ArticleBlood2014
Jumping translocations of 1q12 in multiple myeloma: a novel mechanism for deletion of 17p in cytogenetically defined high-risk disease.
Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Prediction of outcome in newly diagnosed myeloma: a meta-analysis of the molecular profiles of 1905 trial patients.Leukemia · 2018Pooled it
- Concomitant gain of 1q21 and MYC translocation define a poor prognostic subgroup of hyperdiploid multiple myeloma.Haematologica · 2016Trial
- Article
- Fluorescence in situ hybridization reveals the evolutionary biology of minor clone of gain/amp(1q) in multiple myeloma.Leukemia · 2024Article
- The numerous facets of 1q21Oncology letters · 2024Review
- 1q21+ is associated with poor prognosis in newly diagnosed multiple myeloma patients with extramedullary disease: a retrospective study.Annals of hematology · 2024Article
- Chromosomal Damage, Chromosome Instability, and Polymorphisms inInternational journal of molecular sciences · 2024Article
- Multiomic Mapping of Acquired Chromosome 1 Copy-Number and Structural Variants to Identify Therapeutic Vulnerabilities in Multiple Myeloma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Selective pericentromeric heterochromatin dismantling caused by TP53 activation during senescence.Nucleic acids research · 2022Article
- Amp 1q21 is more predictable with dismal survival than gain 1q21 of newly diagnosed multiple myeloma in real-world analysis.Journal of clinical laboratory analysis · 2022Article
- Cytogenetic Abnormalities in Multiple Myeloma: Incidence, Prognostic Significance, and Geographic Heterogeneity in Indian and Western Populations.Cytogenetic and genome research · 2022Article
- Profile of Chromosomal Alterations, Chromosomal Instability and Clonal Heterogeneity in Colombian Farmers Exposed to Pesticides.Frontiers in genetics · 2022Article
- Patient similarity network of newly diagnosed multiple myeloma identifies patient subgroups with distinct genetic features and clinical implications.Science advances · 2021Article
- Single- and double-hit events in genes encoding immune targets before and after T cell-engaging antibody therapy in MM.Blood advances · 2021Article
- Review
- A Journey Through Myeloma Evolution: From the Normal Plasma Cell to Disease Complexity.HemaSphere · 2020Review
- An acquired high-risk chromosome instability phenotype in multiple myeloma: Jumping 1q Syndrome.Blood cancer journal · 2019Article
- Advanced forms of MPNs are accompanied by chromosomal abnormalities that lead to dysregulation of TP53.Blood advances · 2018Article
- The multiple myelomas - current concepts in cytogenetic classification and therapy.Nature reviews. Clinical oncology · 2018Review
- Hyperhaploid karyotypes in multiple myeloma.Oncotarget · 2017Article
Corrections and comments
- Commented on by
Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
Multiple myeloma (MM) is a B-cell malignancy driven in part by increasing copy number alterations (CNAs) during disease progression. Prognostically significant CNAs accumulate during clonal evolution and include gains of 1q21 and deletions of 17p, among others. Unfortunately, the mechanisms underlying the accumulation of CNAs and resulting subclonal heterogeneity in high-risk MM are poorly understood. To investigate the impact of jumping translocations of 1q12 (JT1q12) on receptor chromosomes (RCs) and subsequent clonal evolution, we analyzed specimens from 86 patients selected for unbalanced 1q12 aberrations by G-banding. Utilizing spectral karyotyping and locus-specific fluorescence in situ hybridization, we identified 10 patients with unexpected focal amplifications of an RC that subsequently translocated as part of a sequential JT1q12 to one or more additional RCs. Four patients exhibited amplification and translocation of 8q24 (MYC), 3 showed amplification of 16q11, and 1 each displayed amplification of 18q21.3 (BCL2), 18q23, or 4p16 (FGFR3). Unexpectedly, in 6 of 14 patients with the combination of the t(4;14) and deletion of 17p, we identified the loss of 17p as resulting from a JT1q12. Here, we provide evidence that the JT1q12 is a mechanism for the simultaneous gain of 1q21 and deletion of 17p in cytogenetically defined high-risk disease.
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.