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Gene expression profiling identifies potential relevant genes in alveolar rhabdomyosarcoma pathogenesis and discriminates PAX3 ‐ FKHR positive and negative tumors
Author(s) -
De Pittà Cristiano,
Tombolan Lucia,
Albiero Giada,
Sartori Francesca,
Romualdi Chiara,
Jurman Giuseppe,
Carli Modesto,
Furlanello Cesare,
Lanfranchi Gerolamo,
Rosolen Angelo
Publication year - 2006
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.21698
Subject(s) - alveolar rhabdomyosarcoma , biology , pax3 , gene , gene expression profiling , gene expression , rhabdomyosarcoma , fusion gene , microarray , complementary dna , microarray analysis techniques , reverse transcription polymerase chain reaction , transcription factor , cancer research , genetics , pathology , medicine , sarcoma
We analyzed the expression signatures of 14 tumor biopsies from children affected by alveolar rhabdomyosarcoma (ARMS) to identify genes correlating to biological features of this tumor. Seven of these patients were positive for the PAX3‐FKHR fusion gene and 7 were negative. We used a cDNA platform containing a large majority of probes derived from muscle tissues. The comparison of transcription profiles of tumor samples with fetal skeletal muscle identified 171 differentially expressed genes common to all ARMS patients. The functional classification analysis of altered genes led to the identification of a group of transcripts ( LGALS1 , BIN1 ) that may be relevant for the tumorigenic processes. The muscle‐specific microarray platform was able to distinguish PAX3‐FKHR positive and negative ARMS through the expression pattern of a limited number of genes ( RAC1 , CFL1 , CCND1, IGFBP2 ) that might be biologically relevant for the different clinical behavior and aggressiveness of the 2 ARMS subtypes. Expression levels for selected candidate genes were validated by quantitative real‐time reverse‐transcription PCR. © 2005 Wiley‐Liss, Inc.