ArticleBlood2009
CXCR4 inhibitor AMD3100 disrupts the interaction of multiple myeloma cells with the bone marrow microenvironment and enhances their sensitivity to therapy.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 255 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
255 citing papers in PubMed, 2 syntheses or guidelines pooled it, 422 citations in OpenAlex.
- Clinicopathological significance of CXCR4 in non-small cell lung cancer.Drug design, development and therapy · 2015Pooled it
- A meta-analysis for CXCR4 as a prognostic marker and potential drug target in non-small cell lung cancer.Drug design, development and therapy · 2015Pooled it
- A Phase Ib/II Trial of the First-in-Class Anti-CXCR4 Antibody Ulocuplumab in Combination with Lenalidomide or Bortezomib Plus Dexamethasone in Relapsed Multiple Myeloma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Trial
- Plerixafor is superior to conventional chemotherapy for first-line stem cell mobilisation, and is effective even in heavily pretreated patients.Blood cancer journal · 2014Trial
- Trial
- Ex vivo bone marrow subniches influence the fate of human antibody-secreting cells.Science advances · 2026Article
- Targeting the immune-metabolic axis reverses orthodontics-induced systemic pathology.Signal transduction and targeted therapy · 2026Article
- When Myeloma Escapes the Bone Marrow: Extramedullary Disease in the Immunotherapy Era.Cancers · 2026Review
- Homomultimeric FAP Inhibitor-Based Radioligands for Cancer Theranostics: Design Principles, Structure-Function Relationships, and Preclinical Performance.Molecules (Basel, Switzerland) · 2026Review
- The endosteal niche regulates breast cancer cell dormancy in bone: identification of new molecular determinants.Bone research · 2026Article
- SSTNSignal transduction and targeted therapy · 2026Article
- Myeloid-derived suppressor cells in multiple myeloma: mechanistic insights and therapeutic implications.Frontiers in immunology · 2026Review
- Genes-first and phenotypes-first paths to treatment resistance in hematological malignancies.Cell death & disease · 2025Review
- Immuno-positron emission tomography as a new frontier in imaging hematologic malignancies.World journal of clinical oncology · 2025Review
- Presentation of CXCL12γ by heparan sulfate proteoglycans activates CXCR4 without desensitization in normal and malignant B cells.Blood advances · 2025Article
- Bone Marrow-Targeted Liposomes Loaded with Bortezomib Overcome Multiple Myeloma Resistance.ACS nano · 2025Article
- Acquired Bortezomib Resistance in Multiple Myeloma: From Mechanisms to Strategy.Current treatment options in oncology · 2024Review
- IL-10R inhibition reprograms tumor-associated macrophages and reverses drug resistance in multiple myeloma.Leukemia · 2024Article
- Relationship between adipocytes and hematological tumors in the bone marrow microenvironment: a literature review.Translational cancer research · 2024Review
- In vitro models of the crosstalk between multiple myeloma and stromal cells recapitulate the mild NF-κB activation observed in vivo.Cell death & disease · 2024Article
195 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
24 authors at 4 institutions in 1 country.
Funding
Abstract
The interaction of multiple myeloma (MM) cells with their microenvironment in the bone marrow (BM) provides a protective environment and resistance to therapeutic agents. We hypothesized that disruption of the interaction of MM cells with their BM milieu would lead to their sensitization to therapeutic agents such as bortezomib, melphalan, doxorubicin, and dexamethasone. We report that the CXCR4 inhibitor AMD3100 induces disruption of the interaction of MM cells with the BM reflected by mobilization of MM cells into the circulation in vivo, with kinetics that differed from that of hematopoietic stem cells. AMD3100 enhanced sensitivity of MM cell to multiple therapeutic agents in vitro by disrupting adhesion of MM cells to bone marrow stromal cells (BMSCs). Moreover, AMD3100 increased mobilization of MM cells to the circulation in vivo, increased the ratio of apoptotic circulating MM cells, and enhanced the tumor reduction induced by bortezomib. Mechanistically, AMD3100 significantly inhibited Akt phosphorylation and enhanced poly(ADP-ribose) polymerase (PARP) cleavage as a result of bortezomib, in the presence of BMSCs in coculture. These experiments provide a proof of concept for the use of agents that disrupt interaction with the microenvironment for enhancement of efficacy of cytotoxic agents in cancer therapy.
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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.