ReviewFrontiers in genetics2019
Germline Risk Contribution to Genomic Instability in Multiple Myeloma.
Review in Frontiers in genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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
16 citing papers in PubMed, 21 citations in OpenAlex.
- Targeting BCL-2 with venetoclax and dexamethasone in patients with relapsed/refractory t(11;14) multiple myeloma.American journal of hematology · 2021Trial
- Genetic architecture of multiple myeloma: From somatic alterations to germline susceptibility and clinical implications.Translational oncology · 2026Review
- Multiple myeloma risk linked to DNA damage response genes.Journal of hematology & oncology · 2026Article
- Therapy-related B-cell acute lymphoblastic leukemia after treatment for multiple myeloma.American journal of blood research · 2026Article
- From Germline Susceptibility to Therapeutic Vulnerability: DNA Damage Response Gene Mutations Driving Multiple Myeloma Evolution and Precision Therapy.Human mutation · 2026Review
- Elevated Allele Frequency and Male-Predominance of a CommonCurrent issues in molecular biology · 2025Article
- Multi-omics profiling and AI-driven clinically deployable risk models in MGUS and smoldering myeloma.Clinical and experimental medicine · 2025Review
- FaMMily Affairs: Dissecting inherited contributions to multiple myeloma risk.Seminars in hematology · 2025Review
- The Genetic and Molecular Drivers of Multiple Myeloma: Current Insights, Clinical Implications, and the Path Forward.Pharmacogenomics and personalized medicine · 2024Review
- The Role of DNA Repair in Genomic Instability of Multiple Myeloma.International journal of molecular sciences · 2022Review
- Article
- Review
- Clonal Evolution of Multiple Myeloma-Clinical and Diagnostic Implications.Diagnostics (Basel, Switzerland) · 2021Review
- Non-secretory multiple myeloma with unusual TFG-ALK fusion showed dramatic response to ALK inhibition.NPJ genomic medicine · 2021Article
- Second malignancies in multiple myeloma; emerging patterns and future directions.Best practice & research. Clinical haematology · 2020Review
- Mesothelioma developing in carriers of inherited genetic mutations.Translational lung cancer research · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Genomic instability, a well-established hallmark of human cancer, is also a driving force in the natural history of multiple myeloma (MM) - a difficult to treat and in most cases fatal neoplasm of immunoglobulin producing plasma cells that reside in the hematopoietic bone marrow. Long recognized manifestations of genomic instability in myeloma at the cytogenetic level include abnormal chromosome numbers (aneuploidy) caused by trisomy of odd-numbered chromosomes; recurrent oncogene-activating chromosomal translocations that involve immunoglobulin loci; and large-scale amplifications, inversions, and insertions/deletions (indels) of genetic material. Catastrophic genetic rearrangements that either shatter and illegitimately reassemble a single chromosome (chromotripsis) or lead to disordered segmental rearrangements of multiple chromosomes (chromoplexy) also occur. Genomic instability at the nucleotide level results in base substitution mutations and small indels that affect both the coding and non-coding genome. Sometimes this generates a distinctive signature of somatic mutations that can be attributed to defects in DNA repair pathways, the DNA damage response (DDR) or aberrant activity of mutator genes including members of the
Indexed as
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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.