T
T. Van Maerken
Researcher at Ghent University Hospital
Publications - 9
Citations - 518
T. Van Maerken is an academic researcher from Ghent University Hospital. The author has contributed to research in topics: Neuroblastoma & Mutation frequency. The author has an hindex of 7, co-authored 9 publications receiving 470 citations.
Papers
More filters
Journal ArticleDOI
An integrative genomics screen uncovers ncRNA T-UCR functions in neuroblastoma tumours
Pieter Mestdagh,Erik Fredlund,Erik Fredlund,Filip Pattyn,Ali Rihani,T. Van Maerken,Joëlle Vermeulen,Candy Kumps,Björn Menten,K. De Preter,Alexander Schramm,Johannes H. Schulte,Rosa Noguera,Gudrun Schleiermacher,Isabelle Janoueix-Lerosey,Genevieve Laureys,R. Powel,David Nittner,J-C Marine,Markus Ringnér,Franki Speleman,Jo Vandesompele +21 more
TL;DR: For the first time, a T-UCR expression landscape in neuroblastoma is defined and widespread T- UCR involvement in diverse cellular processes that are deregulated in the process of tumourigenesis is suggested.
Journal ArticleDOI
Clinicopathological significance of indoleamine 2,3-dioxygenase 1 expression in colorectal cancer
Liesbeth Ferdinande,Christine Decaestecker,Laurine Verset,Anne Mathieu,X Moles Lopez,A-M Negulescu,T. Van Maerken,Isabelle Salmon,Claude Cuvelier,Pieter Demetter +9 more
TL;DR: Higher IDO1 expression at the tumour invasion front is involved in CRC progression and correlates with impaired clinical outcome, suggesting that IDO 1 is an independent prognostic indicator for CRC.
Journal ArticleDOI
Astrocyte elevated gene-1 contributes to the pathogenesis of neuroblastoma.
Seok-Geun Lee,Hyun Yong Jeon,Zhao-zhong Su,J E Richards,Vozhilla N,Devanand Sarkar,T. Van Maerken,Paul B. Fisher +7 more
TL;DR: Over-expression of AEG-1 enhanced proliferation and expression of the transformed state in less aggressive neuroblastoma cells through activation of the phosphatidylinositol 3-kinase-Akt-signaling pathway and stabilization of MYCN.
Journal ArticleDOI
Escape from p53-mediated tumor surveillance in neuroblastoma: switching off the p14(ARF)-MDM2-p53 axis.
TL;DR: It is concluded that deregulation of the p14ARF-MDM2-p53 axis seems to be the principal mode of p53 inactivation in neuroblastoma, opening new perspectives for targeted therapeutic intervention.
Escape from p53-mediated tumor surveillance in neuroblastoma: switching off the
TL;DR: In this paper, the authors review the mechanisms for evasion of p53-mediated growth control and conclude that deregulation of the p14ARF-MDM2-p53 axis seems to be the principal mode of inactivation in neuroblastoma.