Arrow-HCC Phd Scholarships

Arrow researchers recognised for their results

We are pleased to report that Arrow funded scientists and PhD students have had the results of their research published in renowned scientific publications as follows:

American Journal of Hematology - January 2011

Article: 'Expression Profiling of Cytogenetically Normal Acute Myeloid Leukemia Identifies MicroRNAs that Target Genes Involved in Monocytic Differentiation.'

Authors: Mark Lutherborrow, Former Arrow/HCC Senior Research Scientist; Adam Bryant, Former Arrow/HCC PhD Scholar; Vivek Jayaswal; David Agapiou; Catalina Palma, Current Arrow/HCC Research scientist; Yee Hwa Yang and David Ma.

BMC Medical Genomics - March 2011

Article: 'Discriminating lymphomas and reactive lymphadenopathy in lymph node biopsies by gene expression profiling'

Authors: T.Loi, Former Arrow/HCC PhD Scholar; A.Campain; A.Bryant, Former Arrow/HCC PhD Scholar; T.Molloy, Former Arrow/HCC Senior Research Scientist; M.Lutherborrow, Former Arrow/HCC Senior Research Scientist; J.Turner; Y.Yang; D.Ma

BMC Genomics - 2011

Article: 'Identification of microRNA-mRNA Cliques using Microarray Data'

Authors: V.Jayaswal; M.Lutherborrow, Former Arrow/HCC Senior Research Scientist; D.Ma; Y. Yang.

 

Adele Baker

Adele Baker - Arrow / HCC PhD scholarship recipient


PhD student, The University of Melbourne. Peter MacCallum Cancer Centre, Melbourne. Gene Regulation Laboratory. Supervisor: A/Prof Ricky Johnstone.


PhD project summary

Development of genetically engineered mouse models of the MLL-ENL and MLL-AF9 mutations to study tumorigenesis.

My projects aim is to identify key molecular targets for the treatment of acute leukaemia's (AL) driven by mixed lineage leukaemia (MLL) fusion p rotein mutations.

The MLL mutation accounts for 60-80% of all infant acute leukaemia's and is classified as aggressive tumours that need high amounts of poly-chemotherapy for treatment, yet still result in a poor prognosis outcome. Genetically, the group of paediatric and adult acute leukaemia patients can be characterized by their distinct genetic rearrangements of the MLL gene located at the 11q23 chromosomal band which is fused to one of over 66 different fusion partner proteins. I will aim to produce mice that develop acute myeloid leukaemia (AML) with the MLL mutation that is fused to two out of the six most common oncogenic fusion partner proteins. These mutations are known as Mixed Lineage Leukaemia-Eleven-Nineteen-Leukaemia (MLL-ENL) [t(11;19)(q23;p13.3)] and Mixed Lineage Leukemia-AF9 (MLL-AF9) [t(p;11)(p22;q23)]. The mice will be utilized to study disease onset and progression and to determine the oncogenic potential of these two different MLL fusion protein mutations. Furthermore, I will aim to investigate what drives or activates the onset and process of these MLL fusion proteins. This will provide a platform for developing new drug targets and therapies for patients expressing the MLL-ENL and MLL-AF9 fusion protein MLL mutation.

 

Bradley Hoad

Bradley Hoad - Arrow / HCC PhD scholarship recipient


Queensland University of Technology, Institute of Health and Biomedical Innovation


PhD project summary

Leukemia's are a cancerous blood disorder that arise when the genes that normally regulate cell growth and maturation are lost through genetic mutation. For decades scientists have been focusing on chemicals and radiation, which cause DNA damage, as the culprits of these mutations. It now appears that the processes governing the repair of DNA damage may be more critical in promoting leukaemia than the damaging event itself. Our study aims to characterise the role of nucleophosmin in DNA repair. Nucleophosmin is a nuclear protein found mutated and over expressed in several cancers however none as frequently as acute myeloid leukaemia. In fact, nucleophosmin is commonly used as a biomarker for the disease. This project will now investigate the apparently critical role nucleophosmin plays in maintaining genome stability. Uncovering nucleophosmins role in this pathway may reveal new targets for anti-leukaemia drugs.

 

Alireza Ardjmand, M.Sc - Arrow / HCC PhD scholarship recipient

PhD Student, School of Biomedical Sciences & Pharmacy, Cancer Research Unit

University of Newcastle


 

PhD Project Summary

The survival of patients with acute leukaemia has gradually improved through the development of new diagnostic and treatment protocols. These advances have been driven by research to identify specific markers expressed by leukaemia cells. Nevertheless, there are still major challenges to overcome, particularly to identify those patients who will fail therapy. Emerging evidence suggests the persistence of a small unique population of drug resistant cells called Leukemic Stem Cells (LSC's) that are ultimately responsible for disease relapse.

Since LSC's share many markers with their normal haemopoeitic counterparts they are difficult to identify. My PhD project tests the hypothesis that Fat1 is a biologically important target protein expressed specifically by LSCs. If substantiated, specific monoclonal antibodies against Fat1 could be used to both identify and kill LSCs. Importantly, since Fat1 is not expressed on normal cells; this approach promises to provide a new treatment that will minimise collateral damage to normal blood cells.

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