ReviewInternational journal of hematology2020
Molecular basis of clonal evolution in multiple myeloma.
Review in International journal of hematology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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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.
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Who cites it
35 citing papers in PubMed, 54 citations in OpenAlex.
- Review
- Genomic profiling enables personalized strategies to overcome drug resistance in multiple myeloma.Discover oncology · 2026Review
- Leveraging quantitative systems pharmacology modeling for elranatamab regimen optimization in relapsed or refractory multiple myeloma.NPJ systems biology and applications · 2025Article
- Impact of proteostasis workload on sensitivity to proteasome inhibitors in multiple myeloma.Clinical and experimental medicine · 2025Review
- Discovery of a novel class NSD2 inhibitor for multiple myeloma with t(4;14)Blood neoplasia · 2025Article
- CAR-T cells in the treatment of multiple myeloma: an encouraging cell therapy.Frontiers in immunology · 2025Review
- Single-cell profiling uncovers PTPRG-driven stemness in malignant plasma cells and signatures of treatment failure in multiple myeloma.Frontiers in immunology · 2025Article
- Anti‑BCMA CAR‑T cell immunotherapy for relapsed or refractory multiple myeloma.Experimental and therapeutic medicine · 2023Article
- EMD originates from hyaluronan-induced homophilic interactions of CD44 variant-expressing MM cells under shear stress.Blood advances · 2023Article
- Review on Bortezomib Resistance in Multiple Myeloma and Potential Role of Emerging Technologies.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Presence of bone marrow fibrosis in multiple myeloma may predict extramedullary disease.International journal of hematology · 2022Article
- Kinase Inhibition in Multiple Myeloma: Current Scenario and Clinical Perspectives.Pharmaceutics · 2022Review
- Gene expression profiling and in vitro functional studies reveal RAD54L as a potential therapeutic target in multiple myeloma.Genes & genomics · 2022Article
- Progress of modern imaging modalities in multiple myeloma.International journal of hematology · 2022Review
- Review
- The Rationale for the Dual-Targeting Therapy for RSK2 and AKT in Multiple Myeloma.International journal of molecular sciences · 2022Article
- The Peptide-Drug Conjugate Melflufen Modulates the Unfolded Protein Response of Multiple Myeloma and Amyloidogenic Plasma Cells and Induces Cell Death.HemaSphere · 2022Article
- [The significance of bone marrow immature plasma cell burden in the prognosis of newly diagnosed multiple myeloma patients].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2022Article
- Chimeric antigen receptor T-cell therapy for multiple myeloma.Frontiers in immunology · 2022Review
- Preclinical evidence of a direct pro-survival role of arginine deprivation in multiple myeloma.Frontiers in oncology · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The treatment outcome of multiple myeloma (MM) is worse than expected from the average numbers of non-synonymous mutations, which are roughly correlated with the prognosis of cancer patients. The refractoriness of MM may be ascribed to the complex genomic architecture and clonal behavior of the disease. In MM, disease progression is accomplished by branching patterns of subclonal evolution from reservoir clones with a propagating potential and/or the emergence of minor clones, which already exist at the MGUS stage and outcompete other clones through selective pressure mainly by therapeutic agents. Each subclone harbors novel mutations and distinct phenotypes including drug sensitivities. In general, mature clones are highly sensitive to proteasome inhibitors (PIs), whereas immature clones are resistant to PIs but could be eradicated by immunomodulatory drugs (IMiDs). The branching evolution is a result of the fitness of different clones to microenvironment and their evasion of immune surveillance; therefore, IMiDs are effective for MM with this pattern of evolution. In contrast, ~ 20% of MM evolve neutrally in the context of strong oncogenic drivers, such as high-risk IgH translocations, and are relatively resistant to IMiDs. Further understanding of the genomic landscape and the pattern of clonal evolution may contribute to the development of more effective treatment strategies for MM.
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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.