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

United Kingdom

(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]

Germany

(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]

Germany

(Ek et al. 2016)

Molecular alterations in bone marrow mesenchymal stromal cells derived from acute myeloid leukemia patients

Leukemia

[23]

Italy

(Bresolin et al. 2010)

Gene expression-based classification as an independent predictor of clinical outcome in juvenile myelomonocytic leukemia

Journal of Clinical Oncology

[24]

USA

(Payton et al. 2009)

High throughput digital quantification of mRNA abundance in primary human acute myeloid leukemia samples

Journal of Clinical Investigation

[25]

USA

(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]

USA

(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]

USA

(Krejci et al. 2008)

p53 signaling in response to increased DNA damage sensitizes AML1-ETO cells to stress-induced death

Blood

[28]

Netherlands

(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]

Germany

(Papaemmanuil et al. 2016)

Genomic Classification and Prognosis in Acute Myeloid Leukemia

New England Journal of Medicine

[14]

Austria

(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]

Japan

(Saito et al. 2011)

CD52 as a molecular target for immunotherapy to treat acute myeloid leukemia with high EVI1 expression

Leukemia

[31]

France

(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]

France

(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]

Netherlands

(Bachas et al. 2015)

Gene Expression Profiles Associated with Pediatric Relapsed AML

Plos One

[33]

Netherlands

(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]

USA

(Guo et al. 2014)

PIM inhibitors target CD25-positive AML cells through concomitant suppression of STAT5 activation and degradation of MYC oncogene

Blood

[35]

China

(Cheung et al. 2009)

A comparative study of bone marrow and peripheral blood CD34+ myeloblasts in acute myeloid leukaemia

British Journal of Haematology

[36]

United Kingdom

(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]

Italy

(Salvestrini et al. 2012)

Purinergic signaling inhibits human acute myeloblastic leukemia cell proliferation, migration, and engraftment in immunodeficient mice

Blood

[38]

Netherlands

(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]

USA

(Falini et al. 2010)

Multilineage dysplasia has no impact on biologic, clinicopathologic, and prognostic features of AML with mutated nucleophosmin (NPM1)

Blood

[40]

USA

(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]

Denmark

(Mora-Jensen et al. 2015)

Cellular origin of prognostic chromosomal aberrations in AML patients

Leukemia

[42]

USA

(Grossmann et al. 2011)

Whole-exome sequencing identifies somatic mutations of BCOR in acute myeloid leukemia with normal karyotype

Blood

[43]