SynthesisScientific reports2021
Meta-analysis of gene signatures and key pathways indicates suppression of JNK pathway as a regulator of chemo-resistance in AML.
Synthesis in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
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- Multi-context modeling of driver pathways reveals common and specific mechanisms across 23 cancer types.PLoS computational biology · 2025Article
- Potential Cause-and-Effect Relationship between Gut Microbiota and Childhood Neuroblastoma: A Mendelian Randomization Analysis.Indian journal of pediatrics · 2025Article
- PELI2 inhibits colorectal cancer development through MAPK signaling pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- Integrated multi-optosis model for pan-cancer candidate biomarker and therapy target discovery.Frontiers in bioinformatics · 2025Article
- Unraveling the role of long non-coding RNAs in therapeutic resistance in acute myeloid leukemia: New prospects & challenges.Non-coding RNA research · 2024Review
- MT1E in AML: a gateway to understanding regulatory cell death and immunotherapeutic responses.Journal of leukocyte biology · 2024Article
- Review
- Genes Co-Expressed withInternational journal of molecular sciences · 2024Article
- Article
- Identification and analysis of methylation signature genes and association with immune infiltration in pediatric acute myeloid leukemia.Journal of cancer research and clinical oncology · 2023Article
- A six-gene prognostic signature for both adult and pediatric acute myeloid leukemia identified with machine learning.American journal of translational research · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathways and robust deregulated gene signatures involved in AML chemo-resistance are not fully understood. Multiple subgroups of AMLs which are under treatment of various regimens seem to have similar regulatory gene(s) or pathway(s) related to their chemo-resistance phenotype. In this study using gene set enrichment approach, deregulated genes and pathways associated with relapse after chemotherapy were investigated in AML samples. Five AML libraries compiled from GEO and ArrayExpress repositories were used to identify significantly differentially expressed genes between chemo-resistance and chemo-sensitive groups. Functional and pathway enrichment analysis of differentially expressed genes was performed to assess molecular mechanisms related to AML chemotherapeutic resistance. A total of 34 genes selected to be differentially expressed in the chemo-resistance compared to the chemo-sensitive group. Among the genes selected, c-Jun, AKT3, ARAP3, GABBR1, PELI2 and SORT1 are involved in neurotrophin, estrogen, cAMP and Toll-like receptor signaling pathways. All these pathways are located upstream and regulate JNK signaling pathway which functions as a key regulator of cellular apoptosis. Our expression data are in favor of suppression of JNK pathway, which could induce pro-apoptotic gene expression as well as down regulation of survival factors, introducing this pathway as a key regulator of drug-resistance development in AML.
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