ArticleLeukemia research2018
Whole exome sequencing identifies novel mutations of epigenetic regulators in chemorefractory pediatric acute myeloid leukemia.
Article in Leukemia research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
17 citing papers in PubMed, 25 citations in OpenAlex.
- KDM5 family of demethylases promotes CD44-mediated chemoresistance in pancreatic adenocarcinomas.Scientific reports · 2023Article
- Triple-negative Thrombocythemia and Subsequent Acute Lymphoblastic Leukemia with Additional Somatic Mutations.Internal medicine (Tokyo, Japan) · 2023Article
- The histone demethylase KDM5C functions as a tumor suppressor in AML by repression of bivalently marked immature genes.Leukemia · 2023Article
- Tumor hypoxia: From basic knowledge to therapeutic implications.Seminars in cancer biology · 2023Review
- KDM5 Lysine Demethylases in Pathogenesis, from Basic Science Discovery to the Clinic.Advances in experimental medicine and biology · 2023Article
- A genomic DNA-based NGS method for the simultaneous detection of multiple fusion genes in pediatric leukemia.Oncology letters · 2023Article
- Targeting Chromatin-Remodeling Factors in Cancer Cells: Promising Molecules in Cancer Therapy.International journal of molecular sciences · 2022Review
- The genesis and evolution of acute myeloid leukemia stem cells in the microenvironment: From biology to therapeutic targeting.Cell death discovery · 2022Review
- The Chromatin-Oxygen Sensor GeneInternational journal of molecular sciences · 2022Article
- Decitabine and vorinostat with FLAG chemotherapy in pediatric relapsed/refractory AML: Report from the therapeutic advances in childhood leukemia and lymphoma (TACL) consortium.American journal of hematology · 2022Article
- Article
- The Cross Marks the Spot: The Emerging Role of JmjC Domain-Containing Proteins in Myeloid Malignancies.Biomolecules · 2021Review
- Emerging epigenetic therapeutics for myeloid leukemia: modulating demethylase activity with ascorbate.Haematologica · 2021Review
- 2-Oxoglutarate-dependent dioxygenases in cancer.Nature reviews. Cancer · 2020Review
- Identification of ryuvidine as a KDM5A inhibitor.Scientific reports · 2019Article
- Biology and targeting of the Jumonji-domain histone demethylase family in childhood neoplasia: a preclinical overview.Expert opinion on therapeutic targets · 2019Review
- Precision medicine in the treatment stratification of AML patients: challenges and progress.Oncotarget · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 7 institutions in 2 countries.
Funding
Abstract
Genomic alterations underlying chemotherapy resistance remains poorly characterized in pediatric acute myeloid leukemia (AML). In this study, we used whole exome sequencing to identify gene mutations associated with chemo-resistance in 44 pediatric AML patients. We identified previously unreported mutations involving epigenetic regulators such as KDM5C, SRIT6, CHD4, and PRPF6 in pediatric AML patients. Despite low prevalence in general pediatric AML, mutations involving epigenetic regulators including splicing factors, were collectively enriched as a group in primary chemo-resistance AML patients. In addition, clonal evolution analysis of secondary chemo-resistance AML patients reveals dominant clone at diagnosis could survive several course of intensified chemotherapy. And gain of new mutations in genes such as MVP, TCF3, SS18, and BCL10, may contribute to chemo-resistance at relapse. These results provide novel insights into the genetic basis of treatment failure in pediatric AML.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.