ArticleFrontiers in oncology2023
Metabolic changes underlying drug resistance in the multiple myeloma tumor microenvironment.
Article in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 21 citations in OpenAlex.
- 3D biomimetic microgel platform for multiple myeloma: Approaching tumor microenvironment on cell lines and patient-derived cells.Materials today. Bio · 2026Article
- Repurposing Camellia sinensis Roots and Ginkgo biloba Leaves for Multiple Myeloma via Wnt/β-Catenin-Dependent Cell Cycle Arrest and Apoptosis.Chemistry & biodiversity · 2026Article
- The Shape-Shifting Myeloma: Adaptive Plasticity as a Hallmark of Relapse and Refractoriness.Cancers · 2026Review
- Extracellular Enolase-1 Promotes CAF-Associated Stromal Reprogramming via the Plasmin/TGF-β Axis in Multiple Myeloma.Cancers · 2026Article
- A metabolic trade-off between malignant plasma cells and mesenchymal stromal cells sustains multiple myeloma growth.Blood neoplasia · 2026Article
- The controversial role of metabolic reprogramming in anti-tumor therapy resistance.Discover oncology · 2026Review
- Genomic profiling enables personalized strategies to overcome drug resistance in multiple myeloma.Discover oncology · 2026Review
- CLL-1: An emerging target for immunotherapy in acute myeloid leukemia.Annals of hematology · 2026Review
- Long non-coding RNAs and therapeutic resistance in multiple myeloma: from molecular insights to clinical applications.Clinical and experimental medicine · 2026Review
- Single-cell and functional profiling identifies an IL6-centered immunometabolic communication circuit in multiple myeloma.Frontiers in immunology · 2026Article
- Targeting drug resistant colorectal cancer with apigenin nanoarchitectures.Translational oncology · 2025Review
- Decoding NF-κB: nucleocytoplasmic shuttling dynamics, synthetic modulation and post-therapeutic behavior in cancer.Molecular biology reports · 2025Review
- Genetic, epigenetic, and molecular determinants of multiple myeloma and precursor plasma cell disorders: a pathophysiological overview.Medical oncology (Northwood, London, England) · 2025Review
- Article
- N6-methyladenosine-mediated upregulation of H19 promotes resistance to bortezomib by modulating the miR-184/CARM1 axis in multiple myeloma.Clinical and experimental medicine · 2025Article
- B cell immunometabolism in health and disease.Nature immunology · 2025Review
- LILRB4 regulates multiple myeloma development through STAT3-PFKFB1 pathway.Cell death & disease · 2024Article
- Deciphering metabolic crosstalk in context: lessons from inflammatory diseases.Molecular oncology · 2024Review
- Engagement of Mesenchymal Stromal Cells in the Remodeling of the Bone Marrow Microenvironment in Hematological Cancers.Biomolecules · 2023Review
- Lipid metabolic vulnerabilities of multiple myeloma.Clinical and experimental medicine · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple myeloma (MM) is characterized by the clonal expansion of malignant plasma cells in the bone marrow (BM). MM remains an incurable disease, with the majority of patients experiencing multiple relapses from different drugs. The MM tumor microenvironment (TME) and in particular bone-marrow stromal cells (BMSCs) play a crucial role in the development of drug resistance. Metabolic reprogramming is emerging as a hallmark of cancer that can potentially be exploited for cancer treatment. Recent studies show that metabolism is further adjusted in MM cells during the development of drug resistance. However, little is known about the role of BMSCs in inducing metabolic changes that are associated with drug resistance. In this Perspective, we summarize current knowledge concerning the metabolic reprogramming of MM, with a focus on those changes associated with drug resistance to the proteasome inhibitor Bortezomib (BTZ). In addition, we present proof-of-concept fluxomics (glucose isotope-tracing) and Seahorse data to show that co-culture of MM cells with BMSCs skews the metabolic phenotype of MM cells towards a drug-resistant phenotype, with increased oxidative phosphorylation (OXPHOS), serine synthesis pathway (SSP), TCA cycle and glutathione (GSH) synthesis. Given the crucial role of BMSCs in conveying drug resistance, insights into the metabolic interaction between MM and BMSCs may ultimately aid in the identification of novel metabolic targets that can be exploited for therapy.
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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 Socratic graph.