PhD prospectus

Institute Cancer Sciences

Phd Studies Institute Cancer Sciences 2017 2

Contents
Message from the Head of the Institute of Cancer Sciences .................................................. 3
Introduction ........................................................................................................................... 4
Institute of Cancer Sciences .................................................................................................. 5
CORE STAFF ....................................................................................................................... 6
Academic Co-ordinator ...................................................................................................... 6
Administrative Support ....................................................................................................... 6
PhD PROJECTS AVAILABLE ......................................................................................... 7-20
APPLICATION PROCEDURE ............................................................................................ 21
ADDITIONAL INFORMATION FOR APPLYING ................................................................. 22
UNIVERSITY COMMUNICATION CHANNELS .................................................................. 23
Online resources and IT services .................................................................................... 23
Library ............................................................................................................................ 23
Research seminars ......................................................................................................... 23
GENERAL INFORMATION ................................................................................................ 24
Attendance ..................................................................................................................... 24
TIER 4 ............................................................................................................................ 24
SENATE/COLLEGE/UNIVERSITY INFORMATION ............................................................ 25
General Information ........................................................................................................ 26
Complaints ..................................................................................................................... 26
Other information ............................................................................................................ 27
Accommodation, Health and Wellbeing ........................................................................... 27
Student Finance & Money ............................................................................................... 28
Other useful information .................................................................................................. 28
International student information ..................................................................................... 28
Phd Studies Institute Cancer Sciences 2017 3

Message from the Head of the Institute of Cancer Sciences

I would like to welcome you to apply to the University of Glasgow to join the Institute of
Cancer Sciences (ICS), PhD training programme.

Founded in 1451, the University of Glasgow is the fourth oldest university in the English -
speaking world with a long standing tradition of Excellence in Research and Teaching.
Among its alumni are amongst others the father of economics Adam Smith, Scotland’s
architect of devolution Donald Dewar, and renowned physicist and engineer Lord Kelvin to
name but a few.

We at the University of Glasgow are very proud of our teaching achievements and are
always striving for excellence by putting students first. The University is a member of the
prestigious Russell Group of leading UK research universities, and has been rated fourth in
the UK for international student satisfaction (among universities participating in the
International Student Barometer Summer 2013), and the most recent national survey placed
the University of Glasgow second equal in the Russell Group and second outright in
Scotland in terms of student satisfaction.

The ICS itself is a broad-based, research intensive institution with a global reach. It spans
fundamental cancer biology, translational and clinical cancer research with a major focus on
cancer genomics and disease-specific research. The ICS also spans four campuses, at the
Garscube Estate (adjacent to the CRUK Beatson Institute), Gartnavel (including the Paul
O’Gorman Leukaemia Research Centre [POG-LRC] and the Beatson West of Scotland
Cancer Centre), Glasgow University Main Campus and the New South Glasgow Hospital. Its
primary goal is to deliver world-class research that can be translated to patient benefit and to
provide a leading-edge environment for research and training.

Our PhD training programme will build on these strengths and aims to prepare you well for
your future career in Cancer Science.

I wish you all an enjoyable and successful time here at Glasgow University.

Prof Jeff Evans

Phd Studies Institute Cancer Sciences 2017 4

Introduction
Thank you for your interest in undertaking your postgraduate training at the University of
Glasgow. This prospectus will provide you with information regarding the PhD projects
currently available within the Institute of Cancer Sciences and guidance on the application
procedure.

The Graduate School supports all postgraduates in our Schools and Institutes, implementing
best practice for training and support. We provide a vibrant, supportive and stimulating
environment where all our postgraduate students experience an excellent multidisciplinary
research environment, excellence in supervision and mentoring, interactive discussion
groups and seminars and an atmosphere that fosters critical thinking and research analysis
at its best. We aim to produce students confident in embracing new techniques and skills
required to answer their particular research problems.

Our over-arching aim is to provide a research training environment that includes:

- provision of excellent facilities and cutting edge techniques
- training in essential research and generic skills
- synergy between research groups and areas
- extensive multidisciplinary and collaborative research
- extensive external collaborations both within and beyond the UK
- a robust generic and specific scientific skills programme

We aim to provide excellent support for our postgraduates through dedicated postgraduate
convenors, highly trained supervisors and pastoral support for each student.
For further information on the Graduate School please follow this link:

http://www.gla.ac.uk/colleges/mvls/graduateschool/

The University of Glasgow mission is to undertake world leading research and to provide
intellectually stimulating learning environments that benefits culture, society and the
economy. The ICS has the ideal infra-structure, facilities and staff to provide excellent
postgraduate training leading to a successful PhD and future career in cancer science.
Phd Studies Institute Cancer Sciences 2017 5

The Institute of Cancer Sciences consists of four main centres on three site;

http://www.gla.ac.uk/researchinstitutes/cancersciences/contact/

Wolfson Wohl Cancer Research CR-UK Beatson Institute, University

Centre, University of Glasgow, of Glasgow, Garscube Estate, G61
Garscube Estate, G61 1QH 1BD

Paul O’Gorman Leukaemia McGregor Building, University of

Research Centre, Gartnavel Hospital Glasgow, University Avenue, G12
Site, G12 0ZD 8QQ
Phd Studies Institute Cancer Sciences 2017 6

CORE STAFF
Academic Co-ordinator

Dr Joanne Edwards is the Post Graduate Convenor for the Institute of Cancer Sciences. In
addition to your two supervisors, you can discuss your academic progress and any
personal issues that are affecting your studies with the PGR Convenor.

Dr Joanne Edwards
PGR convenor
Institute of Cancer Sciences
Wolfson Wohl Cancer Research
Centre, Garscube Estate,
Glasgow G61 1QH
Email:Joanne.Edwards@glasgow.ac.uk
Tel +44(0)141 330 7244

Administrative Support

Fiona Conway is the administrator for the PhD training programme, and should be the
contact for any non-academic questions.

Mrs Fiona Conway

Institute of Cancer Sciences
Wolfson Wohl Building, Garscube Estate
Glasgow, G61 1QH
Email:Fiona.Conway@glasgow.ac.uk
Tel: +44(0)141 330 4890

Dr Sylvia Morrison
Head of Institute Administration
Institute of Cancer Sciences
Wolfson Wohl Building, Garscube Estate
Glasgow, G61 1QH
Email: Sylvia.morrison@glasgow.ac.uk
Tel: +44(0)141 330 2690
Phd Studies Institute Cancer Sciences 2017 7

Step 1: Selection of PhD project

Image courtesy of Dr. Julia Cordero

Stem cells in tissue homeostasis and transformation
Phd Studies Institute Cancer Sciences 2017 8

Title 01: Microenvironment in paediatric and adult acute myeloid leukaemia

Supervisors: Dr Karen Keeshan and Prof Brenda Gibson
E-mail address: Karen.keeshan@glasgow.ac.uk
Webpage: http://www.gla.ac.uk/researchinstitutes/cancersciences/staff/karenkeeshan/

Abstract: Acute myeloid leukaemia (AML) is a genetically and phenotypically heterogeneous

disease that is characterized by a block in myeloid differentiation, as well as enhanced proliferation
and survival. It affects people of all ages with an incidence of 2-3 per 100 000 per annum in children,
increasing to 15 per 100 000 per annum in older adults. The relapse risk for childhood AML remains
unacceptably high and relapse is the commonest cause of death. Multiple courses of chemotherapy
remain the mainstay of treatment in adult and childhood AML but a ceiling of benefit has been
reached and toxicity is significant (Chaudhury et al, 2015). There have been few, if any, new
treatments in the past 30 years and there is a pressing need for novel effective therapies in AML.
The treatment of paediatric AML is in essence extrapolated from that of adults with AML. Our
previous work (Chaudhury et al, 2015) in addition to recent timely publications (Beerman et al 2015)
have questioned the appropriateness of this approach which assumes that a similar aetiology
underlies AML in the young and old. There is additional evidence that disease characteristics differ
between a paediatric and adult population with AML (Appelbaum 2006; Creutzig et al. 2008).
Functional interplay between AML cells and the bone marrow microenvironment is a distinctive
characteristic of AML disease. AML cells in the adult bone marrow BM reside in leukaemic niches
(Colmone et al 2008) that support leukaemic cell survival and expansion. The importance of the
microenvironment in paediatric versus adult AML (fetal liver, cord blood, bone marrow) and its role is
disease characteristics has not been well explored. Our lab focuses on the proliferation and self-
renewal capabilities of the leukaemic cell and the influence of the leukaemic niche. We hypothesize
that the microenvironment influences the initiation, maintenance, and aggressiveness of paediatric
and adult AML disease.
Methods & approaches: This project will investigate the role of the microenvironment in AML disease
initiation and maintenance. W e will focus on genetically distinct subtypes of paediatric and adult
using a number of models and approaches including: Bone marrow transduction and transplantation
(BMT) murine models: expression of AML oncogenes in viral constructs and using CRISPR/Cas9
gene editing approaches; assessments on disease in vivo; Stromal co-cultures and transcriptional
profiling using haematopoietic stem cells; primary AML samples from paediatric and adult patients.
The project will also employ flow cytometry, cellular and molecular biology technologies. This PhD
studentship offers extensive dual training in both fundamental and translational biology of leukaemia,
an environment encompassing clinical and basic researchers, and training opportunities as part of
the college graduate program.

References:
1. Chaudhury SS, Morison JK, Gibson BES, Keeshan K. Insights into cell ontogeny, age and acute
myeloid leukaemia. Experimental Hematology. 2015 Jun 4.
2. Beerman I, Rossi DJ. Epigenetic Control of Stem Cell Potential during Homeostasis, Aging, and
Disease. Cell Stem Cell. 2015 Jun;16(6):613–25.
3. Appelbaum, F.R., 2006. Age and acute myeloid leukemia. Blood, 107(9), pp.3481–3485.
4. Creutzig, U. et al., 2008. Significance of age in acute myeloid leukemia patients younger than 30
years: a common analysis of the pediatric trials AML-BFM 93/98 and the adult trials AMLCG 92/99
and AMLSG HD93/98A. Cancer, 112(3), pp.562–571.
5. Colmone A, Amorim M, Pontier AL, W ang S, Jablonski E, Sipkins DA. Leukemic cells create bone
marrow niches that disrupt the behavior of normal hematopoietic progenitor cells. Science.
2008;322(5909):1861-1865.
Phd Studies Institute Cancer Sciences 2017 9

Title 02: SWATH Proteomic analysis to identify putative biomarkers to predict disease related
complications involved in Polycythaemia Vera
Supervisors: Dr Helen Wheadon and Professor Mhairi Copland
E-mail address: Helen.Wheadon@glasgow.ac.uk; Mhairi.Copland@glasgow.ac.uk
Webpage: http://www.gla.ac.uk/researchinstitutes/cancersciences/staff/helenwheadon/

Abstract: Polycythaemia Vera (PV) is a haemopoietic stem cell disease, with ~95% of patients
having the V617F JAK2 mutation, which results in constitutive activation of the JAK/STAT signalling
pathway, leading to increased myelopoiesis and high erythrocyte counts. Patients also suffer from
symptoms related to chronic inflammation, which is thought to explain, in part, the increased risk of
thrombosis. Chronic inflammation is well recognised as a driver of atherosclerotic plaque formation
and a risk for development of arterial and venous thromboembolism in patients with autoimmune
conditions and other chronic medical illnesses, but the evidence for this in PV is only just starting to
become available. It is known that an elevated white cell count in PV is associated with an increase
in arterial events, and this appears to relate to inappropriate activation of the haemopoietic cells
resulting in a pro-coagulation phenotype, however there is much that remains unclear about what
drives these symptoms. One avenue worth exploring is the role of monocytes in PV related
thrombotic and cardiovascular complications. Intermediate monocyte frequency has recently been
identified as a positive predictor of cardiovascular events playing a significant role in inflammation
through high secretion of TNFand IL-1. Intermediate monocytes also express CCR2 and CCR5,
which are critical for monocyte homing and trans-endothelial migration into atherosclerotic plaques.
Platelet activation and blood coagulation is also initiated at the site of injury by
monocyte/macrophage secreted exosomes which contain tissue factor and P-selectin glycoprotein
ligand-1 (PSGL-1) on their surface. Work from the Wheadon/Copland laboratory has recently
identified significantly higher intermediate monocyte frequency in PV patients compared to normal
aged matched control donors and high levels of pro-inflammatory cytokines/chemokines in PV
patient serum. Recent interest has focused on the role that exosomes play in immune regulation,
especially in neoplasms. Exosomes are homogenous membrane vesicles (40-150nm diameter),
derived from the exocytosis of intraluminal vesicles and released into the extracellular space when
fused to the plasma membrane. The majority of cells including haemopoietic cells release exosomes,
with malignancy specific exosomes, expressing cell of origin cluster of differentiation (CD) antigens
identified in leukaemia and PV. Exosomes are important for the extracellular transfer of proteins,
lipids, mRNAs, microRNAs and DNAs to neighbouring cells where they can alter the function of the
recipient cell. Tumour-derived exosomes (TEX) are released both locally and into the circulation to
interact with a variety of cell types, including immune cells. TEX have been shown to alter
immunoregulatory mechanisms such as; antigen presentation, immune activation, immune
suppression, immune surveillance and cell communication. It is known that erythrocytes retain their
microRNA content during maturation and that they secrete exosomes, however their functional role is
still not clearly defined. One could postulate that the exosomes act as immunosuppressive signals
given that erythrocyte homeostasis requires the constant removal of damaged or aged erythrocytes
6
(2x10 per second) via phagocytes within the liver, spleen or lymph nodes. How erythrocyte
exosomes modulate immune responses and whether this is altered in PV patients still remains to be
investigated, as does the role of monocyte and erythrocyte derived TEX in PV related complications
namely chronic inflammation and thrombotic events.
Hypothesis/research question: Are tumour-derived exosomes involved in the chronic inflammatory
and pro-coagulation symptoms experienced by Polycythaemia Vera patients?
Aims/objectives:
1. Mathematical evaluation to determine cells of origin of exosomes in PV patients and normal aged
matched donor plasma.
2. SWATH profiling to identify novel biomarkers involved in PV pathophysiology
3. Evaluate Ruxolitinib, hydroxycarbamide (HC), statins and aspirin treatment on TEX secretion &
TEX effects on the inflammasome and coagulation.

References:
1.Hasselbalch, H.C., Perspectives on chronic inflammation in essential thrombocythemia, polycythemia
vera, and myelofibrosis: is chronic inflammation a trigger and driver of clonal evolution and
development of accelerated atherosclerosis and second cancer? Blood, 2012. 119(14): p. 3219-25.
2.Hulsmans, M. and P. Holvoet, MicroRNA-containing microvesicles regulating inflammation in
association with atherosclerotic disease. Cardiovasc Res, 2013. 100(1): p. 7-18.
3. Stansfield, B.K. and D.A. Ingram, Clinical significance of monocyte heterogeneity. Clin Transl Med,
2015. 4: p. 5.
4.Caivano, A., et al., High serum levels of extracellular vesicles expressing malignancy-related markers
are released in patients with various types of hematological neoplastic disorders. Tumour Biol, 2015.
5. Greening, D.W., et al., Exosomes and their roles in immune regulation and cancer. Semin Cell Dev
Biol, 2015. 40: p. 72-81.
 Phd Studies Institute Cancer Sciences 2017 10

Title 03: Epigenetic profiling of blood and lung cancer stem cells for precision medicine
Supervisors: Dr. Xu Huang
E-mail address: xu.huang@glasgow.ac.uk
Webpage: http://www.gla.ac.uk/researchinstitutes/cancersciences/staff/xuhuang/

Normal development of adult tissues relies on balanced self-renewal and differentiation of tissue stem
and progenitor cells, whereas the abnormal activation of self-renewal or blockage of differentiation
pathways, could lead to the malignant cell proliferation and oncogenesis. Leukaemia stem cells (LSCs)
as a rare cell population present in Acute Myeloid Leukaemia (AML), confer chemotherapy resistance
and are responsible for maintenance and relapse of the disease. Precision medicine requires
eradication of LSCs for long term remission in AML, yet the detailed mechanism driving the oncogenic
dysregulation in LSC still remains elusive. Epigenetic regulators play essential roles in cooperating with
transcription factors to control gene expression required for LSC maintenance. The recent development
of several pharmacological inhibitors targeting these regulators, such as BRD4 and Dot1L, highlights the
great potential for them as promising anti-tumour targets. We have utilised a high throughput lentivirus
shRNA screen to identify the critical epigenetic regulators, knock-down of which in human AML cells
promoted AML LSC terminal myeloid differentiation and/or led to the loss of their self-renewal capacity,
resulting in rapid cell death while sparing normal haemopoietic stem cell function. This suggests that
targeting these candidates could represent rational novel therapeutic intervention in AML.
Hypothesis In this project, we will focus on further validating the prioritised candidates from our previous
screen, in primary AML patient samples and in our established human AML xenograft mice model. We
hypothesise that these identified epigenetic regulators are required to sustain specific LSC centred
epigenomic profiles, through association with distinct chromatin complex(es) in human AML cells
compared to normal bone marrow cells, which are responsible for selectively maintaining LSC function.
Aims and Methodology The PhD candidate will employ systems biology approaches utilising combined
genomics/proteomics (such as SILAC-IP-MS, RNA-seq and ChIP-seq) and bioinformatics analysis with
following aims:
1) to determine epigenomic profiles in AML LSCs, which are associated with the specified epigenetic
regulator;
2) to investigate the cellular and molecular mechanisms through which the specified regulator selectively
targets human AML LSCs;
i: to identify the components of the unique chromatin complex with which the candidate selectively
associates in human AML.
ii: to identify the candidate’s downstream targets in human AML.
3) to evaluate the use of the available epigenetic inhibitors in AML and provide information to facilitate
and optimise the development of potent preclinical/clinical-grade drug(s).
Overall, this PhD project is expected to advance our understanding underlying the important role of
epigenetic regulators in human AML LSC. The information will be used to initiate the next stage of drug
discovery and propose effective combination treatments with other standard AML therapies. The
knowledge acquired in this study can also be applied to research of other cancer types. Our preliminary
data indicate similar roles of particular epigenetic regulators in both blood and non-small cell lung
carcinoma (NSCLC). The student will also be encouraged to use NSCLC cells as an alternative model
for parallel studies in this project, and broaden our view on the role of epigenetic pathways in other stem
cell derived solid tumours.
References:

1. Huang X et al. Enhancers of Polycomb EPC1 and EPC2 sustain the oncogenic potential of MLL
leukaemia stem cells. Leukemia (2014) 28: 1081-91.

2. Harris WJ et al. The histone demethylase KDM1A sustains the oncogenic potential of MLL-AF9
leukemia stem cells. Cancer Cell (2012) 21: 473-487.

3. Jude JG et al. A targeted knockdown screen of genes coding for phosphoinositide modulators
identifies PIP4K2A as required for acute myeloid leukemia cell proliferation and survival. Oncogene
(2015) 34: 1253-1262.
Phd Studies Institute Cancer Sciences 2017 11

Title 04: Elucidating the role of APOBEC3B in CML stem cell

survival Supervisors: Dr Heather Jørgensen; Mhairi Copland
E-mail address: heather.jorgensen@glasgow.ac.uk; mhairi.copland@glasgow.ac.uk
Webpage: http://www.gla.ac.uk/researchinstitutes/cancersciences/staff/
heatherjorgensen/
Abstract: Small molecule tyrosine kinase inhibitors (TKIs), such as imatinib, form the standard
therapy for BCR-ABL1 driven chronic myeloid leukaemia (CML). However we have shown that CML
leukaemia stem cells (LSC) are insensitive to these drugs, which cause cell cycle arrest rather than
apoptosis resulting in disease persistence in patients that are very unlikely to be cured using TKI
monotherapy. In the search for complementary targets to BCR-ABL1 in CML LSC, we have carried
out global gene expression profiling between normal haematopoietic stem cells (HSC) and CML
LSC. A key finding was that LSC, but not normal HSC, show up-regulation of several genes,
including Apolipoprotein B mRNA editing enzyme (APOBEC3B). One of the major cellular functions
of APOBEC3 proteins is the derepression of microRNA (miR)-mediated protein translation inhibition.
Upregulation of miRs through targeted inhibition of APOBEC3B may have therapeutic effect in CML
by re-enabling tumour suppressor functions of miRs, including down-regulation BCR-ABL1. In this
project, miR signatures will be validated in CML, as they relate to APOBEC3B activity; the effect of
APOBEC3B neutralisation on miR function, and the modulation of miR function on primary BCR-
ABL1+ cell function will be investigated with a view to translating therapeutic targeting to the clinic.

References:
1. Holyoake T, Vetrie D, Cancer: Repositioned to kill stem cells. Nature 2015;525(7569):328.
2. Hershkovitz-Rokah et al, Restoration of miR-424 suppresses BCR-ABL activity and sensitizes
CML cells to imatinib treatment. Cancer Lett 2015;360:245.
3. Huang et al, Derepression of microRNA-mediated protein translation inhibition by apolipoprotein B
mRNA-editing enzyme catalytic polypeptide-like 3G (APOBEC3G) and its family members. J Biol
Chem 2007;282:33632.
4. Swanton C et al, APOBEC Enzymes: Mutagenic fuel for cancer evolution and heterogeneity.
Cancer Discov 2015;5(7):704.
5. Jurkovicova D et al, microRNA expression profiling as supportive diagnostic and therapy prediction
tool in chronic myeloid leukemia. Neoplasma 2015;62(6):949.
Phd Studies Institute Cancer Sciences 2017 12

Title 05: Identify Novel Drug Targets in Chronic Myeloid Leukaemia using a Genome-scale
CRISPR-knockout Approach
Supervisors: Dr Vignir Helgason
E-mail address: Vignir.Helgason@glasgow.ac.uk
Webpage: http://www.gla.ac.uk/researchinstitutes/cancersciences/staff/vignirhelgason/

Abstract: Chronic myeloid leukaemia (CML) is caused by a reciprocal translocation between

chromosomes 9 and 22 leading to transcription of the fusion protein BCR-ABL, a constitutively active
tyrosine kinase. The tyrosine kinase inhibitor (TKI) imatinib has significantly improved life expectancy
in the majority of patients, however, TKI-treated CML patients continue to accumulate mutations over
time and acquired TKI-resistance remains a significant problem for patients who currently need to
continue TKI indefinitely1-3. While the mechanism of BCR-ABL dependent resistance has been
thoroughly investigated (mainly caused by mutations in the tyrosine kinase domain of ABL4),
relatively little is known about the mechanism(s) that drive BCR-ABL independent resistance and the
therapeutic options for this group of patients are limited and expected survival short. It is therefore
hoped that this patient population, that currently experiences rare responses to TKI treatment, may
share an alternative drug target that can be inhibited with a novel compound.
So far, investigation into the mechanism(s) responsible for TKI resistance has been limited by the
lack of availability of suitable cell line modes. We have therefore recently developed TKI-resistant
CML cell lines with acquired BCR-ABL independent resistance (no mutation in kinase domain of
BCR-ABL). To our knowledge this is the first time that TKI-resistant CML cell lines that continue to
proliferate in the absence of BCR-ABL activity have been generated. This provides us with a unique
opportunity to explore what drives BCR-ABL independent resistance in CML.
The aim of this project is to perform genome-scale CRISPR-knockout screens to identify
mechanism(s) of BCR-ABL independent TKI-resistance and search for novel drug targets. W e have
already optimised all methods required to perform loss-of-function genetic screens using the
genome-scale CRISPR-Cas9 knockout (GeCKO) v2 library5. Using this approach we will identify
genes that are critical for survival of TKI-resistant CML cells in the presence of complete BCR-ABL
inhibition. Positive hits will be validated on patient-derived CML cells (from patients not responding to
TKI treatment) and the best pre-clinical murine models available. The ultimate aim is to facilitate the
development of a pre-clinical package to be tested in future clinical trials for patients with CML,
resistant to currently licensed TKIs through a BCR-ABL independent mechanism.

References:
1. Jiang, X., et al. Instability of BCR-ABL gene in primary and cultured chronic myeloid leukemia
stem cells. Journal of the National Cancer Institute 99, 680-93 (2007).
2. Holyoake, T.L., et al. Do we need more drugs for chronic myeloid leukemia? Immunological
reviews 263, 106-23 (2015).
3. Karvela, M., et al. Mechanisms and novel approaches in overriding tyrosine kinase inhibitor
resistance in chronic myeloid leukemia. Expert Rev Anticancer Ther 12, 381-92 (2012).
4. Hochhaus, A., et al. Molecular and chromosomal mechanisms of resistance to imatinib (STI571)
therapy. Leukemia 16, 2190-6 (2002).
5. Sanjana, N.E., et al. Improved vectors and genome-wide libraries for CRISPR screening. Nature
methods 11, 783-4 (2014).
Phd Studies Institute Cancer Sciences 2017 13

Title 06: Identification and characterisation of drug-able neurotransmitter signalling pathways

in acute myeloid leukaemia (AML)
Supervisors: Dr David Vetrie, Dr Xu Huang and Professor Mhairi Copland
E-mail address: David.Vetrie@glasgow.ac.uk; Xu.Huang@glasgow.ac.uk;
Mhairi.Copland@glasgow.ac.uk
Webpage: http://www.gla.ac.uk/researchinstitutes/cancersciences/staff/davidvetrie/

Abstract: Acute myeloid leukaemia (AML) is the most common form of acute leukaemia with an
incidence in the U.K. of ≈ 4 cases/100,000 individuals and with 2250 cases diagnosed each year. It is
characterised by a clonal hierarchy of malignant myeloid blast cells, and within each clone, a sub-
population of cells known as leukaemia stem cells (LSCs) are considered to be the critical cells for
maintenance and relapse of the disease. Standard AML chemotherapies such as daunorubicin and
cytarabine, have evolved slowly since the 1970s and do not eradicate LSCs. Furthermore, AML is
heterogeneous with sub-types characterised by different DNA mutations. DNA rearrangements of the
mixed lineage leukaemia (MLL) gene are found in 70% of childhood and 10% of adult cases, and
these forms of AML have particularly poor prognosis with 5 year survival rates between 11-38%.
Neurotransmitter signalling plays a role in haematopoiesis within the bone marrow and has been
shown to be important for the maintenance of cancer cells in medulloneuroblastoma,
myeloproliferative neoplasms and AML, among others. In AML, dopamine receptors have been
shown to be important for the survival of leukaemic stem and progenitor cells. Treating AML cells
with the dopaminergic antagonist thioridazine, a repurposed anti-psychotic drug (that is non-toxic to
normal haematopoiesis), was shown to kill AML cells in combination with low dosages of cytarabine.
This demonstrated that compounds targeting neurotransmitter signalling may provide novel
therapeutic options for AML – and improve clinical outcome and reduce toxicity associated with
standard chemotherapies. Recently we have demonstrated a role for neurotransmitter signalling in
CML cells and that treatment with thioridazine can result in cell loss, particularly of primitive primary
CD34+ cells. We have extended these observations to perform a compound screen in relevant cell
lines and in primary CML and non-CML CD34+ cells and have identified neurotransmitter signalling
antagonists and agonists that selectively kill CML cells in vitro. We are currently evaluating these
compounds as potential novel therapeutics in CML.
For the reasons stated above, there is a significant unmet clinical need in AML that can only be
addressed through the development of novel therapeutics, particularly for aggressive MLL-AML, and
to eradicate LSCs. Based on previous work in AML and other cancers, and our ongoing
complementary work in CML, we hypothesize that the identification and characterisation of
compounds that modulate neurotransmitter signalling, will allow us to develop novel therapeutics that
can target the selective loss of leukaemic stem and progenitor cells in AML. The aims of this project
are:

Aim 1. To identify compounds which modulate neurotransmitter signalling and selectively reduce the
leukaemic stem and progenitor cell pool, when compared to normal stem and progenitor cells, in
vitro, and in vivo using xenotransplantation.

Aim 2. To validate the molecular mechanism of action (MOA) of compounds and identify specific
genes/proteins which are differentially induced or repressed during modulation of neurotransmitter
signalling in AML progenitor and stem cells LSCs when compared to HSCs.

References:
1. Passegue, E. et al. P.N.A.S. 30: 11842-11849. (2002).
2. Bonnet, D & Dick, JE. Nat. Med. 3: 730-737 (1997).
3. Diamandis, P., et al. Nature Chemical Biology 3: 268-273 (2007).
4. Sachlos, E., et al. Cell 149: 1284-1297 (2012).
5. Arranz, L., et al. Nature 512: 78-81 (2014).
Phd Studies Institute Cancer Sciences 2017 14

Title 07: Investigation of BET and MDM2 inhibitors as a candidate novel combination therapy
for AML
Supervisors: Professor Mhairi Copland and Professor Peter Adams
E-mail address: p.adams@beatson.gla.ac.uk; Mhairi.Copland@glasgow.ac.uk
Webpage: http://www.gla.ac.uk/researchinstitutes/cancersciences/staff/peteradams/

Abstract: In 2015, there will be approximately 2400 new cases of AML in the United Kingdom
(https://www.hmrn.org/statistics/survival). After diagnosis, five year survival is currently ~15.5%.
Therefore, there remains a critical requirement for novel therapies for AML. Bromodomain and extra-
terminal domain (BET) inhibitors are emerging as exciting therapeutic agents for hematopoietic
malignancies, including AML [1]. Pharmacological inhibition of BET bromodomains targets malignant
cells by preventing reading of acetylated lysine residues, thus disrupting chromatin-mediated signal
transduction, which reduces transcription at oncogenic loci, such as c-myc, Bcl-2 and cdk4/6
[1]. Although a heterogeneous disease, most AML retains wild type p53 [2]. However, p53 is often
rendered functionally deficient by over-expression of MDM2 [3]. Accordingly, we hypothesized that
dual inhibition of MDM2 and BET would be synthetic lethal to p53 wild type AML. In extensive
studies, we have confirmed this hypothesis both in vitro and in vivo.

Hypothesis
We hypothesize that BET inhibitors potentiate activation of p53 to promote cell cycle arrest and
apoptosis. W e will: 1) investigate the mechanism by which BET inhibitors potentiate activation of p53
by nutlin; 2) Investigate the mechanism of p53-dependent cell cycle arrest and cell killing.

Objective 1. Investigate mechanism by which BET inhibitors potentiate activation of p53 by

nutlin. We hypothesize that BET inhibitors potentiate activation of p53 by promoting binding of p53
to specific target gene regulatory sides and/or enhancing the activity of chromatin-bound p53. W e
further hypothesize that this depends on the ability of BET inhibitors to control p53 post-translational
modification and/or interaction with associated proteins. W e will dissect these hypotheses to
elucidate the mechanism of p53 activation by BET inhibitors.

Objective 2. Investigate mechanism of cell cycle arrest and cell killing. We hypothesize that
marked G1 cell cycle arrest and apoptosis induced by the drug combination depends, at least in part,
on expression of synergistically activated pro-apoptotic and cell cycle arrest p53 target genes, such
as PUMA and CDKN1A (p21CIP1) respectively.

Completion of these studies will justify the testing of nutlin and BET inhibitors in a human
clinical trial to be led from Glasgow.

References:
1. Gallipoli P, Giotopoulos G, Huntly BJ: Epigenetic regulators as promising therapeutic targets in
acute myeloid leukemia. Ther Adv Hematol 2015, 6:103-119.
2. Hou HA, Chou WC, Kuo YY, Liu CY, Lin LI, Tseng MH, Chiang YC, Liu MC, Liu CW, Tang JL, et
al: TP53 mutations in de novo acute myeloid leukemia patients: longitudinal follow-ups show the
mutation is stable during disease evolution. Blood Cancer J 2015, 5:e331.
3. Kojima K, Konopleva M, Samudio IJ, Shikami M, Cabreira-Hansen M, McQueen T, Ruvolo V, Tsao
T, Zeng Z, Vassilev LT, Andreeff M: MDM2 antagonists induce p53-dependent apoptosis in AML:
implications for leukemia therapy. Blood 2005, 106:3150-3159.
Phd Studies Institute Cancer Sciences 2017 15

Title 08: The role of the extracellular matrix and stromal heparan-sulphate proteoglycans
(HSPGs) in the regulation of growth factor-induced mammary branching and breast cancer
cell growth
Supervisors: Dr Torsten Stein and Professor Joanna Morris
E-mail address: Torsten.Stein@glasgow.ac.uk
Webpage:http://www.gla.ac.uk/researchinstitutes/cancersciences/research/units/pathology/tst
ein/research/

Abstract: Epithelial-stromal interactions are crucial for the dramatic morphological changes
encountered during mammary gland development, and many of the associated mechanisms have
been shown to be deregulated in breast cancer and required for tumour growth1. Therefore, studying
how the stroma influences epithelial cell behaviour during normal development will help to better
understand the stromal effects on epithelial cancer cell growth, migration and invasion.
Postnatal ductal branching morphogenesis during mammary gland development can be described as
controlled multicellular invasion. It is tightly controlled by local growth factors and associated with
significant changes in the surrounding extracellular matrix (ECM). Many of these growth factors need
to bind to heparan-sulphate proteoglycans (HSPGs) for full activity2. Indeed, HSPGs have been
described as ‘master modulators’ of paracrine signalling between fibroblasts and both normal and
cancer epithelial cells3. However, which HSPGs play a role in controlling growth factor-induced
mammary branching morphogenesis or breast cancer growth is poorly understood.
We have recently identified several HSPG-encoding RNAs in mammary fibroblasts from early
pregnant mice (manuscript in preparation), and in collaboration with Prof R. Hynes’ group, MIT, have
identified HSPGs specifically localised around the growing mammary epithelium. Further, recent
studies have shown that heparanase, which removes HS groups, is localised around the growing tips
of the growing pubertal mammary ducts (terminal end buds) and influences mammary branching
morphogenesis4. W e therefore hypothesise that HSPGs are involved in regulating ductal epithelial
lateral branching in a paracrine fashion, and may be associated with breast cancer growth.
In a previous study, we have shown that the ECM surrounding growing mammary epithelium is very
distinct5. We have now optimised ECM enrichment conditions from mouse mammary glands, which
will allow us to characterise the ECM proteins associated with mammary epithelial outgrowth using
proteomic analysis. We hypothesise that the ECM proteins associated with the growing epithelium
may also be found in breast cancer, enhancing cancer growth and invasion.
Aim 1: The characterisation of the role of the previously identified stromal HSPGs in controlling
growth factor-induced mammary branching morphogenesis and in breast cancer.
Aim 2: The identification of ECM proteins associated with the onset of mammary branching
morphogenesis, their localisation in the growing mouse mammary gland during branching
morphogenesis, and their expression in the breast cancer microenvironment in vivo;
Objectives:
For aim 1: A) To measure the effect of over-expression or shRNA-mediated knock-down of
previously identified pregnancy-associated stromal HSPGs on mammary epithelial branching
morphogenesis, using an in vitro 3D co-culture model; B) To assess the effect of fibroblast HSPG
expression on breast cancer cell line growth in 3D co-culture; C) To measure expression
(epithelial/stromal) of these HSPGs by IHC using breast cancer tissue microarrays.
For aim 2: A) To isolate ECM-enriched protein fractions from pooled mammary glands from 3-day
pregnant and age-matched control mice; B) To perform quantitative mass spectrometric analysis on
these samples, using TMT-labelling and ion-trap mass spectrometry, and identify differentially
expressed ECM proteins by bioinformatic analysis; C) To localise identified differentially-expressed
proteins in the mammary gland and in breast cancer tissue microarrays by immunohistochemistry.

References:
1. Lanigan F et al., Molecular links between mammary gland development and breast cancer. Cell
Mol Life Sci. 2007 Dec;64(24):3159-84.
2. Yayon A et al., Cell surface, heparin-like molecules are required for binding of basic fibroblast
growth factor to its high affinity receptor. Cell 1991, 64:841-848.
3. Friedl A. Proteoglycans: Master Modulators of Paracrine Fibroblast - Carcinoma Cell Interactions.
Semin Cell Dev Biol. 2010 Feb;21(1):66-71.
4. Gomes AM et al., Mammary Branching Morphogenesis Requires Reciprocal Signaling by
Heparanase and MMP-14. J Cell Biochem. 2015 Mar 3. [Epub ahead of print]
5. Olijnyk D et al., Fibulin-2 is involved in early extracellular matrix development of the outgrowing
mouse mammary epithelium. Cell Mol Life Sci. 2014 Oct;71(19):3811-28.
Phd Studies Institute Cancer Sciences 2017 16

Title 09: Killing cancer cells - screen if you want to go faster

Supervisors: Dr Stephen Tait and Prof Kevin Ryan
E-mail address: stephen.tait@glasgow.ac.uk
Webpage: http://www.gla.ac.uk/researchinstitutes/cancersciences/staff/stephentait/

Abstract: Inhibition of cell death both promotes cancer and makes it more difficult to treat -
consequently intense interest surrounds restoring cell death sensitivity to tumour cells in order to kill
them. The major form of programmed cell death is apoptosis. Apoptosis requires a key event called
mitochondrial outer membrane permeabilisation in order to kill the cell. Mitochondrial integrity is
tightly controlled by pro- and anti-apoptotic members of the Bcl-2 protein family. Many cancers inhibit
apoptosis by up-regulating anti-apoptotic Bcl-2 protein expression; this has led to development of
potent new drugs - called BH3-mimetics - that neutralise anti-apoptotic Bcl-2 function thereby
restoring apoptotic sensitivity to cancer cells.
While BH3-mimetics work very well as single agents in certain types of leukemia, their efficacy in
other cancer types is less pronounced. Additionally, as with all targeted therapies, inherent or
acquired resistance to BH3-mimetic treatment limits their effectiveness. Using this rationale, this
project aims to identify regulators of sensitivity to BH3-mimetic induced killing. It will use genome-
wide screens, applying CRISPR/Cas-9 genome editing, to identify sensitizing targets, followed by
subsequent mechanistic basis of action studies. Finally, we will apply this knowledge to assess the
impact of targeting selected hits on the effectiveness of BH3-mimetic treatment in vivo.

References:
1. Ichim G et al. Limited mitochondrial permeabilization causes DNA damage and genomic instability
in the absence of cell death. (2015) Molecular Cell 57:860.
2. Haller M et al. Ubiquitination and proteasomal degradation of ATG12 regulates its pro- apoptotic
activity. (2014) Autophagy 10:2269.
3. Lopez J and Tait SW. Mitochondrial apoptosis: killing cancer using the enemy within. (2015) British
Journal of Cancer 112:957.
4. Tait SW et al. Widespread mitochondrial depletion via mitophagy does not compromise
necroptosis. (2013) Cell Reports 5:878.
5. Tait SW et al. Resistance to caspase-independent cell death requires persistence of intact
mitochondria. (2010) Developmental Cell 18:802.
Phd Studies Institute Cancer Sciences 2017 22

APPLICATION PROCEDURE

Step 2: Contact the supervisor to discuss the proposed project in detail and to confirm their
willingness to host you in their laboratory group.

Step 3: Apply through the MVLS postgraduate on-line system

Application process

Follow the link below which will guide you through the application process;

http://www.gla.ac.uk/research/opportunities/howtoapplyforaresearchdegree/

Please ensure that all supporting documents are uploaded at point of application:
 Academic ability evidence
 CV/Resume
 Degree certificate
 Language test (if relevant)
 Passport
 Personal statement
(This should provide any other required information in support of the application,
such as evidence of previous academic or professional experience that qualifies you
for the programme (projects; placements; voluntary work etc.). You should state the
reasons why you selected this programme and what benefit you hope to achieve
through successful completion of the programme. The statement should include
information about lab techniques you have used and research projects in which you
have been involved. The statement should not be longer than two A4 page).
 Reference 1 (should be from an academic who has knowledge of your academic
ability from your most recent study/programme)
 Reference 2 (should be from an academic who has knowledge of your academic
ability)
 Transcript

Step 4: All documents will be assessed by the recruitment and international office (RIO) to
assess whether you have the correct level of qualifications and English standard to enter into
Post-graduate training at the University of Glasgow.

Step 5: Once approved by RIO you will be given a written English task followed by a formal
panel interview with members of the ICS staff via Skype.

Step 6: Formal offer letter will be issued with proposed start date to commence your
postgraduate training at the University of Glasgow, School of MVLS, within the Institute of
Cancer Sciences.
Phd Studies Institute Cancer Sciences 2017 23

ADDITIONAL INFORMATION

Connect to the MVLS website

http://www.gla.ac.uk/colleges/mvls/graduateschool/researchopportunities/internationalstudents/

Here you will find the following booklets and advice on the following topics;

 International student handbook

 Extending your student visa
 Entry Clearance Correction Scheme
 Inviting family members
 Immigration advice
Phd Studies Institute Cancer Sciences 2017 24

UNIVERSITY COMMUNICATION CHANNELS

Online resources and IT services

When you start the programme you will be given a GUID. The GUID is your
registration/matriculation number followed by the first letter of your surname, and allows you
access to:-
Computer clusters (CSCE)
Remote CSCE desktop service
Moodle
Email
IT Services training courses online booking
Helpdesk self service
Wireless and remote access
Library access to all Ejournals and databases
MyGlasgow including MyCampus

Please use the following links for:-Information on registration, enrolment and inductions-
http://www.gla.ac.uk/studentlife/support/
IT Services- http://www.gla.ac.uk/services/it/forstudents/

Library

Your student card allows you access to the James Herriot Library on the Garscube campus,
and the main library on the Gilmorehill campus. The college librarian can help you find
information and show you how to use databases effectively.
http://www.gla.ac.uk/services/library/

Student-staff feedback

The Staff-Student Liaison Committee (SSLC) provides a forum for staff and students to
discuss matters of mutual interest.

The SSLC is important because:

1. It allows staff and students to discuss ideas and to solve problems

2. It forms the basis for the representation of students’ views within the Subject, School or
Graduate School and identifies concerns which require consideration beyond the Subject,
School or Graduate School
3. It is a formal, qualitative means of consulting students and gauging opinion on academic
matters and soliciting suggestions for improvements/enhancements
4. It provides a mechanism for obtaining student feedback and communicating action taken
in response to feedback.

A SSLC meeting will be held every 4 months. We 2 years we ask for 2 student
representative for the SSLC, whose role is to consult their fellow research students and
represent their views at the SSLC meeting held with the PGR convenor, assistant PGR
Phd Studies Institute Cancer Sciences 2017 25

convenors and PGR support staff. SSLC representatives will be asked to attend a training
session, and their role will be recorded on their transcript.

Research Seminars
You are encouraged to attend seminars related to your PhD and any others that you are
interested in.

The Friday ICS seminar series will be held on a fortnightly basis, at 3:30 pm on alternate
Fridays, in the WWCRC Seminar Room, followed by drinks in the WWCRC Cafe. The list of
speakers will be posted on the ICS website.

Regular seminars by local and visiting speakers are also held in the Robertson Trust Lecture
Theatre (Beatson Institute of Cancer Research) and elsewhere in the university. You will
receive a note of the seminars via email.

GENERAL INFORMATION

ATTENDANCE
The University has a Student Absence Policy and covers attendance requirements and
procedures for reporting absences. Students must complete a MyCampus absence report
for any significant absence from the University, and should email Fiona Conway to confirm
this. Significant absence includes:
1) an absence of more than seven consecutive days during working periods;
2. an absence of any duration if it prevents a student from:
a. attending an examination, or
b. fulfilling any other published minimum requirements for the award of credit (e.g.
compulsory attendance at a tutorial or laboratory class or meeting a deadline for
handing in an assignment).

Supporting documentary evidence will be required and should be scanned electronically. For
details on our absence policies please refer to:
http://www.gla.ac.uk/services/registry/

TIER 4

In 2008, the UK Government introduced the Points Based System (PBS) of immigration for
non-EEA/Swiss nationals who wish to work and study in the UK. There are 5 tiers of
immigration under the PBS with Tier 4 being the student category. The University acts as a
sponsor for non-EEA/Swiss students under Tier 4 (Sponsor Licence Number: TRAW6PAA8)
and the Tier 4 Compliance Team within the Registry is responsible for ensuring that a range
of areas relating to the University’s Sponsor Licence are met.
You are expected to participate fully in your studies whilst you are in the UK, ensuring that
you meet the attendance requirements of your course and comply with the University’s
procedures for monitoring student attendance. As your visa sponsor, the University has a
Phd Studies Institute Cancer Sciences 2017 26

duty to notify the Home Office if you withdraw from your programme of study or if, having
failed to engage with your studies or attended a number of scheduled contact points, it is felt
that you are no longer academically active and should be withdrawn. Your permission to
remain in the UK will, as a consequence, be withdrawn by the Home Office.

The University of Glasgow is required by the Home Office to hold a copy of the passport
photo ID page, visa (or Leave to Enter the UK) and Biometric Residence Permit (if you have
been issued with one) for all international students, including those on a Tier 4 Visa. You
must also provide the University with further copies of these documents if they are updated
or renewed during your studies. In addition, the University must notify the Home Office if
students holding a Tier 4 student visa to study at the University of Glasgow do not register.
You will therefore need to register your visa with the University when you arrive in Glasgow.

If you fail to complete registration, you will not be able to begin your studies. Students
arriving out with the main registration periods are required to bring their passport and visa to
the Student Services Enquiry Desk- http://www.gla.ac.uk/students/sset/ on Level 2 of the
Fraser Building between the following times:

Monday to Friday, 0900 - 1600 (except Wednesday, 0930 - 1600)

Your attendance at previous check-ins, as well as attendance at your course contact points
during the current academic year, will be assessed to determine whether you are still
present and engaged with you studies, if you still have valid permission to study in the UK, or
whether you should be withdrawn from your program of study. If you are withdrawn, we will
notify the Home Office who will take steps to curtail your visa.

SENATE/COLLEGE/UNIVERSITY INFORMATION

Please consult the following weblinks for the most up to date information on these topics:
Phd Studies Institute Cancer Sciences 2017 27

General Information

 MyCampus - http://www.gla.ac.uk/students/myglasgow/
 Student Information Directory - Further information on all services and facilities
available to you at the University can be found at: http://www.gla.ac.uk/students/
 Students’ Representative Council (SRC)- https://www.glasgowstudent.net/
 Role of the SRC in supporting students- https://www.glasgowstudent.net/about/
 Executive Officers- http://www.glasgowstudent.net/
 Advice Centre- http://www.glasgowstudent.net/advice/
 University Calendar (Regulations) College Section
http://www.gla.ac.uk/services/senateoffice/calendar
 Data Protection and Freedom of Information-
http://www.gla.ac.uk/services/dpfoioffice/
 University and Public Holidays-
http://www.gla.ac.uk/services/humanresources/all/worklife/publicholidays/public/
 Student Voice Website - Find out how you can provide the University with feedback
on your experience as a student at Glasgow.
(http://www.gla.ac.uk/services/senateoffice/qea/studentengagement/studentrepresent
ationstudentvoice/)
 Social Networking Guidelines: Students, and the University, are increasingly using
social media to interact personally and with learning. Engagement with social media
can be a useful and supportive tool for learning but it can also lead to very public
declarations or statements. Students are encouraged to use social media but to
approach it sensibly and be conscious of security settings, the permanence of
information online and the context of comments. The SRC have some food for
thought here: http://www.glasgowstudent.net/advice/health-and-safety/social-
networking/

Complaints

If you have a complaint please raise it with a member of staff in the area concerned. We aim
to provide a response to the complaint within five working days. This is Stage 1.
If you are not satisfied with the response provided at Stage 1 you may take the complaint to
Stage 2 of the procedure. Similarly, if your complaint is complex, you may choose to go
straight to Stage 2. At this stage the University will undertake a detailed investigation of the
complaint, aiming to provide a final response within 20 working days.
You can raise a Stage 2 complaint in the following ways:
by e-mail: complaints@glasgow.ac.uk; by phone: 0141 330 2506
by post: The Senate Office, The University of Glasgow, Glasgow, G12 8QQ
in person: The Senate Office, Gilbert Scott Building, The University of Glasgow.
Complaints do not have to be made in writing but you are encouraged to submit the
completed Complaint Form (available at
http://www.gla.ac.uk/services/senateoffice/studentcodes/students/complaints/) whether it is
at Stage 1 or Stage 2. This will help to clarify the nature of the complaint and the remedy that
you are seeking.
Remember that the SRC Advice Centre is available to provide advice and assistance if you
are considering making a complaint. (Tel: 0141 339 8541; e-mail: advice@src.gla.ac.uk).
Phd Studies Institute Cancer Sciences 2017 28

Other information

 Certifying letter- http://www.gla.ac.uk/students/sset/

 Change of contact details- http://www.gla.ac.uk/services/registry/registration/
 Changing or leaving course- http://www.gla.ac.uk/services/registry/registration/
 Fraser Building: Student Service enquiry team-
http://www.gla.ac.uk/students/enquiries/
 Graduation- http://www.gla.ac.uk/services/registry/graduation/
 ID cards- http://www.gla.ac.uk/students/sset/idcards/
 Language support- http://www.gla.ac.uk/schools/mlc/eas/
 Library- http://www.gla.ac.uk/services/library/
 References- http://www.gla.ac.uk/services/registry/registration/
 Registration- Certifying letter- http://www.gla.ac.uk/services/registry/registration/
 Student learning service- http://www.gla.ac.uk/services/sls/
 Transcripts- http://www.gla.ac.uk/services/registry/registration/
 Useful forms- http://www.gla.ac.uk/services/registry/registration/
 University Bookshop- http://www.johnsmith.co.uk/gla
 Computing & IT:
 IT helpdesk - www.gla.ac.uk/services/it/helpdesk/
 IT training - www.gla.ac.uk/services/it/training/
 Residential IT support -
http://www.gla.ac.uk/services/residentialservices/residentialitsupport/
 Student webmail- http://www.gla.ac.uk/students/myglasgow/
 Virtual Learning Environments:
 Moodle- http://www.gla.ac.uk/services/moodle/

Accommodation, Health and Wellbeing

 Council tax - http://www.gla.ac.uk/services/registry/registration/

 Halls minibus - http://www.glasgowstudent.net/services/minibus/
 Residential IT support -
http://www.gla.ac.uk/services/residentialservices/residentialitsupport/
 Residential services - http://www.gla.ac.uk/services/residentialservices/
 TV License- http://www.glasgowstudent.net/advice/accommodation/tv-licensing/
 Advice and counselling - http://www.gla.ac.uk/services/counselling/
 Childcare - http://www.gla.ac.uk/services/nursery/
 Student disability - http://www.gla.ac.uk/services/disability/
 Disabled Access Campus Map - http://www.gla.ac.uk/services/disability/
 Health and wellbeing, doctors and dentists -
http://www.gla.ac.uk/students/wellbeing/supportservices/
 SRC advice on prescription charges - http://www.glasgowstudent.net/advice/health-
and-safety/healthcare/
 Spirituality and religion - http://www.gla.ac.uk/services/chaplaincy/worship/
 Sport and recreation - http://www.gla.ac.uk/services/sport/
 SRC advice centre - http://www.glasgowstudent.net/advice
Phd Studies Institute Cancer Sciences 2017 29

 The student network -

http://www.gla.ac.uk/studentlife/studentunionsandorganisations/
 Barclay Medical Centre- http://www.universitybarclay.com/

Student Finance & Money

 What can I apply for?- http://www.gla.ac.uk/services/registry/finance/

 Available help- http://www.gla.ac.uk/services/registry/finance/
 Tuition fee assistance- http://www.gla.ac.uk/scholarships/fees/
 Scholarships- http://www.gla.ac.uk/scholarships/
 Loans- http://www.gla.ac.uk/services/registry/finance/
 Other schemes- http://www.gla.ac.uk/services/registry/finance/
 Emergency money- http://www.gla.ac.uk/services/registry/finance/funds/
 Other money matters:
 Further advice- http://www.gla.ac.uk/services/registry/finance/
 Contact us- http://www.gla.ac.uk/services/registry/contact/
 Tuition fees- http://www.gla.ac.uk/scholarships/fees/
 Opening a bank account - http://www.gla.ac.uk/international/support/livinginuk/
 Cost of living - http://www.gla.ac.uk/international/support/livinginuk/costofliving/
 Student Awards Agency for Scotland- http://www.saas.gov.uk/

Other Useful Information

 Campus map - http://www.gla.ac.uk/about/maps/

 Emergencies -
www.gla.ac.uk/services/central/trafficandsecurity/emergencyresponseguidanceforstaf
fandstudents/
 Food - http://www.gla.ac.uk/services/hospitality/
 Travel- www.gla.ac.uk/about/maps/

International

 International student support - http://www.gla.ac.uk/international/support/

 Careers advice for international students-
http://viewer.zmags.com/publication/0d722362
 English as a foreign language - http://www.gla.ac.uk/schools/mlc/languagecentre/
 International student handbook -
http://www.gla.ac.uk/international/support/internationalstudenthandbook/
 International family network -
http://www.gla.ac.uk/international/support/familynetwork/
 Study abroad & exchange- http://www.gla.ac.uk/international/abroadexchange/
Phd Studies Institute Cancer Sciences 2017 30