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Project information
ALK Activation as a target of TRAanslational Science (ALKATRAS): Break free from cancer (ALKATRAS)

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Project Identification
675712
Project Period
9/2015 - 8/2019
Investor / Pogramme / Project type
European Union
  • Horizon 2020
  • MSCA Marie Skłodowska-Curie Actions (Excellent Science)
MU Faculty or unit
Central European Institute of Technology
Cooperating Organization
University of Cambridge

Anaplastic Lymphoma Kinase (ALK) is an increasingly prevalent oncogene in a number of human malignancies and therefore represents a prominent clinical problem. ALK was first discovered in 1994 when Steve Morris, St. Jude, Memphis, USA cloned this gene from cases of ALCL. Since that time, ALK has been implicated in a number of cancers ranging from neuroblastoma to Non-Small Cell Lung Cancer (NSCLC) and inflammatory myofibroblastic tumours to name a few. In the case of ALCL, ALK is activated as the consequence of a chromosomal translocation whereby the oligomerisation domains of the Nucleophosmin (NPM) gene are juxtaposed to the kinase domain of ALK. The resultant NPM-ALK fusion protein is constitutively active. In the case of NSCLC, an inversion event fuses the Echinoderm microtubule-associated protein-like 4 (EML4) gene to ALK and for neuroblastoma activating point mutations are present, most notably the F1174L ALK mutant. The consistent presence of this oncogene in a number of cancer sub-types suggests not only that common underlying mechanisms of tumorigenesis may exist, but also a unique therapeutic target in ALK. However, as has been the case for a number of kinase inhibitors that have entered the clinical arena, resistance mechanisms have emerged and therefore it is imperative that we pre-empt these activities in order to design better therapeutics. Hence, ERIA was established to discover other ALK-induced processes in order that better therapies can be designed and the ALKATRAS ETN will build on this network to consolidate our collaborations. Our integrated programme will pursue the following objectives: 1) Increase our understanding of the biological mechanisms of ALK-induced tumorigenesis; 2) Develop our understanding of the status and role of the (epi)genome in ALK-induced malignancies; 3) Develop novel therapies and biomarkers; 4) Understand mechanisms of treatment resistance and develop methods to overcome these

Publications

Total number of publications: 10

2023

2021

2020

2019

2018

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