ArticleHaematologica2021
Halting the vicious cycle within the multiple myeloma ecosystem: blocking JAM-A on bone marrow endothelial cells restores angiogenic homeostasis and suppresses tumor progression.
Article in Haematologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 59 citations in OpenAlex.
- Junctional Adhesion Molecule-A (JAM-A) Associates With High-Risk Disease in Multiple Myeloma Patients and a Structure-Based Rationally-Designed Peptide Inhibitor Attenuates Tumorigenic Features In Vitro and In Vivo.European journal of haematology · 2026Article
- Drug Resistance in Multiple Myeloma: Tumor-Intrinsic Mechanisms and the Bone Marrow Microenvironment.Cell biochemistry and function · 2026Review
- Tight Spaces, Big Discoveries: Decoding Human Adhesion Biology with Avian Chorioallantoic Membrane Xenograft Models.Cancers · 2026Review
- Mechanisms and intervention strategies of microenvironment-mediated drug resistance in multiple myeloma.Cancer cell international · 2026Review
- Prognostic impact of the immune microenvironment in multiple myeloma: a meta-analysis of current studies.Haematologica · 2025Article
- Article
- Targeting of mitochondrial fission through natural flavanones elicits anti-myeloma activity.Journal of translational medicine · 2024Article
- The relationship between peripheral T follicular helper cells and disease severity in systemic sclerosis.Clinical and experimental medicine · 2024Article
- Article
- Breaking through Multiple Myeloma: A Paradigm for a Comprehensive Tumor Ecosystem Targeting.Biomedicines · 2023Review
- Article
- Visualizing the Interactions Shaping the Imaging of the Microenvironment in Human Cancers.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Increased Circulating Soluble Junctional Adhesion Molecules in Systemic Sclerosis: Association with Peripheral Microvascular Impairment.Life (Basel, Switzerland) · 2022Article
- Pathways of Angiogenic and Inflammatory Cytokines in Multiple Myeloma: Role in Plasma Cell Clonal Expansion and Drug Resistance.Journal of clinical medicine · 2022Review
- SARS-CoV-2 and Endothelial Cells: Vascular Changes, Intussusceptive Microvascular Growth and Novel Therapeutic Windows.Biomedicines · 2022Review
- The Route of the Malignant Plasma Cell in Its Survival Niche: Exploring "Multiple Myelomas".Cancers · 2022Review
- Junctional adhesion molecule C expression specifies a CD138low/neg multiple myeloma cell population in mice and humans.Blood advances · 2022Article
- The Rationale for the Dual-Targeting Therapy for RSK2 and AKT in Multiple Myeloma.International journal of molecular sciences · 2022Article
- Using the Power of Junctional Adhesion Molecules Combined with the Target of CAR-T to Inhibit Cancer Proliferation, Metastasis and Eradicate Tumors.Biomedicines · 2022Article
- Microfluidic device engineered to study the trafficking of multiple myeloma cancer cells through the sinusoidal niche of bone marrow.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
31 authors at 10 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interactions of malignant multiple myeloma (MM) plasma cells (MM-cells) with the microenvironment control MM-cell growth, survival, drug-resistance and dissemination. As in MM microvascular density increases in the bone marrow (BM), we investigated whether BM MM endothelial cells (MMECs) control disease progression via the junctional adhesion molecule A (JAM-A). Membrane and cytoplasmic JAM-A levels were upregulated in MMECs in 111 newly diagnosed (NDMM) and 201 relapsed-refractory (RRMM) patients compared to monoclonal gammopathy of undetermined significance (MGUS) and healthy controls. Elevated membrane expression of JAM-A on MMECs predicted poor clinical outcome. Mechanistically, addition of recombinant JAM-A to MMECs increased angiogenesis whereas its inhibition impaired angiogenesis and MM growth in 2D and 3D in vitro cell culture and chorioallantoic membrane-assays. To corroborate these findings, we treated MM bearing mice with JAM-A blocking mAb and demonstrated impaired MM progression corresponding to decreased MM-related vascularity. These findings support JAM-A as an important mediator of MM progression through facilitating MM-associated angiogenesis. Collectively, elevated JAM-A expression on bone marrow endothelial cells is an independent prognostic factor for patient survival in both NDMM and RRMM. Blocking JAM-A restricts angiogenesis in vitro, in embrio and in vivo and represents a suitable druggable molecule to halt neoangiogenesis and MM progression.
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