Pathway simulations in common oncogenic drivers of leukemic and rhabdomyosarcoma cells: a systems biology approach.
A part of current research has intensively been focused on the proliferation             and metabolic processes governing biological systems. Since the advent of high             throughput methodologies such as microarrays, the load of genomic data has increased             geometrically and along with that the need for computational methods to interpret             these data. In the present study, we investigated in vitro the common proliferation             and metabolic processes, associated with common oncogenic pathways, as far as             gene expression is concerned, between the T-cell acute lymphoblastic leukemia             (CCRF-CEM) and the rhabdomyosarcoma (TE-671) cell lines. We present a computational             approach, using cDNA microarrays, in order to identify commonalities between diverse             biological systems. Our analysis predicted that JAK1, STAT1, PIAS2 and CDK4 are             the driving forces in the two cell lines. This type of analysis may lead to the             understanding of the common mechanisms that transform physiological cells to malignant,             and may reveal a new holistic approach to understanding the dynamics of tumor             onset as well as the mechanistics behind oncogenic drivers.
First Department of Pediatrics, Choremeio Research Laboratory, University of Athens, Athens 11527, Greece. glamprou@med.uoa.gr
George I
GI
Lambrou
Apostolos
A
Zaravinos
Maria
M
Adamaki
Demetrios A
DA
Spandidos
Fotini
F
Tzortzatou-Stathopoulou
Spiros
S
Vlachopoulos
D002453:Cell Cycle / Q000235:genetics; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D048430:Cell Shape / Q000235:genetics; D002471:Cell Transformation, Neoplastic / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D003198:Computer Simulation; D051358:Cyclin-Dependent Kinase 4 / Q000235:genetics; D030541:Databases, Genetic; D020869:Gene Expression Profiling / Q000379:methods; D015973:Gene Expression Regulation, Leukemic; D015972:Gene Expression Regulation, Neoplastic; D053263:Gene Regulatory Networks; D020022:Genetic Predisposition to Disease; D006801:Humans; D053613:Janus Kinase 1 / Q000235:genetics; D020411:Oligonucleotide Array Sequence Analysis; D009857:Oncogenes; D010641:Phenotype; D054218:Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D050828:Protein Inhibitors of Activated STAT / Q000235:genetics; D012208:Rhabdomyosarcoma / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D050794:STAT1 Transcription Factor / Q000235:genetics; D049490:Systems Biology
C501001:PIAS2 protein, human; D050828:Protein Inhibitors of Activated STAT; D050794:STAT1 Transcription Factor; C494079:STAT1 protein, human; C507904:JAK1 protein, human; D053613:Janus Kinase 1; C495900:CDK4 protein, human; D051358:Cyclin-Dependent Kinase 4