Trial reportPloS one2015
Gene expression profiles associated with pediatric relapsed AML.
Trial report in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed.
- Identification of single-cell blasts in pediatric acute myeloid leukemia using an autoencoder.Life science alliance · 2024Article
- Acute myeloid leukemia: novel mutations and their clinical implications.American journal of blood research · 2023Review
- Transcriptomic analysis reveals proinflammatory signatures associated with acute myeloid leukemia progression.Blood advances · 2022Article
- Long noncoding RNA SATB1-AS1 contributes to the chemotherapy resistance through the microRNA-580/ 2'-5'-oligoadenylate synthetase 2 axis in acute myeloid leukemia.Bioengineered · 2021Article
- Deciphering molecular heterogeneity in pediatric AML using a cancer vs. normal transcriptomic approach.Pediatric research · 2021Article
- Harnessing Gene Expression Profiles for the Identification of Ex Vivo Drug Response Genes in Pediatric Acute Myeloid Leukemia.Cancers · 2020Article
- Phosphotyrosine-based Phosphoproteomics for Target Identification and Drug Response Prediction in AML Cell Lines.Molecular & cellular proteomics : MCP · 2020Article
- Targeting the RNA mCell stem cell · 2019Article
- Development and validation of GMI signature based random survival forest prognosis model to predict clinical outcome in acute myeloid leukemia.BMC medical genomics · 2019Article
- Decreased SATB1 expression promotes AML cell proliferation through NF-κB activation.Cancer cell international · 2019Article
- Reduced expression but not deficiency of GFI1 causes a fatal myeloproliferative disease in mice.Leukemia · 2019Article
- Mechanisms of drug resistance in acute myeloid leukemia.OncoTargets and therapy · 2019Review
- Self-nanoemulsifying system improves oral absorption and enhances anti-acute myeloid leukemia activity of berberine.Journal of nanobiotechnology · 2018Article
- Epigenetic heterogeneity affects the risk of relapse in children with t(8;21)RUNX1-RUNX1T1-rearranged AML.Leukemia · 2018Article
- Molecular and genetic alterations associated with therapy resistance and relapse of acute myeloid leukemia.Journal of hematology & oncology · 2017Review
- MicroRNA-106b~25 cluster is upregulated in relapsed MLL-rearranged pediatric acute myeloid leukemia.Oncotarget · 2016Article
- Article
- LIN28B is over-expressed in specific subtypes of pediatric leukemia and regulates lncRNA H19.Haematologica · 2016Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Development of relapse remains a problem for further improvements in the survival of pediatric AML patients. While virtually all patients show a good response to initial treatment, more patients respond poorly when treated at relapse. The cellular characteristics of leukemic blast cells that allow survival of initial treatment, relapse development and subsequent resistance to salvage treatment remain largely elusive. Therefore, we studied if leukemic blasts at relapse biologically resemble their initial diagnosis counterparts. We performed microarray gene expression profiling on paired initial and relapse samples of 23 pediatric AML patients. In 11 out of 23 patients, gene expression profiles of initial and corresponding relapse samples end up in different clusters in unsupervised analysis, indicating altered gene expression profiles. In addition, shifts in type I/II mutational status were found in 5 of these 11 patients, while shifts were found in 3 of the remaining 12 patients. Although differentially expressed genes varied between patients, they were commonly related to hematopoietic differentiation, encompassed genes involved in chromatin remodeling and showed associations with similar transcription factors. The top five were CEBPA, GFI1, SATB1, KLF2 and TBP. In conclusion, the leukemic blasts at relapse are biologically different from their diagnosis counterparts. These differences may be exploited for further development of novel treatment strategies.
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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.