Increased vascularization in myeloma

Laroche, Michel; Brousset, Pierre; Ludot, I.; Mazières, B; Thiéchart, M.; Attal, Michel

doi:10.1034/j.1600-0609.2001.00191.x

Cited by 20 publications

(4 citation statements)

References 13 publications

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“…Several studies have demonstrated the presence of increased bone marrow angiogenesis in patients with multiple myeloma (Vacca et al , 1994; Rajkumar et al , 1999a; Ahn et al, 2001; Laroche et al, 2001). It continues to be debated whether this finding is related to the pathogenesis of the disease or whether it is merely an epiphenomenon or a surrogate marker of other biological features that are important in myeloma.…”

Section: Discussionmentioning

confidence: 99%

Bone marrow angiogenesis in multiple myeloma: effect of therapy

et al. 2002

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Summary. Recent studies have demonstrated that angiogenesis has a role in haematological malignancies, including multiple myeloma. Multiple myeloma is characterized by inevitable relapse after standard or high-dose chemotherapy. To study the effect of chemotherapy on bone marrow angiogenesis in patients with multiple myeloma, we used two methods to evaluate bone marrow angiogenesis in patients with newly diagnosed multiple myeloma, comparing these findings with those from bone marrow obtained after standard chemotherapy. Before therapy, an increased degree of bone marrow angiogenesis and a high bone marrow plasma cell labelling index (PCLI) were predictive of poorer survival. As estimated by microvessel density (MVD), the median survivals for patients with lowgrade, intermediate-grade and high-grade angiogenesis were 77, 30 and 14 months respectively. After therapy, the MVD did not change significantly. However, when patients with at least a partial response were considered separately, they showed a decrease in MVD. Post-therapy PCLI was predictive of survival, but post-therapy MVD was not. There was good correlation between angiogenesis estimated by visual grading and that determined by MVD assessment. We conclude that the degree of bone marrow angiogenesis is a prognostic marker in patients with multiple myeloma and does not decrease significantly after therapy.

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Section: Discussionmentioning

confidence: 99%

Bone marrow angiogenesis in multiple myeloma: effect of therapy

et al. 2002

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“…2, 3, 4 There is a direct correlation between BM microvessel density and parameters of disease progression. 5 Moreover, increased BM vascularization in MM patients is correlated with a poor prognosis.…”

Section: Introductionmentioning

confidence: 99%

Syndecan-1 promotes the angiogenic phenotype of multiple myeloma endothelial cells

et al. 2011

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Angiogenesis is considered a hallmark of multiple myeloma (MM) progression. In the present study, we evaluated the morphological and functional features of endothelial cells (ECs) derived from bone marrow (BM) of patients affected by MM (MMECs). We found that MMECs compared with normal BM ECs (BMECs) showed increased expression of syndecan-1. Silencing of syndecan-1 expression by RNA interference technique decreased in vitro EC survival, proliferation and organization in capillary-like structures. In vivo, in severe combined immunodeficient mice, syndecan-1 silencing inhibited MMEC organization into patent vessels. When overexpressed in human umbilical vein ECs and BMECs, syndecan-1 induced in vitro and in vivo angiogenic effects. Flow-cytometric analysis of MMECs silenced for syndecan-1 expression indicated a decreased membrane expression of vascular endothelial growth factor (VEGF) receptor-2 (VEGFR-2). Immunoprecipitation and confocal analysis showed colocalization of VEGFR-2 with syndecan-1. Absence of nuclear translocation of VEGFR-2 in syndecan-1-knockdown cells together with the shift from perinuclear localization to recycling compartments suggest a role of syndecan-1 in modulation of VEGFR-2 localization. This correlated with an in vitro decreased VEGF-induced invasion and motility. These results suggest that syndecan-1 may contribute to the highly angiogenic phenotype of MMECs by promoting EC proliferation, survival and modulating VEGF–VEGFR-2 signalling.

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“…Focusing on non-solid tumors, different authors have reported altered angiogenesis in association with different hematological malignancies. Laroche et al reported that the number of arterioles and capillaries increased in myeloma from its initial stages according to the gravity of the disease [ 119 ]. Increased BM angiogenesis and increased levels of associated factors, such as VEGF, have also been described in relation to AML, ALL, B-CLL or CML, among others, leading to the development of therapeutic applications based on disruption of this mechanism [ 120 ].…”

Section: Unresolved Questions In Modeling Bm and Non-solid Tumorsmentioning

confidence: 99%

In Vitro Modeling of Non-Solid Tumors: How Far Can Tissue Engineering Go?

Clara-Trujillo

Ferrer

Ribelles

2020

IJMS

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In hematological malignancies, leukemias or myelomas, malignant cells present bone marrow (BM) homing, in which the niche contributes to tumor development and drug resistance. BM architecture, cellular and molecular composition and interactions define differential microenvironments that govern cell fate under physiological and pathological conditions and serve as a reference for the native biological landscape to be replicated in engineered platforms attempting to reproduce blood cancer behavior. This review summarizes the different models used to efficiently reproduce certain aspects of BM in vitro; however, they still lack the complexity of this tissue, which is relevant for fundamental aspects such as drug resistance development in multiple myeloma. Extracellular matrix composition, material topography, vascularization, cellular composition or stemness vs. differentiation balance are discussed as variables that could be rationally defined in tissue engineering approaches for achieving more relevant in vitro models. Fully humanized platforms closely resembling natural interactions still remain challenging and the question of to what extent accurate tissue complexity reproduction is essential to reliably predict drug responses is controversial. However, the contributions of these approaches to the fundamental knowledge of non-solid tumor biology, its regulation by niches, and the advance of personalized medicine are unquestionable.

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Increased vascularization in myeloma

Cited by 20 publications

References 13 publications

Bone marrow angiogenesis in multiple myeloma: effect of therapy

Bone marrow angiogenesis in multiple myeloma: effect of therapy

Syndecan-1 promotes the angiogenic phenotype of multiple myeloma endothelial cells

In Vitro Modeling of Non-Solid Tumors: How Far Can Tissue Engineering Go?

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