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Table 1 AML gene expression datasets used to prioritize the gene expression signatures

From: Development and validation of GMI signature based random survival forest prognosis model to predict clinical outcome in acute myeloid leukemia

Data Set Country Control group Experimental Group Author Title Journal Reference
GSE14924 United Kingdom 21 20 (Le et al. 2009) Peripheral blood T cells in acute myeloid leukemia (AML) patients at diagnosis have abnormal phenotype and genotype and form defective immune synapses with AML blasts Blood [21]
GSE68172 Germany 5 72 (Schneider et al. 2015) Leukemic progenitor cells are susceptible to targeting by stimulated cytotoxic T cells against immunogenic leukemia-associated antigens International Journal of Cancer [22]
GSE84881 Germany 4 19 (Ek et al. 2016) Molecular alterations in bone marrow mesenchymal stromal cells derived from acute myeloid leukemia patients Leukemia [23]
GSE14858 Italy 20 20 (Bresolin et al. 2010) Gene expression-based classification as an independent predictor of clinical outcome in juvenile myelomonocytic leukemia Journal of Clinical Oncology [24]
GSE12662 USA 15 91 (Payton et al. 2009) High throughput digital quantification of mRNA abundance in primary human acute myeloid leukemia samples Journal of Clinical Investigation [25]
GSE10746 USA 3 8 (Mougeot et al. 2011) Microarray analyses of oral punch biopsies from acute myeloid leukemia (AML) patients treated with chemotherapy Oral Surgery Oral Medicine Oral Pathology Oral Radiology & Endodontology [26]
GSE17054 USA 4 9 (Majeti et al. 2009) Dysregulated gene expression networks in human acute myelogenous leukemia stem cells Proceedings of the National Academy of Sciences of the United States of America [27]
GSE8023 USA 3 9 (Krejci et al. 2008) p53 signaling in response to increased DNA damage sensitizes AML1-ETO cells to stress-induced death Blood [28]
GSE17061 Netherlands 0 35 (Silva et al. 2009) Gene expression profiling of minimally differentiated acute myeloid leukemia: M0 is a distinct entity subdivided by RUNX1 mutation status Blood [29]
GSE70124 Germany 0 46 (Papaemmanuil et al. 2016) Genomic Classification and Prognosis in Acute Myeloid Leukemia New England Journal of Medicine [14]
GSE10258 Austria 0 15 (Zatkova et al. 2009) AML/MDS with 11q/MLL amplification show characteristic gene expression signature and interplay of DNA copy number changes Genes Chromosomes & Cancer [30]
GSE35159 Japan 0 12 (Saito et al. 2011) CD52 as a molecular target for immunotherapy to treat acute myeloid leukemia with high EVI1 expression Leukemia [31]
GSE50928 France 0 13 (Khaznadar et al. 2015) Defective NK Cells in Acute Myeloid Leukemia Patients at Diagnosis Are Associated with Blast Transcriptional Signatures of Immune Evasion Journal of Immunology [32]
GSE34885 France 0 14 (Khaznadar et al. 2015) Defective NK Cells in Acute Myeloid Leukemia Patients at Diagnosis Are Associated with Blast Transcriptional Signatures of Immune Evasion Journal of Immunology [32]
GSE52891 Netherlands 0 23 (Bachas et al. 2015) Gene Expression Profiles Associated with Pediatric Relapsed AML Plos One [33]
GSE22056 Netherlands 0 98 (de Jonge et al. 2010) High VEGFC expression is associated with unique gene expression profiles and predicts adverse prognosis in pediatric and adult acute myeloid leukemia Blood [34]
GSE59808 USA 0 32 (Guo et al. 2014) PIM inhibitors target CD25-positive AML cells through concomitant suppression of STAT5 activation and degradation of MYC oncogene Blood [35]
GSE12326 China 0 10 (Cheung et al. 2009) A comparative study of bone marrow and peripheral blood CD34+ myeloblasts in acute myeloid leukaemia British Journal of Haematology [36]
GSE44857 United Kingdom 0 18 (Leonard et al. 2014) Sequential Treatment with Cytarabine and Decitabine Has an Increased Anti-Leukemia Effect Compared to Cytarabine Alone in Xenograft Models of Childhood Acute Myeloid Leukemia Plos One [37]
GSE30903 Italy 0 24 (Salvestrini et al. 2012) Purinergic signaling inhibits human acute myeloblastic leukemia cell proliferation, migration, and engraftment in immunodeficient mice Blood [38]
GSE22845 Netherlands 0 154 (Taskesen et al. 2011) Prognostic impact, concurrent genetic mutations, and gene expression features of AML with CEBPA mutations in a cohort of 1182 cytogenetically normal AML patients: further evidence for CEBPA double mutant AML as a distinctive disease entity Blood [39]
GSE18018 USA 0 19 (Falini et al. 2010) Multilineage dysplasia has no impact on biologic, clinicopathologic, and prognostic features of AML with mutated nucleophosmin (NPM1) Blood [40]
GSE21261 USA 0 79 (Miesner et al. 2010) Multilineage dysplasia (MLD) in acute myeloid leukemia (AML) correlates with MDS-related cytogenetic abnormalities and a prior history of MDS or MDS/MPN but has no independent prognostic relevance: a comparison of 408 cases classified as “AML not otherwise specified” (AML-NOS) or “AML with myelodysplasia-related changes” (AML-MRC) Blood [41]
GSE56237 Denmark 0 10 (Mora-Jensen et al. 2015) Cellular origin of prognostic chromosomal aberrations in AML patients Leukemia [42]
GSE30442 USA 0 11 (Grossmann et al. 2011) Whole-exome sequencing identifies somatic mutations of BCOR in acute myeloid leukemia with normal karyotype Blood [43]