ECTS PhD Studentship

2008 Award Announcement

The 2009 grant applications are now closed.
The 2010 awards will be announced in June 2009.

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 total amount available is €75,000 (Euro) payable in instalments of €25,000 (Euro) per annum for 3 years

The purpose of these grants 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

Eligibility:

Candidates must fulfill the following criteria:

• first year PhD student
• member of ECTS
• based in Europe
• PhD project must be relevant to field of bone biology

Please note:

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 instalment will be payable on receipt of the report.

2008 Awards

Four 2008 ECTS PhD Studentships were presented on Wednesday 28 May to Marta Capannolo (University of L’Aquila, Italy), Dieudonné Francois-Xavier (Hopital Lariboisière, France), Arlene Gallagher (Universiteit Utrecht, The Netherlands) and Bram Perdu (University Wirijk, Belgium).

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2008 award winners Marta Capannolo, Dieudonne Francois-Xavier, Arlene Gallagher and Bram Perdu

The student projects that the ECTS will be funding include:

ECTS PhD Studentship – Marta Capannolo
“Generation and characterization of a clc7 knock-in mouse as a model of Autosomal Dominant Osteopetrosis ADO”

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.

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.

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.

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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