3 and FOXP3-regulated
microRNAs suppress SATB1 in
breast cancer cells. Oncogene.
2011 Jul 11. doi: 10.1038/
onc.2011.293
2. Zuo, T., et al., FOXP3 is a novel
transcriptional repressor for the
breast cancer oncogene SKP2. The
Journal of Clinical Investigation,
2007. 117(12): p. 3765-3773.
3. Zuo, T., et al., FOXP3 is an x-linked
breast cancer suppressor gene
and an important repressor of
the HER-2/ErbB2 oncogene. Cell,
2007. 129: p. 1275-1286.
ANIMAL STEM CELLS
NEUROVASCULAR
RESEARCH
ANIMAL
REPRODUCTION
CONTACT DETAILS
FACULTY: Animal Sciences
SCHOOL: Animal and Veterinary Science
SUPERVISOR
Professor Paul J Verma
Pluripotent stem cells such as Embryonic

Stem Cells (ESC) have potentially unlimited
proliferative capacity and the ability to
form every cell type of the body. Therefore
they provide a unique tool understand
development and potentially provide
cells for biomedical and biotechnology
applications. They also have potential
application in livestock development and
species conservation. Recently it has been
shown that introduction of a few embryonic
genes, can reprogram adult cells into
embryonic stem cell equivalents, know as
induced pluripotent stem cells (iPSCs).
While at Monash University, Pauls lab
was the first to develop iPSCs in Australia
from mice1, humans2, livestock3-4 and
endangered species5. At SARDI we are
exploring application of this exciting
approach to benefit the livestock industry
and for preserving biodiversity.
Project 1: Generation and

characterization of pluripotent stem
cells from large animals
Generation of pluripotent stem cells from
large animals are of interest for a number
of reasons; they provide a unique source
of cells from livestock that allow specific
traits to be engineered for agricultural
purposes and to develop unique
biomedical models to understand human
diseases and can be useful for species
conservation.
References:
paul.verma@sa.gov.au
1. Liu J, Ashton MP, Sumer H, OBryan

MK, Brodnicki TC, Verma PJ.
(2011) Generation of Stable
Pluripotent Stem Cells from NonObese Diabetic (NOD) Mouse
Tail-Tip Fibroblasts. Diabetes;
60(5):1393-8.
HONOURS COORDINATOR
2. Liu J, Sumer H, Leung J, Upton K,

Dottori M, Pbay A and Verma
PJ. (2010) Late passage human
fibroblasts induced to pluripotency
are capable of directed neuronal
differentiation. Cell Transplantation;
20(2):193-203.
Professor Peter Cockcroft
3. Sumer H, Liu J, Malaver-Ortega LF,

Lim ML, Khodadi K. and Verma
PJ. (2011) Nanog is a key factor for
induction of pluripotency in bovine
adult fibroblasts. Journal of Animal
Science; 89(9):2708-16.
4. Liu J, Balehosur D, Murray B, Kelly
JM, Sumer H and Verma PJ. (2011)
Generation and characterization
of reprogrammed sheep induced
pluripotent stem cells. Theriogenology
77(2):338-46
Dr Karen Kind
+61 8 8313 7972
karen.kind@adelaide.edu.au
+61 8 8313 7883

peter.cockfort@adelaide.edu.au
5. Verma R, Holland MK, Temple-Smith

P, Verma PJ. (2011) Inducing
pluripotency in somatic cells from
the snow leopard (Panthera uncia),
an endangered felid. Theriogenology
77(1):220-8, 228.e1-2.
Below: Professor Paul Verma
Project 2: Genome editing of

pluripotent livestock stem cells
Recently we6,7 and others have shown
that cutting edge molecular techniques
including TALENs (transcription activatorlike effector nucleases) and CRISPR/Cas9
(clustered regularly interspaced short
palindromic repeat) and Cas proteins)
have the ability to effect precise genome
modifications that were inconceivable only
a few years ago. Using these techniques
it is possible to edit the genome at the
zygote stage, and we are exploring this
technology in livestock species
23
24
MYELOMA
RESEARCH
MYELOMA RESEARCH
LABORATORY
CONTACT DETAILS
SCHOOL: Medicine
SUPERVISORS
Prof Andrew Zannettino
Our laboratory studies the molecular

and cellular basis for the development
of the bone marrow cancer, multiple
myeloma. Myeloma is characterised
by the clonal proliferation of malignant
plasma cells (an immune cell type
that normally protects us against
infection). Myeloma is the second
most common blood cancer affecting
humans, with over 1,500 Australians
diagnosed each year. Despite recent
advances in treatment, myeloma
remains almost universally fatal with a
10 year survival rate of approximately
17%. The main clinical manifestations
of myeloma are the development of
osteolytic bone lesions, bone pain,
hypercalcaemia, renal insufficiency,
suppressed immunoglobulin production
and increased BM angiogenesis
(blood vessel formation). It is now
widely accepted that most, if not
all, cases of myeloma are preceded

by a premalignant (asymptomatic)
monoclonal gammopathy of uncertain
significance (MGUS) stage. However,
the genetic factors which trigger the
progression from this asymptomatic
stage of the disease to overt malignant
myeloma remains to be determined.
Moreover, recent studies suggest that
the bone marrow microenvironment
plays a central role in disease
progression. Our laboratorys research
is focussed on identifying the key genes
which are responsible for disease
progression and the role played by
the bone microenvirnment in disase
pathogenesis. We believe that these
approaches will enable us to identify
new molecular markers of disease
risk and to design drugs against novel
therapeutic targets.
+61 8 8222 3455

andrew.zannettino@adelaide.edu.au
Dr Stephen Fitter
Dr Duncan Hewett
Dr Sally Martin
Dr Jacqueline Noll
Dr Kate Vandyke
Dr Stanley Cheung
Dr Melissa Cantley
HONOURS COORDINATOR
A/Prof Chris Rayner
+61 8 8222 2916
Chris.rayner@adelaide.edu.au
Prof David Callen
+61 8 8222 3145
David.callen@adelaide.edu.au
Dr Lisa Butler
+61 8 8222 3270
Below: Professor Andrew Zannettino
Project 1 (a)
the development of MM. The cause

of this difference in susceptibility
remains to be determined. The
project is aimed at identifying genetic
differences between KaLwRij and
C57BL/6 mice that may underlie the
propensity of each strain to succumb
to, or resist myeloma disease
development, respectively.
Project 3: Determining the effects
of myeloma plasma cells on
mesenchymal stem cell (MSC)
differentiation
Project 1 (b)
Project 1: Identification of genetic

factors which trigger the progression
from asymptomatic MGUS to overt
malignant MM
What causes an individual patient to
progress from MGUS to MM is still
incompletely understood. Our group is in
the unique position of having assembled
a biospecimen bank comprised of
a large number of matched MGUS
and MM clinical samples taken from
patients at the time of diagnosis. Using
a comprehensive genomics approach,
we will identify structural and gene
expression changes between paired
MGUS/MM samples and to investigate
the biological roles of the candidate
myeloma genes using established
in vitro models and a mouse model
of myeloma that recapitulates human
disease
Project 2: Defining the role of the
bone marrow microenvironment in the
development MM
There is a growing appreciation of
the role played by the non-cancerous
or microenvironmental cells in the
development of malignancy. One area of
our research is dedicated to identifying
factors in the BM microenvironment that
contribute to the development of MM.
We have previously compared the gene
expression and cellular characteristics of
two strains of mice; the commonly used
laboratory strain C57BL/6 and the related
strain C57BL/KaLwRij. Although very
similar, subtle differences have developed
over time, the most striking being the
susceptibility of C57BL/KaLwRij mice to
Lytic lesions are a common feature

of MM. Notably; these lesions persist
beyond disease remission, suggesting
that MM PC mediate long-term changes
to the normal bone remodelling
process by inhibiting osteoblast
function. Osteoblasts are specialised
bone forming cells derived from
precursor pluripotent mesenchymal
stem cells (MSCs) that reside within
the bone marrow microenvironment.
We hypothesise that infiltration and
proliferation of MM plasma cells in
the BM could potentially alter the
differentiative potential of MSCs leading
to a deficiency in bone forming function
of osteoblasts. Using gene expression
profiling of MSC prior to and following
exposure to MM PC we aim to identify
the molecular mechanisms by which MM
plasma cells influence stem cell biology.
the components of these complexes

are common to both, they can be
distinguished by the presence of either
the Raptor protein or the Rictor protein.
Recent studies from our laboratory
have demonstrated that mTOR plays a
crucial role in bone development, with
inhibition of mTOR causing an increase
in bone formation. However, due to a
lack of specific inhibitors for Raptor
and Rictor, we are unable to delineate
which of the two mTOR complexes (or
perhaps both) is involved in this process.
We have developed a sophisticated
animal knockout model in which either
Raptor or Rictor expression is specifically
knocked out in bone cells. We will
use these animals to examine what
happens to bone growth in response
to bone-specific deletion of Raptor or
Rictor. These studies will enable us
to develop specific inhibitors of either
Raptor or Rictor in order to stimulate
bone formation in patients with myelomaassociated bone loss.
Project 4: Identifying the role of the

mTOR pathway in mesenchymal stem
cell biology and bone formation
mTOR is a key signalling protein
which regulates a number of cellular
processes by forming one of two multiprotein complexes. These multi-protein
complexes have both overlapping
and distinct roles, and while most of
Project 2
25
26
Zannettino AC. Imatinib mesylate

causes growth plate closure in vivo.
Leukemia. 2009;23(11):2155-2159.
5. Gronthos S, Zannettino AC.
Methods for the purification and
characterization of human adiposederived stem cells. Methods Mol
Biol. 2011;702:109-20. PubMed
PMID: 21082398.
6. Martin SK, Diamond P, Gronthos
S, Peet DJ, Zannettino AC. The
emerging role of hypoxia, HIF-1
and HIF-2 in multiple myeloma.
Leukemia. 2011 Oct;25(10):1533-42.
doi: 10.1038/leu.2011.122. Epub
2011 Jun 3. Review. PubMed PMID:
21637285.
Project 4 (a)
Project 4 (b)
Key References:
1. Diamond P, Labrinidis A, Martin SK,
Farrugia AN, Gronthos S, To LB,
Fujii N, OLoughlin PD, Evdokiou
A, Zannettino AC. Targeted
disruption of the CXCL12/CXCR4
axis inhibits osteolysis in a murine
model of myeloma-associated
bone loss. J Bone Miner Res. 2009
Jul;24(7):1150-61. Review. PubMed
PMID: 19335218.
2. Martin SK, Diamond P, Williams SA,
To LB, Peet DJ, Fujii N, Gronthos
S, Harris AL, Zannettino AC.
Hypoxia-inducible factor-2 is a
novel regulator of aberrant CXCL12
expression in multiple myeloma
plasma cells. Haematologica.
2010 May;95(5):776-84. Epub
2009 Dec 16. PubMed PMID:
20015878; PubMed Central PMCID:
PMC2864384.
3. Vandyke K, Dewar AL, Farrugia
AN, Fitter S, Bik To L, Hughes
TP, Zannettino AC. Therapeutic
concentrations of dasatinib inhibit in
vitro osteoclastogenesis. Leukemia.
2009;23(5):994-997.
7. Fitter S, Vandyke K, Gronthos S,

Zannettino AC. Suppression of
PDGF-induced PI3 kinase activity
by imatinib promotes adipogenesis
and adiponectin secretion. J Mol
Endocrinol. 2012 May 8;48(3):22940. Print 2012 Jun. PubMed PMID:
22474082.
8. Noll JE, Williams SA, Purton LE,
Zannettino AC. Tug of war in the
haematopoietic stem cell niche: do
myeloma plasma cells compete for
the HSC niche? Blood Cancer J.
2012 Sep 14;2:e91. doi: 10.1038/
bcj.2012.38. PubMed PMID:
PMC3461708.
9. Thomas D, Powell JA, Green BD, Barry
EF, Ma Y, Woodcock J, Fitter S,
Zannettino AC, Pitson SM, Hughes
TP, Lopez AF, Shepherd PR, Wei AH,
Ekert PG, Guthridge MA. Protein
kinase activity of phosphoinositide
3-kinase regulates cytokinedependent cell survival. PLoS Biol.
2013 Mar;11(3):e1001515. doi:
10.1371/journal.pbio.1001515.
Epub 2013 Mar 19. PubMed PMID:
PMC3601961.
10. Vandyke K, Chow AW, Williams SA,
To LB, Zannettino AC. Circulating
N-cadherin levels are a negative
prognostic indicator in patients with
multiple myeloma. British journal of
haematology. 2013;161(4):499-507.
4. Vandyke K, Dewar AL, Fitter S,

Menicanin D, To LB, Hughes TP,
CSN Therapeutics Laboratory
CSN THERAPEUTICS LABORATORY
Lysosomal Disease Research

Unit
LYSOSOMAL DISEASE
RESEARCH
CONTACT DETAILS
DISCIPLINE: Paediatrics
SUPERVISOR
Dr Kim Hemsley
The CNS Therapeutics Lab, located in the

new SAHMRI building, consists of 2 postdoctoral scientists, 5 scientists, 3 technical
officers and one PhD student and is part
of the Lysosomal Diseases Research Unit
(LDRU). The LDRUs research goal is early
diagnosis and treatment for all lysosomal
storage disorders (LSD). A large, wellestablished and multidisciplinary team,
the LDRU has been extremely successful
at both basic science and translating this
to successful clinical and commercial
outcomes.
LSD are inborn errors of metabolism
in which there is a mutation in a gene
encoding a lysosomal enzyme, resulting
in low or no production of that lysosomal
enzyme and subsequent accumulation
of substrate within cells. Progressive
neurodegeneration is seen in the majority
of LSD and most of these disorders have
no treatment at present, so affected
children often die in their early teens.
The CNS Therapeutics Lab primarily
utilises a mouse model of a
neurodegenerative LSD, known as MPS
IIIA (1, 2). Other disease models are also
being established. MPS IIIA is presently
untreatable and so we are examining
the cascade of neuropathological
changes that occur within the MPS IIIA
brain as a result of the accumulation
of substrate, and their response to
experimental treatments (3). Gaining a
better understanding of how the disorder
manifests will permit effective application
of therapies.
regions during development will be

evaluated, in order to determine their
contribution to cognitive dysfunction.
Students involved in these studies
will gain experience in a variety of
techniques including the handling
and use of a viral (gene therapy)
vector, performance of stereotaxic
surgery, mouse handing, post-surgical
monitoring and post-mortems and the
performance of immunohistochemistry
techniques using epifluorescence
and confocal microscopy-based
imaging and analysis. Molecular and
biochemical assays may also be
utilised.
+61 8 8128 4906

kim.hemsley@sahmri.com
HONOURS COORDINATOR
Dr Cheryl Shoubridge
+61 8 8161 8105
cheryl.shoubridge@adelaide.edu.au
A/Prof Simon Barry
+61 8 8161 8105
References:
1. Bhaumik et al (1999). A mouse model
for mucopolysaccharidosis type III A
(Sanfilippo syndrome). Glycobiology.
9: 1389-1396.
2. Crawley et al (2006) Characterization
of a C57BL/6 congenic mouse strain
of mucopolysaccharidosis type IIIA.
Brain Res. 1104: 1-17.
3. Hassiotis et al (2014) Disease stage
determines the efficacy of treatment
of a pediatric neurodegenerative
disorder. Eur. J. Neurosci. 39: 21392150.
Project: (Basic) Elucidating the

basis of cognitive dysfunction in
a murine model of a paediatric
neurodegenerative disorder
The Honours projects on offer in the
lab will examine the anatomical and
physiological basis for the development of
cognitive disease in the MPS IIIA mouse
model. Both structural and neurochemical
changes occurring in discrete brain
27
28
OVARIAN
DEVELOPMENTAL
BIOLOGY
OVARIAN DEVELOPMENTAL
BIOLOGY LABORATORY
CONTACT DETAILS
SUPERVISOR
Prof Ray Rodgers
+61 8 8313 3932
Which comes first the chicken or the

egg? Whatever the correct answer is,
without ovaries there would be no eggs.
The primary function of the adult ovary
is to mature and release eggs and
additionally secrete hormones such as
oestrogen and progesterone. These
control the reproductive cycle and
gestation. Understanding the formation
of the ovary and its ovarian follicles that
contain the germ cells is paramount.
The study of developmental biology
of the ovary and the role of stem cells
offers unique opportunities for student
to develop cell and developmental
biology knowledge and skills. Our team
has a long history in this area being the

first to describe stem cells in the ovary
in 1994 [1] through to developing a new
model on how the ovary develops [2]
and identifying a stem cell niche [3]. We
offer a number of projects but prefer
to tailor projects to suit the skill and
knowledge base of students. We are a
cell and molecular biological laboratory
using cell culture, molecular biology
including bioinformatic approaches and
immunohistochemistry to name a few.
Initial enquiries should be directed to
Prof Ray Rodgers.
ray.rodgers@adelaide.edu.au
HONOURS COORDINATOR
Dr Kathy Gatford
+61 8 8313 4158
+61 8 8313 4093 / +61 8 8313 4090
Below: Professor Ray Rodgers
Project 1: Granulosa Stem Cells

Within the ovary eggs mature inside
follicles and these in turn grow by
replication of the cells of the follicle
wall, namely granulosa and thecal
cells. These cells produce the ovarian
hkrmones, oestrogen and progesterone.
Therefore, replication of granulosa cells
is critically important, both for hormone
production and for maturation of eggs.
In fact, the number of eggs released
and the timing of egg release is partially
regulated via the cell fate decisions
of the granulosa cells. Our group
focuses on the roles of extracellular
matrix in regulating cell behaviour in
the mammalian follicle. We were the
first to identify that granulosa cells
arise from a population of stem cells
and to characterize them (reviewed
in [1]). However, limited studies have
been conducted on these cells. They
could be critical to understanding
conditions such as premature ovarian
failure, sterility induced by radiation
treatment for cancer, infertility, hormone
imbalances, as well as for developing
new in vitro technologies for maturing
eggs.
Project 2: Regulation of GREL Cell
Lineages
The precursor cell to both the surface
epithelium of the ovary and to the
somatic epithelial cells of the ovarian
follicle called granulosa cells, are
GREL cells of the developing ovary [2].
We first identified these cells in fetal
ovaries and called them gonadal-ridge
epithelial-like cells. We have isolated
these cells and conducted expression
microarray analyses to identify markers
of them. However, they have not been
well characterised yet. Additionally
what controls the decision of their cell
fate is still unknown. Knowing this has
implication for understanding some
forms of ovarian cancer and also the
development of the ovarian reserve of
primordial follicles.
Using antibodies to extracellular matrix

motifs found in stem cell niches in a
variety of other tissues we identified a
niche around smaller growing follicles
and associated with larger vessels
that develop and surround the larger
growing follicles. This has not been
investigated further at this stage.
Knowing how thecal cells arise is very
important for the study of polycystic
ovary syndrome [5] where there is
excess theca and excess androgens
produced. PCOS is the commonest
endocrine condition of women of
reproductive age, affecting about 5% of
that population.
3. Glister C, Satchell L, Bathgate RA,

Wade JD, Dai Y, Ivell R, AnandIvell R, Rodgers RJ, Knight PG
(2013) A functional link between
Bone Morphogenetic Proteins and
Insulin-like Peptide 3 signaling
in modulating ovarian androgen
production. Proc Natl Acad
Sci USA 110, doi =10.1073/
pnas.1222216110.
4. Hatzirodos N, Nigro J, Irving-Rodgers
HF, Vashi AV, Caterson B, Sullivan
TR and Rodgers RJ (2012)
Glycomic analyses of ovarian
follicles during development and
atresia. Matrix Biology 31, 45-56.
5. Hatzirodos N, Bayne RA, IrvingRodgers HF, Hummitzsch K,
Sabatier L, Lee S, Bonner W,
Gibson MA, Rainey WR, Carr BR,
Mason HD, Reinhardt DP, Anderson
RA, Rodgers RJ (2011) Linkage
of regulators of TGF activity in
the fetal ovary to polycystic ovary
syndrome. FASEB Journal 25,
2256-2265.
References:
1. Rodgers RJ, Lavranos TC, van Wezel
IL, Irving-Rodgers HF. Development
of the ovarian follicular epithelium.
Mol Cell Endocrinol 1999; 151:
171-179.
2. Hummitzsch K, Irving-Rodgers HF,
Hatzirodos N, Bonner W, Sabatier
L, Reinhardt DP, Sado Y, Ninomiya
Y, Wilhelm D, Rodgers RJ (2013)
A new model of development of
the mammalian ovary and follicles.
PLOS ONE 8(2):e55578.
Fig 1: Ovarian Stem cells (Modified from [1])
Fig 2: Proposed new model on how the ovary forms (from [2]).
Figure 7
a
Project 3: Thecal Stem Cells

A specialised stromal layer called the
theca interna, develops around each
ovarian follicle as it grows and enlarges
following its activation. The primary
role of the thecal cells is to synthesise
androgens, which act as precursors
for forming oestrogens [3]. Many have
speculated that thecal cells could
arise from a population of stem cells.
Where these reside is also conjectured.
Surface epithelium
Stromal cell
GREL cell
Fibre
Primordial germ cell
Granulosa cell
Capillary
Oogonia, oocyte
Basal lamina
29
30
DEVELOPMENT GENETICS
LABORATORY
DEVELOPMENTAL
GENETICS
CONTACT DETAILS
FACULTY: Sciences
SCHOOL: Molecular & Biomedical Science
DISCIPLINE: Biochemistry
SUPERVISORS
Prof Paul Thomas
+61 8 8313 7047
The development of the human brain

into a complex structure containing one
hundred billion cells is a fascinating
process that requires thousands of
genes. Mutations in genes that control
brain development in humans cause
common neurological disorders such
as mental retardation. Genetic studies
performed in mice have demonstrated
that the signaling systems and
transcriptional networks that coordinate
the differentiation of neuronal cell
types are highly conserved throughout
vertebrate evolution. Therefore,
genetically modified mice provide an
excellent system with which to investigate
the genetic control of neurogenesis and
to model human neurodevelopmental
disorders.
Our laboratory has shown that
duplication and mutation of the
transcription factor gene SOX3 is
associated with the mental retardation
syndrome X-linked Hypopituitarism (XH).
SOX3 is expressed in the stem cells
of the developing brain and is a key
regulator of neural differentiation. We
have developed mouse models with
altered dosage of SOX3 using gene
knockout and transgenic technology.
These mice exhibit abnormalities in brain
development that resemble patients
with XH. Our aim for the future is to
understand how SOX3 controls the
maintenance and differentiation of neural
stem cells at the molecular and cellular
level. Our research uses a range of
cutting-edge molecular genetic and cell
biology techniques including microarray,
fluorescence immunohistochemistry,
proteomics and gene targeting in
Embryonic Stem Cells.
that are regulated by this important

transcription factor. The aim of this
project is to identify genes that are
activated by SOX3 in the developing
mouse brain. This project is based
on microarray screens that we are
currently performing using mouse
embryos/neurospheres that lack SOX3
or overexpress SOX3. Differentially
expressed genes (ie putative SOX3 target
genes) will be validated using RealtimePCR and in situ hybridisation analysis of
wildtype, knock-out and transgenic Sox3
embryos. This is a fast moving area,
so if you would like an update or further
details please drop in for a chat!
References:
1. Jacqueline T.T. Wong, Peter G. Farlie,
Sebastien Holbert, Paul J. Lockhart
and THOMAS PQ (2007) Polyalanine
expansion mutations in the X-linked
hypopituitarism gene SOX3 result
in aggresome formation and
impaired transactivation. Frontiers in
Bioscience, 12, 2085-2095
2. Woods KS, Cundall M, Turton J, Rizotti
K, Mehta A, Palmer R, Wong J,
Chong WK, Al-Zyoud M, El-Ali M,
Otonkoski T, Martinez-Barbera JP,
Thomas PQ, Robinson IC, LovellBadge R, Woodward KJ, Dattani
MT. (2005) Over- and Underdosage
of SOX3 Is Associated with
Project 1: Identifying SOX3 target

genes (Honours or PhD project)
We have shown that SOX3 is a key
regulator of neurogenesis in mice and
humans. However, little is currently
known about the genes/pathways
Paul.thomas@adelaide.edu.au
Dr James Hughes
HONOURS COORDINATOR
Dr Keith Shearwin
+61 8 8313 5361
Keith.shearwin@adelaide.edu.au
Dr Kirk Jensen
+61 8 8313 3793
Kirk.jensen@adelaide.edu.au
Infundibular Hypoplasia and

Hypopituitarism. Am J Hum Genet.
76, 833-49
3. Rizzoti, K., Brunelli, S., Carmignac, D.,
Thomas, P.Q., Robinson, I.C.A.F.
and Lovell-Badge, R. (2004) SOX3
is required during the formation
of the hypothalamo-pituitary axis.
Nature Genetics, 36, 247-55
4. Solomon, N. M., Nouri, S., Warne,
G.L., Lagerstrom-Fermer, M.,
Forrest, S.M. and Thomas, P.Q.
(2002) Increased gene dosage
at Xq26-q27 is associated with
X-linked hypopituitarism (XH).
Genomics 79, 1-7
Below: Professor Paul Thomas
PERIODONTAL REPAIR
LABORATORY
PERIODONTAL
REPAIR
CONTACT DETAILS
SCHOOL: Dentistry
SUPERVISOR
Prof Mark Bartold
+61 8 8313 3436
Mark.bartold@adelaide.edu.au
To date repair of damaged periodontal

tissues relies on implantation of
structural substitutes with little or no
reparative potential. More recently,
tissue-engineering, based on an
understanding of the cell and molecular
biology of the periodontium, has
emerged as an interesting alternative
to existing therapies for periodontal
regeneration.
mesenchymal stem cell lineages.

Studies will assess the capacity
of differentiated iPS cells to form
functional periodontal tissues.
Prof Stan Gronthos
Project 3: Induction of Neural

Crest Cell Differentiation
from Periodontla iPS cells
Characterization and Utilization of
iPS cells for Dental Regeneration
+61 8 8313 3295
We have established the presence of

mesenchymal stem-like cells (PDLSC)
in both periodontal tissues capable
of sustained renewal and tissue
regeneration. We have also developed
induced-pluiropotent stem cells from
periodntla cells. We now hypothesize
that PDLSC can be used for cellular
based therapies to treat damaged
periodontal tissues.
These studies are aimed at

determining which cells from oral
sites allow for ease and efficiency
of obtaining neural crest cells from
periodontal iPS cells and to use the
most efficient source of oral cells
and investigate their utility for tissue
regeneration around teeth and dental
implants.
We collaborate extensively with the

Mesenchymal Stem Cell Research
Group, led by Associate Professor
Stan Gronthos at the Hanson Institute/
Institute of Medical and Veterinary
Sciences.
References:
Project 1: Dental mesenchymal stem

cells for tissue regeneration
2. Gronthos S, Mrozik K, Shi S,

Bartold PM. Ovine periodontal
ligament stem cells: Isolation,
characterization and differentiation
potential. Calcified Tissue
International 79: 310-317; 2006.
These studies involve the identification

and characterization of human and
ovine periodontal ligament stem
cells (PDLSC) and dental pulp stem
cells (DPSC). Studies will determine
the efficacy of different stem cell
preparations and biomaterials to repair
alveolar bone, cementum, dentin and
periodontal tissues using both ovine
models representative of different dental
defects.
1. Seo B-M, Miura M, Gronthos S,

Bartold PM, Batouli S, Brahim J,
Young M, Robey PG, Wang C-Y, Shi
S. Multipotent postnatal stem cells
from human periodontal ligament.
Lancet 364:149-155; 2004.
HONOURS COORDINATOR
Toby Hughes
Toby.hughes@adelaide.edu.au
Dr Neville Gully
+61 8 8313 3887
Neville.gully@adelaide.edu.au
3. Wada N, Wang B, LinN-H, Laslett

AL, Gronthos S, Bartold PM.
Induced pluripotent stem cell lines
derived from human gingival and
periodontal ligament fibroblasts
Journal of Periodontal Research
46: 438-447; 2011.
4. Xiong J, Mrozik K, Gronthos S,
Bartold PM. Epithelial cell rests of
Malassez contain unique stem cell
populations capable of undergoing
epithelial-mesenchymal transition.
Stem Cells & Development
(Accepted November 26, 2011)
5. Hynes KE, Menicanin D, Gronthos S,
Bartold PM Clinical utility of stem
cells for periodontal regeneration.
Periodontology 2000 59: 203-227;
2012.
Below: Professor Mark Bartold
Project 2: Induced Pluripotent Stem

Cells to regenerate Periodontal
Tissues
This work will explore whether induced
pluripotent stem cells derived from
periodntal tissues have the capacity
to develop down pathways towards
31
32
EMBRYONIC STEM
CELLS
REPRODUCTIVE
BIOTECHNOLOGY
LABORATORY
CONTACT DETAILS
SUPERVISORS
A/Prof Mark Nottle
The Reproductive Biotechnology

Laboratory has an international
reputation in the development of cutting
edge reproductive biotechnologies
for use in biomedical and agricultural
research.
These include the development of
somatic cell nuclear transfer, or cloning,
as it is more commonly known. The
groups research is increasingly
focused in the area of embryonic and
adult stem cells and uses the pig as
a model for humans in these fields.
The following topics are being offered
as Honours projects in 2010. These
projects will expose candidates to first
class research equipping them with a
wide range of skills in the general areas
of embryology, molecular and cellular
biology.
Project 1: Making embryos for
research
Our Laboratory uses in vitro produced
(IVP) pig embryos for much of its
research. This uses abattoir derived
ovaries from which oocytes are

removed, matured in culture, fertilised
and then cultured up to six days. While
IVP can produce embryos for research
purposes these are of a lesser quality
than those that would be found in the
reproductive tract. The current project
aims to improve one or more step in
this process so that we can ultimately
produce embryos of the same quality.
Honours and PhD project s are
available in this general area. And
will provide students with research
experience across a range of areas
including molecular and cell biology and
embryology
Project 2: Saving endangered
species
Somatic cell nuclear transfer or cloning
a sit more commonly know has
been proposed as a way of saving
endangered species. However this
approach is limited because not enough
oocytes are available from endangered
females. The use of oocytes from
+61 8 8313 4087

Mark.nottle@adelaide.edu.au
Dr Ivan Vassiliev
HONOURS COORDINATOR
Dr Kathy Gatford
+61 8 8313 4158
+61 8 8313 4093 / +61 8 8313 4090
another species has been proposed

as a way of overcoming this shortage.
However so called interspecies nuclear
transfer is still in its infancy. The current
project aims improve the efficiency of
interspecies nuclear transfer.
Honours and PhD projects are available
in this general area. And will provide
Below: Associate Professor Mark Nottle
students with research experience

across a range of areas including
molecular and cell biology and
embryology
Project 3: Reducing early embryonic
loss
Around 30% of embryos are lost early in
pregnancy. The reason for this unknown.
Our Lab is examining the hypothesis
that the majority of these losses are
due to difference in oocytes quality
as a result of changes in nutrition,
season, disease etc. In particular we are
examining how these influence oocytes
quality and embryo development
Honours and PhD project s are
available in this general area. And
will provide students with research
experience across a range of areas
including molecular and cell biology and
embryology
Project 4: Isolation and

characterisation of embryonic stem
cells
As human stem cell research advances
there is an increasing need for a
large animal model for bridging the
gap between mouse studies and
clinical trials. We have developed a
new method for isolating ESCs and
are using this to develop the pig as
a large animal model for stem cell
research. This includes the isolation
and characterisation of embryonic stem
cells from a range of sources including
parthenogenetic embryos.
Honours and PhD project s are available
in this general area. And will provide
students with research experience in cell
biology, embryology and stem cells
References:
1. Beebe LFS, McIlfatrick SM, Nottle
MB (2009) Adding essential
amino acids at a low concentration
improves the development of in
vitro fertilized porcine oocytes .
Reproduction and Development
55:373-377.
2. Beebe LFS, McIlfatrick SM, Nottle
MB. Effect of cytochalasin B
and Trichostatin A on somatic cell
nuclear transfer efficiencies in the
pig . Cloning and Stem Cells. 2009.
11:477-482
3. Vassiliev I, Vassilieva S, Beebe,
LFS, McIlfatrick SM, Harrison, SJ,
Nottle MB. In vitro and in vivo
characterisation of putative porcine
embryonic stem cells. Cloning and
Stem Cells. 2010 . 12: 223-230.
4. Vassiliev I, Vassilieva S, Truong KP,
Beebe LF, McIlfatrick SM, Harrison
SJ, Nottle MB. Isolation and in vitro
characterisation of putative porcine
embryonic stem cells from cloned
embryos treated with Trichostatin A.
Cellular Reprogramming 2011 13:
205-213.
5. Campbell JM, Nottle M, Vassiliev
I, Mitchell M , Lane M. insulin
increases epiblast cell number of in
vitro cultured mouse embryos via
the insulin P13K/GSK/p53 pathway.
Stem Cells and Development 2012
E pub ahead of print
Porcine retinal epithelial cells produced by the directed differentiation in vitro of

porcine embryonic stem cells in our Laboratory
33
34
STROKE RESEARCH
LABORATORY
STROKE
RESEARCH
CONTACT DETAILS
SCHOOL: Medicine
SUPERVISOR
Prof Simon Koblar
+61 4 06 928 658
A challenge for stem cell research in

neuroscience in the 21st century is how
to repair the brain following damage
from neurological disease or injury.
Stroke is the leading cause of disability
in the western world, and in Australia in
2010 there were 60,000 new cases of
stroke and over 250,000 people living
with the effects of stroke.
Neural stem cells have been found in
the brain, and studies suggest that in
the human brain following stroke there
is a stimulus to activate neurogenesis,
however this may be too little too late to
have any significant therapeutic benefit.
One therapeutic strategy to treat stroke
is to transplant stem cells derived from
adult tissues that have the ability to
differentiate into neurons and interact
with the brain.
The SRP investigates the use of stem

cells derived from the dental pulp of
the human tooth- dental pulp stem
cells (DPSC). We have investigated
the effects of DPSC delivered directly
to the brain in a rat model that has
undergone a surgically induced stroke,
demonstrating significant improvements
in motor function in rats treated with
DPSC compared to those that did not
receive any stem cells. From this study,
we want to investigate how these DPSC
are exhibiting their beneficial effects on
the stroke-affected animals.
Simon.koblar@adelaide.edu.au
HONOURS COORDINATOR
A/Prof Chris Rayner
+61 8 8222 2916
Prof David Callen
+61 8 8222 3145
The focus of this research is to use

a range of molecular, cellular and
electrophysiological tools to translate
stem cell therapy to the neurology clinic
and to one day improve the functional
outcome for patients disabled by stroke.
Below: Professor Simon Koblar
Project 1: Stem cell therapy in

stroke
Our aim is to understand how to repair
the brain following ischaemic stroke.
Stem cells have been shown to have
therapeutic potential, however, it
remains unknown as to which stem cells
will be most useful and how stem cells
will achieve this goal.
In 2000 Stan Gronthos, a collaborator,
discovered an adult human stem cell
from teeth, known as a Dental Pulp
Stem Cell (DPSC). We have published
that under optimum environmental
conditions DPSC may generate
functionally active neurons and, indeed,
coordinate neuroplastic changes in a
host neural system.
In 2009-10 we undertook our first preclinical study using DPSC in a rat model
of stroke. 24-hours following stroke we
injected 600,000 adult human DPSC
into the stroke brain. The animals were
closely monitored four weeks after
treatment and we found a significant
neuro-behavioural improvement
following DPSC treatment in comparison
to control animals (Leong et al 2012).
pulp derived cells, differs. This will allow

us to identify the best population of cells
for treatment after stroke.
The age of the dental pulp donor is another
factor that could impact on the neurogenic
potential of DPSC. We are interested
in determining whether autologous
transplantation may be possible for stroke
patients, 80% of which are over 55 years
of age. Thus, we will examine DPSC
from older teeth, and their potential to
differentiate into functional neurons.
Project 3: Mechanisms through
which DPSC improve functional
outcome after stroke
We have demonstrated that the intracerebral injection of DPSC results in
an improvement in brain function in a
rat model of stroke. However, we have
found, as have others, that few stem cells
survive long-term in the brain and the idea
that improvement is due to neural cell
replacement is highly unlikely. There are a
number of possible mechanisms of action
which may underlie how DPSC improve
brain function, which we are interested in
investigating:
We now hope to determine whether the

less invasive, more clinically relevant,
intravenous administration of DPSC can
also result in an improvement in stroke
outcomes.
How transplanted DPSC interact with

and influence endogenous neural
stem cells;
Project 2: Investigating the

neurogenic potential of DPSC

and influence the glial scar, which
forms in response to stroke and can
limit the repair of damaged tissue.
DPSC are a heterogeneous population

of cells, which have neurogenic potential.
We have been able to induce DPSC
to differentiate into cells with neuronal
morphology, expressing neuronal
markers, in vitro. However, the challenge
is to produce cells that have the
electrophysiological properties required
by functional neurons. We now plan to
investigate different methodologies for
neuronal induction of DPSC, with the aim
of generating functional neurons.

and influence the perineuronal net,
and thus promote neuroplasticity;
References
1. Leong WK, Lewis MD, Koblar SA.
(2013) Preclinical studies on
human cell-based therapy in rodent
ischemic stroke models: where are
we now after a decade? Stem Cells
31: 1040-1043
2. Arthur A, Rychkov G, Shi S, Koblar
SA, Gronthos S. (2008) Adult
Human Dental Pulp Stem Cells
differentiate towards functionally
active neurons under appropriate
environmental cues. Stem Cells 26
(7): 1787-1795
3. Arthur A, Shi S,Zannettino ACW,
Fujii N, Gronthos S, Koblar SA.
(2009) Implanted Adult Human
Dental Pulp Stem Cells induce
Endogenous Axon Guidance. Stem
Cells 27(9): 2229-2237
4. Leong WK, Henshall TL, Arthur A,
Kremer KL, Lewis MD, Helps
SC, Field J, Hamilton-Bruce MA,
Warming S, Manavis J, Vink R,
Gronthos S, Koblar SA. (2012)
Human adult dental pulp stem
cells enhance poststroke functional
recovery through non-neural
replacement mechanisms. Stem
Cells Translational Medicine 1:177187
5. Lees JS, Sena ES, Egan KJ, Antonic
A, Koblar SA, Howells DW, Macleod
MR. (2012) Stem cell-based
therapy for experimental stroke: a
systematic review and meta-analysis.
International journal of stroke : official
journal of the International Stroke
Society 7: 582-588
We also hope to investigate the

neurogenic potential of sub-populations
of dental pulp derived cells. In particular,
we are interested in p75 positive neural
stem cells, which are already dedicated
to differentiating down the neuronal
lineage. We plan to determine how the
neurogenic potential of p75 positive cells
alone, or in combination with other dental
35
36
RENAL AND
TRANSPLANTATION
RENAL AND
TRANSPLANTATION
LABORATORY
CONTACT DETAILS
SCHOOL: Medicine
SUPERVISORS
A/Prof Toby Coates
The Renal and Transplantation

Laboratory is developing cell-based
therapies to repair and replace tissues.
These include transplanting pancreatic
islet cells to treat Type-1 diabetes and
using mesenchymal stem cells and
endothelial progenitor cells to treat
kidney disease. We also investigate the
potential of Dendritic cells for preventing
the rejection of transplanted organs.
For up to date information on project
opportunities within this laboratory
please contact us.
Project 1: Enhancing pancreatic islet
transplantation for Type 1 Diabetes.
Type 1 Diabetes occurs when the
insulin-producing beta cells within the
Islets of Langerhans in the pancreas
are destroyed by a patients own
immune system. A potential cure is
islet transplantation, which is at the

clinical trial stage in Australia. As part
of the Australian Islet Consortium, our
laboratory examines ways in which islet
transplantation might be improved.
+61 8 8222 0934

Toby.coates@adelaide.edu.au
Dr Claire Jessup
Dr Robert Carroll
One factor limiting the success of

islet transplantation is that 70% of the
transplanted islets die after transplant.
Our research focuses on how islet
transplantation may be improved.
Techniques include gene therapy to
express anti-apoptotic or survival factors
and codelivery of vasculogenic cells to
increase the regrowth of blood vessels
in the pancreatic islets.
Dr Matthew Stephenson
Project 2: Cellular therapy to treat

kidney disease and kidney repair
after transplantation and injury
Prof David Callen
Dr Daisy Mohanasundaram
HONOURS COORDINATOR
A/Prof Chris Rayner
+61 8 8222 2916
+61 8 8222 3145

Endothelial progenitor cells are bonemarrow derived cells that are involved
in the formation and repair of blood
Below: Associate Professor Toby Coates
vessels. Mesenchymal stem cells are

multipotent cells that have the ability
to differentiate into a multitude of cells
types, and have immunosuppressive
properties.
Both of these cell types may be used
to improve the outcome of organ
transplants and potentially to repair
damaged organs before or after
organ transplantation. We are also
investigating the use of these rare
cell types to prevent or treat kidney
diseases.
Project 3: Dendritic cell therapy to
improve kidney transplantation
Dendritic cells are important for initiating
and directing immune responses
including those against transplanted
organs. A variety of approaches
are available to modify the function
of Dendritic cells to promote organ
acceptance after transplantation. These
include gene therapy to inhibit Dendritic
cell maturation and pharmacological
manipulation using NF-KB inhibitors to
promote the formation of T regulatory
cells (T reg). These approaches may
ultimately lead to the development of
organ transplant tolerance strategies,
to promote drug-free organ
transplantation.
References:
1. Cloning Stem Cells. 2007
Winter;9(4):564-70.
2. Bishop A.G., Ierino, F.L., Sharland,
A.F., Hall, B.M, Alexander, S.A.,
Sandrin, M.S., Coates P.T. ,
McCaughan, G.W., Approaching
the promise of Operational
Tolerance in clinical transplantation.
Transplantation 2011;91:1065-1074
regulatory T cells in vitro and in

vivo. Clinical and Experimental
Immunology 2010, 162 (3), 460473.
6. Sen, S, McDonald, S.P., Coates,
P.T. , Bonder C.S. , Endothelial
progenitor cells: novel biomarkers
and promising cell therapy for
cardiovascular diseases. Clin Sci
2011;120:263-83
3. Penko, D., Mohanasundaram, D.,

Sen, S., Drogemuller, C., Mee,
C., Bonder, C. S., Coates, P. T.,
Jessup, C. F., Incorporation of
endothelial progenitor cells into
mosaic pseudoislets. Islets 2011, 3
(3).73-79
4. Prasad, S.; Kireta, S.; Leedham,
E.; Russ, G. R.; Coates, P. T. ,
Propagation and characterisation
of dendritic cells from G-CSF
mobilised peripheral blood
monocytes and stem cells in
common marmoset monkeys.
Journal of Immunological Methods
2010, 352 (1-2), 59-70.
5. Rogers, N. M.; Kireta, S.; Coates, P.
T. Curcumin induces maturationarrested dendritic cells that expand
We are investigating the potential of

Dendritic cells to induce tolerance prior
to kidney transplantation.
Mouse islets | Dr Claire Jessup
37
38
VASCULAR BIOLOGY
AND CELLULAR
RECRUITMENT
VASCULAR BIOLOGY AND

CELLULAR RECRUITMENT
LABORATORY
CONTACT DETAILS
SCHOOL: Medicine
Delivery of blood occurs via an intricate

network of vessels distributed throughout
the body. As well as maintaining bodily
functions under normal conditions,
blood vessels are essential to support
tissue regeneration and the progression
of diseases such as cancer and
cardiovascular dusease. Improved
understanding of how blood vessels form
and the control of their development may
provide therapeutic opportunities and
great public health potential. The Vascular
Biology and Cell Trafficking Laboratory
focuses on endothelial cells (ECs) which
line the lumen of all blood vessels and thus
play a pivotal role in normal and disease
states.
The VBCT laboratory has three main
areas of interest. Firstly, during allergic
inflammation, ECs regulate leukocyte
recruitment via adhesion molecule
expression, we are interrogating this

process with an aim to block neutrophil
recruitment and attenuate allergic
inflammation. Secondly, endothelial
progenitor cells (EPCs) directly contribute
to blood vessel formation (vasculogenesis)
in the pathological settings of
cardiovascular disease, cancer, organ
transplantation. We recently identified
a new sub-population of EPCs and are
now interrogating these to identify new
targets for therapeutic application. Finally,
breast cancer and melanoma progress
via the a process called vasculaogenic
mimicry (VM). This is a process wherein
cancer cells themselves form vascular-like
structures to provide access to the blood
supply for nutrients and oxygen. We are
investigating the processes by which VM
occurs and are defining targets to prevent
cancer progression.
SUPERVISOR
Dr Claudine Bonder
+61 8 8222 3504
Claudine.bonder@health.sa.gov.au
Dr Lisa Ebert
HONOURS COORDINATOR
A/Prof Chris Rayner
+61 8 8222 2916
Prof David Callen
+61 8 8222 3145
Dr Lisa Butler
+61 8 8222 3270
Below: Doctor Claudine Bonder
Project 1: Endothelial progenitor cells

(EPCs) in disease
We recently identified a new population of
immature, non-adherent EPCs. These cells
are distinct from currently defined EPCs by
their non-adherence and immature phenotype
and likely represent the true circulating EPCs
which constantly survey the vasculature,
ready to respond to vascular injury for repair.
Examining these cells for therapeutic potential
is a major goal of the laboratory.
Project 2: EPCs in islet transplantation
naEPCs HUVEC matrigel_tagged
Pancreatic islet transplantation is an emerging

cure for Type 1 Diabetes but success is
limited by death of insulin producing beta
cells post-transplantation. EPCs have the
potential to improve islet engraftment and
function. Further development of an EPC:islet
interaction will greater advance the cure
for diabetes. This project is in collaboration
with Assoc/Prof Toby Coates and Dr Claire
Jessup.
Project 3: Vasculogenic mimicry in
cancer
Aggressive, invasive and metastatic breast
cancers correlate with increased vascular
density of the tumour through at least two
processes, (i) EPCs and (ii) vasculogenic
mimicry (VM) wherein cancer cells themselves
generate non-endothelial cell lined channels.
We have identified a unifying mechanism that
has the potential advantage of explaining
both of these processes for increased
vascularisation associated with breast cancer
progression. Investigating this is a major goal of
the laboratory.
References:
1. Appleby S, Cockshell M, Pippal J,
Thompson E, Barrett J, Tooley K, Sen S,
Sun W, Grose R, Nicholson I, Levina V,
Cooke I, Talbo G, Lopez A and Bonder
CS. Characterization of a distinct
population of human endothelial forming
cells and their recruitment via ICAM-3.
PloS ONE, 7(11): e46996, 2012
FITClectin insulin mouse islet
melanoma VM.
WY, Drogemuller C, Coates PTH, Bonder

CS, Jessup CJ. Endothelial progenitor
cells enhance islet engraftment,
influence beta cell function and
modulate connexin 36 expression. Cell
Transplantation, in press
See http://www.centreforcancerbiology.org.
au/Bonder.htm for recent publications and
additional details of the Research Group and
projects.
2. Sen S, McDonald S, Coates PTH and

Bonder C.S. Endothelial Progenitor
Cells: Novel Biomarker and Promising
Cell Therapy for Cardiovascular Disease.
Clinical Science 120(7):263-83, 2011
3. Penko D, Mohanasundaram D, Drogemuller
D, Bonder CS, Coates PTH, Jessup CJ.
Incorporation of endothelial progenitor
cells into mosaic pseudoislets. Islets,
3(3), 1-7, 2011
4. Penko D, Rojas-Canales D, Peiris H, Sun
39
40
NOTES
NOTES
41
FOR FURTHER
INFORMATION
For further information on Honours
and/or postgraduate study opportunities
please speak with your potential supervisor.
For further information regarding enrolment
please contact the relevant faculty or the
Student Centre:
Faculty of Health Sciences
T: +61 8 8313 5336
F: +61 8 8313 3788
E: health.sciences@adelaide.edu.au
W: www.health.adelaide.edu.au/
For general enquiries relating to the Centre

for Stem Cell Research please contact us
directly:
The Centre for Stem Cell Research
Level 6, Medical School North Building
The University of Adelaide
South Australia 5005 Australia
E: stemcell@adelaide.edu.au
W: www.adelaide.edu.au/stemcell
Faculty of Sciences
T: +61 8 8313 3890
F: +61 8 8313 4386
E: faculty.sciences@adelaide.edu.au
W: www.sciences.adelaide.edu.au/
Student Centre
T: +61 8 8313 5208
E: studentcentre@adelaide.edu.au
W: www.adelaide.edu.au/student/future/
2 THE UNIVERSITY OF ADELAIDE
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CENTRE FOR

STEM CELL RESEARCH

POSTGRADUATE RESEARCH OPPORTUNITIES

STUDENT PROJECT BOOKLET FOR 2015

Human nerve and glial cells | Wai Khay, PhD student

THE 4 STEPS TO ENROLMENT

ABOUT THE CENTRE

A/Prof Mark Nottle & Prof Stan Gronthos

BROWSE this booklet to determine a group or project

REFER to the blue panel on each of the research group

CONTACT a specific supervisor directly to discuss a

WHEN the supervisor agrees to take you on as an

ABOUT THE CENTRE

What are the entry requirements?

What is involved in Honours?

The Centre does not have subject

The Honours program varies depending

Assessment of the Honours year will

Some Honours programs also include

A critical assessment of relevant

If the supervisor agrees to take you

Students from any University who have

Throughout the year candidates are

Critical literature review: 15%

If you have decided that you would

The Masters Program

The PhD Program

A Masters degree involves one to

A PhD is the basic qualification for a

The decision to undertake Masters

A PhD thesis may comprise a

demonstrated the capacity to evaluate

demonstrate a deep knowledge of the

presented a clear and well-written

relate the research topic to the

Whilst a number of Masters degrees

If the supervisor agrees to take you

Information for Future Students

The University offers a range of Honours

The University of Adelaide scholarships

More information on scholarships is also

There are a number of professional

Student Centre, level 4, Wills Building

University of Adelaides Research

Information for International Students

The candidates school or discipline

Marketing & Strategic Communications Office - The University of Adelaide

Vascular Biology and Cellular Recruitment Laboratory

Project 1: Mesenchymal stem cells in skeletal tissue regeneration

Project 1: Molecular identification of Regulatory T cells

Project 1: Granulosa Stem Cells

Project 1: Identifying SOX3 target genes

Project 1: Dental mesenchymal stem cells for tissue regeneration

Project 1: Making embryos for research

Project 1: Stem cell therapy in stroke

Project 1: Enhancing pancreatic islet transplantation for Type 1 Diabetes

Project 1: Endothelial progenitor cells (EPCs) in disease

Our major focus is to understand the

leukaemia. These receptor-activated

Below: Professor Richard DAndrea

+61 8 8222 3636

Project 1: -catenin activation and