ReviewChromosoma2014
DNA damage accumulation and repair defects in acute myeloid leukemia: implications for pathogenesis, disease progression, and chemotherapy resistance.
Review in Chromosoma, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 86 citations in OpenAlex.
- Polθ activity modulates sensitivity to standard therapies in DNMT3A-deficient leukemia.Cell reports. Medicine · 2026Article
- Identification and validation of lymphangiogenesis-related genes for predicting acute myeloid leukemia prognosis: insights from bulk RNA sequencing and single-cell RNA sequencing analyses.Clinical and experimental medicine · 2026Article
- Energy Deficiency-Induced ATG4B Nuclear Translocation Inhibits PRMT1-Mediated DNA Repair and Promotes Leukemia Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Curcumin and acute myeloid leukemia: a golden hope, updated insights.Molecular biology reports · 2025Review
- Epigenetic mechanisms of drug resistance in acute myeloid leukemia: advances in small-molecule targeted therapy.Frontiers in pharmacology · 2025Review
- A Combinatorial Functional Precision Medicine Platform for Rapid Therapeutic Response Prediction in AML.Cancer medicine · 2024Article
- JAK2 inhibitors for the treatment of Philadelphia-negative myeloproliferative neoplasms: current status and future directions.Molecular diversity · 2024Review
- PTIP epigenetically regulates DNA damage-induced cell cycle arrest by upregulating PRDM1.Scientific reports · 2024Article
- Silencing of the DNA damage repair regulator PPP1R15A sensitizes acute myeloid leukemia cells to chemotherapy.Annals of hematology · 2024Article
- AZD-7648, a DNA-PK Inhibitor, Induces DNA Damage, Apoptosis, and Cell Cycle Arrest in Chronic and Acute Myeloid Leukemia Cells.International journal of molecular sciences · 2023Article
- Simultaneous Targeting of DNA Polymerase Theta and PARP1 or RAD52 Triggers Dual Synthetic Lethality in Homologous Recombination-Deficient Leukemia Cells.Molecular cancer research : MCR · 2023Article
- Genetic and chemical targeting of the ATPase complex TIP48 and 49 impairs acute myeloid leukemia.Leukemia · 2023Article
- A real-world disproportionality analysis of Rucaparib: Post-marketing Pharmacovigilance Data.BMC cancer · 2023Article
- Review
- High FAAP24 expression reveals poor prognosis and an immunosuppressive microenvironment shaping in AML.Cancer cell international · 2023Article
- DNA Damage Response-Related Proteins Are Prognostic for Outcome in Both Adult and Pediatric Acute Myelogenous Leukemia Patients: Samples from Adults and from Children Enrolled in a Children's Oncology Group Study.International journal of molecular sciences · 2023Article
- Reverse Phase Protein Array Profiling Identifies Recurrent Protein Expression Patterns of DNA Damage-Related Proteins across Acute and Chronic Leukemia: Samples from Adults and the Children's Oncology Group.International journal of molecular sciences · 2023Article
- DNA Repair Genes Polymorphisms: Impact on Acute Myeloid Leukemia Patients Outcome.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- Targeting Chemotherapy to Decondensed H3K27me3-Marked Chromatin of AML Cells Enhances Leukemia Suppression.Cancer research · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
DNA damage repair mechanisms are vital to maintain genomic integrity. Mutations in genes involved in the DNA damage response (DDR) can increase the risk of developing cancer. In recent years, a variety of polymorphisms in DDR genes have been associated with increased risk of developing acute myeloid leukemia (AML) or of disease relapse. Moreover, a growing body of literature has indicated that epigenetic silencing of DDR genes could contribute to the leukemogenic process. In addition, a variety of AML oncogenes have been shown to induce replication and oxidative stress leading to accumulation of DNA damage, which affects the balance between proliferation and differentiation. Conversely, upregulation of DDR genes can provide AML cells with escape mechanisms to the DDR anticancer barrier and induce chemotherapy resistance. The current review summarizes the DDR pathways in the context of AML and describes how aberrant DNA damage response can affect AML pathogenesis, disease progression, and resistance to standard chemotherapy, and how defects in DDR pathways may provide a new avenue for personalized therapeutic strategies in AML.
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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.