Mast cells contribute to vasculogenic mimicry in multiple myeloma
Stem Cells and Development, ISSN: 1547-3287, Vol: 17, Issue: 1, Page: 19-22
2008
- 63Citations
- 26Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations63
- Citation Indexes63
- 63
- CrossRef33
- Captures26
- Readers26
- 26
Article Description
The angiogenic response is amplified during the induction phase of multiple myeloma (MM) and appears to exert a key role in the development of the disease [1]. Thus, inhibitors of angiogenesis have proven therapeutic potential in the treatment of patients with MM. Angiogenesis induced during the development of MM involves the direct production of proangiogenic cytokines by plasma cells within the marrow microenvironment. Mast cells (MCs) contribute to the the composition of the cellular components of the microenvironment in patients with MM, but their role in the pathophysiology of the disease is not clear. In this report, we used electron and confocal microscopy approaches to investigate the participation of MCs in the formation of the vessel wall in biopsy specimens from patients with MM. Results were compared to those obtained from the biopsy material of patients with a benign lesion, namely monoclonal gammopathy of undetermined significance (MGUS). Our results show that patients with MM exhibit typical tryptase-positive MCs, which interact physically with the endothelial cells (ECs) lining the vascular lumina, perhaps as a result of dysregulated vasculogenic development. This evidence highlights the importance of the stromal microenvironment during angiogenesis in the pathophysiology of MM and provides a novel perspective into the complex interplay between stromal and vascular components in the bone marrow microenvironment involved in the induction of hyervascularization in MM. © 2008 Mary Ann Liebert, Inc.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=39449125282&origin=inward; http://dx.doi.org/10.1089/scd.2007.0132; http://www.ncbi.nlm.nih.gov/pubmed/18205547; https://www.liebertpub.com/doi/10.1089/scd.2007.0132; http://www.liebertonline.com/doi/abs/10.1089/scd.2007.0132; http://online.liebertpub.com/doi/abs/10.1089/scd.2007.0132
Mary Ann Liebert Inc
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