ArticleBlood2016
Clonal selection and double-hit events involving tumor suppressor genes underlie relapse in myeloma.
Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers, 2 of them syntheses 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
150 citing papers in PubMed, 2 syntheses or guidelines pooled it, 211 citations in OpenAlex.
- International Myeloma Society/International Myeloma Working Group Consensus Recommendations on the Definition of High-Risk Multiple Myeloma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2025Guideline
- Chromosome 1q21 abnormalities refine outcome prediction in patients with multiple myeloma - a meta-analysis of 2,596 trial patients.Haematologica · 2021Pooled it
- An enhanced genetic model of relapsed IGH-translocated multiple myeloma evolutionary dynamics.Blood cancer journal · 2020Trial
- Trial
- Prevalence and timing of TP53 mutations in del(17p) myeloma and effect on survival.Blood cancer journal · 2017Trial
- Longitudinal fluorescenceHaematologica · 2017Trial
- A single-cell atlas of multiple myeloma defines malignant archetypes and proliferative states.Nature genetics · 2026Article
- Article
- IMS-IMWG 2025 consensus genomic staging predicts outcomes with daratumumab-based quadruplet regimens for NDMM.Blood advances · 2026Article
- Outcomes of Double-Hit and Single High-Risk Cytogenetic Newly Diagnosed Myeloma in Transplant-Eligible Patients.Current oncology (Toronto, Ont.) · 2026Article
- The evolution to hepta-refractory myeloma involves sequential loss of CD38, BCMA and GPRC5D.Leukemia · 2026Article
- Review
- Article
- Temporal genomic dynamics shape clinical trajectory in multiple myeloma.Nature genetics · 2025Article
- Resistance to immunomodulatory drugs in multiple myeloma: the cereblon pathway and beyond.Haematologica · 2025Review
- Risk factors for multiple myeloma and its precursor diseases.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Review
- Current State of Evidence on Definitions and Management of High-Risk Multiple Myeloma.Current oncology reports · 2025Review
- Refining High-Risk Multiple Myeloma: Advancements in Genomic, Clinical, and Prognostic Criteria.Mediterranean journal of hematology and infectious diseases · 2025Review
- CAR-T cell therapy in Multiple Myeloma: current status and future challenges.Blood cancer journal · 2024Review
- Review
90 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
25 authors at 1 institution in 1 country.
Funding
Abstract
To elucidate the mechanisms underlying relapse from chemotherapy in multiple myeloma, we performed a longitudinal study of 33 patients entered into Total Therapy protocols investigating them using gene expression profiling, high-resolution copy number arrays, and whole-exome sequencing. The study illustrates the mechanistic importance of acquired mutations in known myeloma driver genes and the critical nature of biallelic inactivation events affecting tumor suppressor genes, especially TP53, the end result being resistance to apoptosis and increased proliferation rates, which drive relapse by Darwinian-type clonal evolution. The number of copy number aberration changes and biallelic inactivation of tumor suppressor genes was increased in GEP70 high risk, consistent with genomic instability being a key feature of high risk. In conclusion, the study highlights the impact of acquired genetic events, which enhance the evolutionary fitness level of myeloma-propagating cells to survive multiagent chemotherapy and to result in relapse.
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.