Stratification of pediatric acute myeloid leukemia through cancer cell gene-expression profiling

2011 ◽  
Vol 11 (3) ◽  
pp. 355-357 ◽  
Author(s):  
Bjørn Tore Gjertsen
Keyword(s):  
Gene Expression ◽  
Acute Myeloid Leukemia ◽  
Gene Expression Profiling ◽  
Cancer Cell ◽  
Expression Profiling ◽  
Myeloid Leukemia ◽  
Pediatric Acute Myeloid Leukemia ◽  
Cell Gene Expression ◽  
Cell Gene ◽  
Acute Myeloid

scholarly journals Integrated genome-wide genotyping and gene expression profiling reveals BCL11B as a putative oncogene in acute myeloid leukemia with 14q32 aberrations

Haematologica ◽  
2014 ◽  
Vol 99 (5) ◽  
pp. 848-857 ◽  
Author(s):  
S. Abbas ◽  
M. A. Sanders ◽  
A. Zeilemaker ◽  
W. M. C. Geertsma-Kleinekoort ◽  
J. E. Koenders ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acute Myeloid Leukemia ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Myeloid Leukemia ◽  
Genome Wide ◽  
Acute Myeloid

Use of Gene-Expression Profiling to Identify Prognostic Subclasses in Adult Acute Myeloid Leukemia

2004 ◽  
Vol 350 (16) ◽  
pp. 1605-1616 ◽  
Author(s):  
Lars Bullinger ◽  
Konstanze Döhner ◽  
Eric Bair ◽  
Stefan Fröhling ◽  
Richard F. Schlenk ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acute Myeloid Leukemia ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Myeloid Leukemia ◽  
Acute Myeloid

Gene expression profiling of minimally differentiated acute myeloid leukemia: M0 is a distinct entity subdivided by RUNX1 mutation status

Blood ◽  
2009 ◽  
Vol 114 (14) ◽  
pp. 3001-3007 ◽  
Author(s):  
Fernando P. G. Silva ◽  
Sigrid M. A. Swagemakers ◽  
Claudia Erpelinck-Verschueren ◽  
Bas J. Wouters ◽  
Ruud Delwel ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acute Myeloid Leukemia ◽  
B Cell ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Myeloid Leukemia ◽  
Loss Of Function ◽  
Transcription Regulators ◽  
Runx1 Mutation ◽  
Acute Myeloid

Minimally differentiated acute myeloid leukemia (AML-M0) is defined by immature morphology and expression of early hematologic markers. By gene expression profiling (GEP) and subsequent unsupervised analysis of 35 AML-M0 samples and 253 previously reported AML cases, we demonstrate that AML-M0 cases express a unique signature that is largely separated from other molecular subtypes. Hematologic transcription regulators such as CEBPA, CEBPD, and ETV6, and the differentiation associated gene MPO appeared strongly down-regulated, in line with the primitive state of this leukemia. AML-M0 frequently carries loss-of-function RUNX1 mutation. Unsupervised analyses revealed a subdivision between AML-M0 cases with and without RUNX1 mutations. RUNX1 mutant AML-M0 samples showed a distinct up-regulation of B cell–related genes such as members of the B-cell receptor complex, transcription regulators RUNX3, ETS2, IRF8, or PRDM1, and major histocompatibility complex class II genes. Importantly, prediction with high accuracy of the AML-M0 subtype and prediction of patients carrying RUNX1 mutation within this subtype were possible based on the expression level of only a few transcripts. We propose that RUNX1 mutations in this AML subgroup cause lineage infidelity, leading to aberrant coexpression of myeloid and B-lymphoid genes. Furthermore, our results imply that AML-M0, although originally determined by morphology, constitutes a leukemia subgroup.

Gene Expression Profiling in Acute Myeloid Leukemia

2005 ◽  
Vol 23 (26) ◽  
pp. 6296-6305 ◽  
Author(s):  
Lars Bullinger ◽  
Peter J.M. Valk
Keyword(s):  
Gene Expression ◽  
Acute Myeloid Leukemia ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Myeloid Leukemia ◽  
Molecular Taxonomy ◽  
Detailed Knowledge ◽  
New Information ◽  
Therapeutic Decision Making ◽  
Acute Myeloid

Over the last decades, significant advances have been made in the knowledge and treatment of acute myeloid leukemia (AML). The WHO has recognized this new information by incorporating into its classification morphologic, immunophenotypic, genetic, and clinical features in an attempt to define biologically and clinically relevant entities. Nevertheless, well-defined cytogenetic subgroups exhibit considerable heterogeneity, and in many AML subtypes the pathogenic event is still not known. A classification system based on the underlying molecular pathogenetic abnormalities would be ideal, but such detailed knowledge is not yet available. Novel approaches in genomics, such as surveying the expression levels of thousands of genes in parallel using DNA microarray technology, open possibilities to further refine the studies on AML. Today, gene expression profiling in AML is becoming well established and has already been proven to be valuable in diagnosing different cytogenetic subtypes, discovering novel AML subclasses, and predicting clinical outcome. Recently, gene expression profiling studies in AML showed a remarkable level of concordance in findings, which may ultimately lead to an increasingly refined molecular taxonomy. While many challenges remain to be overcome, a combination of gene expression profiling with other microarray-based applications, high-throughput mutational analyses and proteomic approaches will not only significantly contribute to the classification and therapeutic decision making of AML, but also give important insights into the true pathobiologic nature of this type of leukemia.

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