Trial reportInternational journal of oncology2018
Gene expression profiling of acute myeloid leukemia samples from adult patients with AML-M1 and -M2 through boutique microarrays, real-time PCR and droplet digital PCR.
Trial report in International journal of oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
54 citing papers in PubMed, 79 citations in OpenAlex.
- ENO1 promotes acute myeloid leukemia progression through SCD1-mediated lipid metabolism reprogramming.Blood advances · 2026Article
- The multifaceted roles of ribosomal P complex in cancer.World journal of surgical oncology · 2025Review
- Advantages of a genomic DNA-based next-generation sequencing assay for detection of mutant NPM1 measurable residual disease in AML.Blood advances · 2025Article
- Evaluation of circ_0002232 and circ-vimentin gene expressions as valuable biomarkers in acute myeloid leukemia patients.Molecular biology reports · 2025Article
- Diagnostic value of procalcitonin and hemocyte parameters in neonates with bloodstream infection: Role of activated hemocyte-related genes.Pediatric discovery · 2024Article
- MicroRNA-450b-5p modulated RPLP0 promotes hepatocellular carcinoma progression via activating JAK/STAT3 pathway.Translational oncology · 2024Article
- Decoding Acute Myeloid Leukemia: A Clinician's Guide to Functional Profiling.Diagnostics (Basel, Switzerland) · 2024Review
- Antioxidant Enzymes and Their Potential Use in Breast Cancer Treatment.International journal of molecular sciences · 2024Review
- Stellae-123 gene expression signature improved risk stratification in taiwanese acute myeloid leukemia patients.Scientific reports · 2024Article
- Parkin inhibits proliferation and migration of bladder cancer via ubiquitinating Catalase.Communications biology · 2024Article
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- In Silico, In Vitro, and In Vivo Evaluation of Caffeine-Coated Nanoparticles as a Promising Therapeutic Avenue for AML through NF-Kappa B and TRAIL Pathways Modulation.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Identification of Cell Type-Specific Effects ofMolecules and cells · 2023Article
- In Silico and In Vitro Studies of Novel Azomethines on DNA Repair Genes in Gastric Cell Lines.Life (Basel, Switzerland) · 2023Article
- Vacuolar ATPase Is a Possible Therapeutic Target in Acute Myeloid Leukemia: Focus on Patient Heterogeneity and Treatment Toxicity.Journal of clinical medicine · 2023Article
- Shift of N-MYC Oncogene Expression in AML Patients Carrying the FLT3-ITD Mutation.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Article
- Super-enhancer-associated gene CAPG promotes AML progression.Communications biology · 2023Article
- Azacitidine Is Synergistically Lethal with XPO1 Inhibitor Selinexor in Acute Myeloid Leukemia by Targeting XPO1/eIF4E/c-MYC Signaling.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is the most common and severe form of acute leukemia diagnosed in adults. Owing to its heterogeneity, AML is divided into classes associated with different treatment outcomes and specific gene expression profiles. Based on previous studies on AML, in this study, we designed and generated an AML-array containing 900 oligonucleotide probes complementary to human genes implicated in hematopoietic cell differentiation and maturation, proliferation, apoptosis and leukemic transformation. The AML-array was used to hybridize 118 samples from 33 patients with AML of the M1 and M2 subtypes of the French-American‑British (FAB) classification and 15 healthy volunteers (HV). Rigorous analysis of the microarray data revealed that 83 genes were differentially expressed between the patients with AML and the HV, including genes not yet discussed in the context of AML pathogenesis. The most overexpressed genes in AML were STMN1, KITLG, CDK6, MCM5, KRAS, CEBPA, MYC, ANGPT1, SRGN, RPLP0, ENO1 and SET, whereas the most underexpressed genes were IFITM1, LTB, FCN1, BIRC3, LYZ, ADD3, S100A9, FCER1G, PTRPE, CD74 and TMSB4X. The overexpression of the CPA3 gene was specific for AML with mutated NPM1 and FLT3. Although the microarray-based method was insufficient to differentiate between any other AML subgroups, quantitative PCR approaches enabled us to identify 3 genes (ANXA3, S100A9 and WT1) whose expression can be used to discriminate between the 2 studied AML FAB subtypes. The expression levels of the ANXA3 and S100A9 genes were increased, whereas those of WT1 were decreased in the AML-M2 compared to the AML-M1 group. We also examined the association between the STMN1, CAT and ABL1 genes, and the FLT3 and NPM1 mutation status. FLT3+/NPM1- AML was associated with the highest expression of STMN1, and ABL1 was upregulated in FLT3+ AML and CAT in FLT3- AML, irrespectively of the NPM1 mutation status. Moreover, our results indicated that CAT and WT1 gene expression levels correlated with the response to therapy. CAT expression was highest in patients who remained longer under complete remission, whereas WT1 expression increased with treatment resistance. On the whole, this study demonstrates that the AML-array can potentially serve as a first-line screening tool, and may be helpful for the diagnosis of AML, whereas the differentiation between AML subgroups can be more successfully performed with PCR-based analysis of a few marker genes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.