ECTS PhD Studentship
2010 Award Announcement
Applications for the 2011 award is now open. The 2011 award(s)will be announced during the 3rd Joint meeting of the European Calcified Tissue Society and International Bone and Mineral Society 7-11 May 2011 in Athens, Greece
Deadline 12 November 2010
Online Application Form (Members Only)
Description
Grants are available for European PhD students to assist with expenses incurred for their PhD research project, which must be relevant to the field of calcified tissues and related topics. Successful applicants will be expected to attend the ECTS annual PhD training course.
The purpose of this grant is:
- to help meet some of the immediate costs of initiating a PhD research project
- to support and stimulate research on calcified tissues and related topics
- to assist in attracting young researchers to specialise in the field of calcified tissues
- to assist in attracting young researchers to join the ECTS
Amount
The total amount available is €30,000 (Euro) payable in 3 installments
Eligibility
Candidates must fulfill the following criteria:
- PhD student commencing or during their first year of studies
- European member of ECTS and be working in a European institution. Applications will be considered from European members who are working in an International institution if a strong case can be presented for performing the research outside of Europe
- applicant may only apply for one award (i.e. applicants for PhD studentship may not apply for any other ECTS award in the current year)
- PhD project must be relevant to field of bone biology
- previous recipients of an ECTS Postdoctoral Fellowship, ECTS/Amgen/GSK Bone Biology Fellowship, ECTS/Servier Fellowship, ECTS Career Establishment award or ECTS PhD Studentship are not eligible to apply
Please note
- applicants are encouraged to seek funding from alternative sources for their research. However, successful applicants will be requested to complete a declaration form to state that they have not gained simultaneous funding from another organization towards the support of his/her salary for the same research project. Accordingly, the successful applicant is expected to inform ECTS in this event and the ECTS Board will make appropriate adjustments to the award, up to a complete withdrawal if the amount obtained from the other source covers 100% of the applicant’s salary
- funds are not to be used for university/institution overheads
- Grants can be used for salary, consumables, travel, fees or supplies
- applications must be made on-line from the ECTS web site
Review Procedure
All applications are reviewed by an independent panel of reviewers and any conflicts of interest are identified and dealt with appropriately.
Report
Successful candidates will be required to submit a written report on the progress of their research at the end of the grant period and the final installment will be payable on receipt of the report.
Online Application Form (Members Only)
2010 award
The 2010 award was presented during the 37th European Symposium on Calcified Tissues in Glasgow on Tuesday 29 June to Eman Azzam.
Professor Roland Baron – ECTS President (left) presents Eman Azzam with the ECTS PhD Studentship award
Title: |
The role of autophagy in the pathogenesis of Paget’s Disease of Bone |
Abstract of research: |
Autophagy “eating yourself” is a highly organised waste disposal system that acts together with the ubiquitin proteasomal system UPS to effectively use nutrients and ensure efficient clearance of misfolded or aggregated proteins, and dysfunctional organelles. A key protein in both autophagy and the UPS is sequestosome-1/p62. Intriguingly, p62 is often mutated in Paget’s Disease of Bone PDB, a disease of deregulated bone turnover, driven by enlarged and hyperactive osteoclasts. The mechanisms by which mutations in p62 appear to specifically affect osteoclasts remain unknown. I will use stable cell lines expressing Pagetic mutations in p62 and investigate how these cells respond to induction of autophagy. Furthermore, I will develop and use an “autophagy toolkit” to allow me to study the specific role of autophagy in osteoclasts. As autophagy has not been systematically investigated in these cells, my studies have relevance for osteoclast biology as well as for the understanding of PDB. |
Previous award winners
2009 ECTS PhD Studentship – Allison Marion
TITLE OF PROJECT: Calpain-6, a new target in osteosarcoma cells
ABSTRACT
Osteosarcoma is characterized by frequent metastasis and high rate of resistance to chemotherapy. Our purpose is to find new targets to improve osteosarcoma management. We explored by microarray analysis downstream genes of the tumor suppressor syndecan-2. We found that calpain-6 is a candidate molecule downregulated by syndecan-2. We showed that calpain-6 is abnormally expressed in osteosarcoma cells and is involved in survival and proliferation. We aim to study calpain-6 expression in human tumours and to compare with normal bone. We will determine the effect of calpain-6 inhibition by shRNA delivered by lentiviral vectors on bone tumour development in a osteosarcoma mouse model. To target calpain-6 we also aim to determine its functions in osteosarcoma cells by looking for molecular partners. In silico analysis of calpain-6 protein led us to study interaction with other calpains. We will also study its expression during the cell cycle and the subcellular location and shuttling.
2009 ECTS PhD Studentship – Carmen Flores
TITLE OF PROJECT: Development of stem cell based gene therapy for infantile malignant osteopetrosis
ABSTRACT
The aim of this project is the genetic targeting of osteoclasts to understand and treat human bone disease, primarily osteopetrosis. In this lethal disorder osteoclasts are unable to resorb bone due to defects in acidification. The gene mutated in most patients is TCIRG1 that codes for a subunit of a proton pump used by the osteoclast to acidify the resorption area. Lack of resorption leads to dense, fragile bone, bone marrow failure and blindness through compression of nervus opticus. Stem cell transplantation is the only curative treatment. We have recently published the first successful proof-of-principle gene therapy experiments in a murine model of the disease, the oc/oc mouse. We will continue gene therapy development in the mouse model using clinically relevant conditions and newly developed osteoclast-specific lentiviral vectors. Disease mechanisms will be further investigated and work moved to human disease-specific cell lines and patient cells.
2009 ECTS PhD Studentship – Sander Pouwels
TITLE OF PROJECT: Five-year Fracture risk in patients with Parkinson’s disease and neuromuscular diseases or movement disorders
ABSTRACT
Patients with neuromuscular disease or movement disorders NMDs / Parkinson’s disease may be at increased risk of osteoporotic fracture due to instability, immobility, and a higher risk of falling. Patients suffering from Myasthenia Gravis, the Guillain-Barré syndrome, and muscular dystrophies are treated with high dosages of oral corticosteroids, which further contribute to fracture risk. Unfortunately, there is scarce evidence that patients who suffer from Parkinson’s disease or NMDs are at increased risk of fracture. Using the UK General Practice Research Database, which also contains information from e.g. neurologists and hospitals, we will conduct a cohort study including 16,500 patients with NMD, matched to 50,000 control patients without the disease. 5-year and 10-year risk of fracture in will be estimated in order to create a clinical risk score that will include data on the duration of the disease, BMI, smoking, exposure to steroids and dopaminergics drugs and other risk factors.
ABSTRACT
Osteopetrosis is a heterogenous genetic bone disease
often resulting in severe morbidity and early death.
It is due to osteoclast failure which causes persistence
of old bone, increase of bone density and obstruction
of the internal cavities containing vital organs such
as the bone marrow and the nervous system. Short stature,
deformities and pathological fractures are typical symptoms,
along with severe haematological and neural failures.
Currently no efficacious pharmacological cure is available.
Approximately 70 of patients with the less severe autosomal
dominant form ADO harbour a single allele mutation of
CLC7 gene. This project has the aim to generate the
first disease animal model for ADO, which would consist
in a heterozygous knock-in mouse carrying the most frequent
missense mutation of the clc7 gene found in ADO patients,
G215R. This could offer an effective system to study
in detail the typical ADO phenotypic variability and
to test new in vivo therapies.
2008 ECTS PhD Studentship – Dieudonneé
Francois-Xavier
“Syndecan-2: A new therapeutic target in osteosarcoma”
- Dieudonné Francois-Xavier
ABSTRACT
Osteosarcoma is the most common primary malignant
bone tumor. The disease-free survival rate remains below
70 due to high resistance to treatments which is linked
to abnormal control of cell death. We previously showed
that syndecan-2 regulates cell death, contributes to
the cytotoxic action of chemotherapeutic agents and
is downregulated in human osteosarcoma. We hypothesize
that this default in syndecan-2 contributes to cell
resistance to cytotoxic drugs. We propose to identify
the transcription factors and intracellular signalling
processes that control syndecan-2 expression in osteosarcoma
cells. We will then target specific molecular mechanisms
that control syndecan-2 expression in order to amplify
syndecan-2 expression and induce cell death in osteosarcoma
cells. Finally, we will use this knowledge to target
specific molecules and reduce tumorigenesis in an established
osteosarcoma model in mice. The results may lead to
develop new specific treatments which may improve the
management of osteosarcoma.
2008 ECTS PhD Studentship – Arlene Gallagher
“The Million Fractures Study: Use of Thiazolidinediones
and Absolute Risk of Fracture in the United Kingdom,
the Netherlands and Denmark” – Arlene Gallagher
ABSTRACT
Thiazolidinediones are frequently used in patients
with increased sugar levels diabetes mellitus Recent
estimates from the USA indicate that there are more
than 2 million Americans who are prescribed these drugs.
But, recently, it has been suggested that the use of
these drugs may increase the risk of fractures, particularly
at the hand. However, it is unclear whether these drugs
may also increase the risk of other types of fractures,
particularly at the hip fractures. If a patient suffers
a hip fracture, many may die or have to move into a
nursing home. Also, it is unclear whether any increase
in the risk of fractures due to thiazolidinediones is
reversible after stopping these drugs. This study will
also estimate the likelihood that a patient may suffer
a fracture. The study will use data from three large
European databases, allowing the study of broad populations
of users of thiazolidinediones.
2008 ECTS PhD Studentship – Bram Perdu
“Genetic and functional analysis of the pathogenic
mechanisms underlying two osteopetrotic rat models ia
and op” – Bram Perdu
ABSTRACT
The general aim of this project is to gain novel insights
into the bone resorption process and the mechanisms
by which this is performed by the osteoclasts. We will
try to achieve this by studying two well-known natural
mutants of the rat characterized by osteopetrosis, the
incisors-absent ia and the osteopetrotic op rat.
This project can therefore be divided in two parts.
First, we will further characterize the role of the
Plekhm1 protein in osteoclasts, since a mutation in
this gene underlies the ia rat model. Yeast two-hybrid
experiments and colocalisation studies will be undertaken
and the effect of silencing PLEKHM1 on the morphology
and activity of osteoclasts will be studied. Secondly,
we aim to identify the gene that is responsible for
the op ratmodel, screen this new osteopetrosis gene
in human osteopetrotic patients and characterize this
op gene and protein. Further functional characterisation
of these genes will provide better insight into the
pathogenesis of these bone diseases
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