ReviewCancers2021
DNA Damage Response in Multiple Myeloma: The Role of the Tumor Microenvironment.
Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 32 citations in OpenAlex.
- Genetic architecture of multiple myeloma: From somatic alterations to germline susceptibility and clinical implications.Translational oncology · 2026Review
- Dynamic changes in blood-derived inflammatory and bone metabolic markers for disease monitoring and prognostic assessment in multiple myeloma.American journal of translational research · 2026Article
- Structure-based design of new potent and highly selective PARP-1 inhibitor for treating colorectal cancer.Journal of enzyme inhibition and medicinal chemistry · 2025Article
- Therapeutic potential of PRMT1 as a critical survival dependency target in multiple myeloma.BMC cancer · 2025Article
- DNA Damage Response and Redox Status in the Resistance of Multiple Myeloma Cells to Genotoxic Treatment.International journal of molecular sciences · 2025Article
- Polymerase theta inhibition impairs tumor growth and amplifies melphalan-induced DNA damage in multiple myeloma.Journal of translational medicine · 2025Article
- Review
- Glioma-astrocyte connexin43 confers temozolomide resistance through activation of the E2F1/ERCC1 axis.Neuro-oncology · 2025Article
- Germline predisposition in multiple myeloma.iScience · 2025Article
- The Interplay between the DNA Damage Response (DDR) Network and the Mitogen-Activated Protein Kinase (MAPK) Signaling Pathway in Multiple Myeloma.International journal of molecular sciences · 2024Review
- Understanding DNA Epigenetics by Means of Raman/SERS Analysis for Cancer Detection.Biosensors · 2024Article
- Gene interaction network analysis in multiple myeloma detects complex immune dysregulation associated with shorter survival.Blood cancer journal · 2023Article
- Article
- 2-Hydroxy-3-methylanthraquinone inhibits homologous recombination repair in osteosarcoma through the MYC-CHK1-RAD51 axis.Molecular medicine (Cambridge, Mass.) · 2023Article
- Understanding human aging and the fundamental cell signaling link in age-related diseases: the middle-aging hypovascularity hypoxia hypothesis.Frontiers in aging · 2023Article
- Transcriptome profiling of high and low somatic embryogenesis rate of oil palm (Frontiers in plant science · 2023Article
- THZ531 Induces a State of BRCAness in Multiple Myeloma Cells: Synthetic Lethality with Combination Treatment of THZ 531 with DNA Repair Inhibitors.International journal of molecular sciences · 2022Article
- Multiple Myeloma Patient Tumors With High Levels of Cereblon Exon-10 Deletion Splice Variant Upregulate Clinically Targetable Pro-Inflammatory Cytokine Pathways.Frontiers in genetics · 2022Article
- Review
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
No grant is acknowledged in the PubMed record.
Abstract
Multiple myeloma (MM) is an incurable plasma cell malignancy characterized by genomic instability. MM cells present various forms of genetic instability, including chromosomal instability, microsatellite instability, and base-pair alterations, as well as changes in chromosome number. The tumor microenvironment and an abnormal DNA repair function affect genetic instability in this disease. In addition, states of the tumor microenvironment itself, such as inflammation and hypoxia, influence the DNA damage response, which includes DNA repair mechanisms, cell cycle checkpoints, and apoptotic pathways. Unrepaired DNA damage in tumor cells has been shown to exacerbate genomic instability and aberrant features that enable MM progression and drug resistance. This review provides an overview of the DNA repair pathways, with a special focus on their function in MM, and discusses the role of the tumor microenvironment in governing DNA repair mechanisms.
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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.