TY - JOUR
TI - Proteomic studies of pediatric medulloblastoma tumors with 17p deletion
AU - Anagnostopoulos, A.K.
AU - Papathanassiou, C.
AU - Karamolegou, K.
AU - Anastasiadou, E.
AU - Dimas, K.S.
AU - Kontos, H.
AU - Koutsopoulos, A.
AU - Prodromou, N.
AU - Tzortzatou-Stathopoulou, F.
AU - Tsangaris, G.T.
JO - Journal of Proteome Research
PY - 2015
VL - 14
TODO - 2
SP - 1076-1088
PB - American Chemical Society
SN - 1535-3893, 1535-3907
TODO - 10.1021/pr501219f
TODO - initiation factor 4E;  mammalian target of rapamycin;  phosphatidylinositol 3 kinase;  proteasome;  proteome, actin filament;  Article;  child;  childhood cancer;  chromosome 17p;  chromosome aberration;  chromosome deletion;  chromosome loss;  clinical article;  comparative genomic hybridization;  controlled study;  enzyme activity;  female;  human;  human tissue;  image analysis;  immunoblotting;  infant;  male;  mass spectrometry;  medulloblastoma;  pathophysiology;  priority journal;  protein content;  protein expression;  protein protein interaction;  protein synthesis;  proteomics;  quantitative analysis;  signal transduction;  two dimensional electrophoresis;  Western blotting;  central nervous system tumor;  chromosome 17;  genetics;  medulloblastoma;  metabolism;  preschool child, Central Nervous System Neoplasms;  Child, Preschool;  Chromosome Deletion;  Chromosomes, Human, Pair 17;  Female;  Humans;  Infant;  Male;  Medulloblastoma;  Proteomics
TODO - CNS tumors are the leading cause of cancer-related death in children. Medulloblastoma is the commonest pediatric CNS malignancy, wherein, despite multimodal therapy with surgery, radiation, and chemotherapy, 5 year survival rates merely approach 60%. Until present, gene expression and cytogenetic studies have produced contradicting findings regarding the molecular background of the specific disease. Through integration of genomics, bioinformatics, and proteomics, the current study aims to shed light at the proteomic-related molecular events responsible for MBL pathophysiology, as well as to provide molecular/protein/pathway answers concerning tumor-onset. Experiments were performed on tissues collected at surgery. With 17p loss being the commonest chromosomal aberrance observed in our sample set, array-CGH were employed to first distinguish for 17p-positive cases. 2-DE coupled to mass spectrometry identification exposed the MBL-specific protein profile. Protein profiles of malignant tissues were compared against profiles of normal cerebellar tissues, and quantitative protein differences were determined. Bioinformatics, functional and database analyses, characterization, and subnetwork profiling generated information on MBL protein interactions. Key molecules of the PI3K/mTOR signaling network were identified via the techniques applied herein. Among the findings IGF2, PI3K, Rictor, MAPKAP1, S6K1, 4EBP1, and ELF4A, as part of the IGF network (implicating PI3K/mTOR), were founded to be deregulated. © 2015 American Chemical Society.
ER -