Tumor vasculogenic mimicry predicts poor prognosis in cancer patients: a meta-analysis

Yang, Jin-Hao; Liao, Yuning; Junior, D. M.; Xie, Peng; Qiang, Yuan Yuan; Zheng, Lixin; Wang, M. Y.; Yan, Mei; Meng, Dongfang; Xu, Lanxi; Cao, Longhui; Yang, Qi; Yang, Xue-Fei; Wang, W. B.; Peng, Li‐Xia; Huang, Bi‐Jun; Qian, Chao Nan

doi:10.1007/s10456-016-9500-2

Cited by 109 publications

(96 citation statements)

References 63 publications

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“…Most notably, melanoma cells can align along a deposited basement membrane forming interconnecting vessel‐like structures with lumen, a process known as vasculogenic mimicry (VM). First described in 1999 in uveal melanoma, 94 VM is considered a signature of aggressive cancers, and the occurrence of VM has now been found to correlate with poor prognosis in many cancers such as cutaneous melanoma, breast cancer and glioblastoma 95 . Moreover, it is observed that VEGF inhibition resulted in adaptive resistance in melanoma xenografts, in turn leading to increased VM 96 .…”

Section: Vasculogenic Mimicry Channels: An Alternative Route Of Leukomentioning

confidence: 99%

Control of immune cell entry through the tumour vasculature: a missing link in optimising melanoma immunotherapy?

et al. 2017

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Metastatic melanoma remains a fatal disease to many worldwide, even after the breakthrough introduction of targeted therapies such as BRAF inhibitors and immune checkpoint blockade therapies such as CTLA-4 and PD-1 inhibitors. With advances in our understanding of this disease, as well as the increasing data gathered from patient studies, the significance of the host immune response to cancer progression and response to treatment is becoming clear. More specifically, the presence of intratumoral CD8+ cytotoxic T-cells correlates with better prognosis whereas the accumulation of monocytes/macrophages and neutrophils in the tumour is often associated with worse prognosis. Access and infiltration of circulating leukocytes into the tumour is governed by adhesion molecules and chemokines expressed by the endothelial cells of the vasculature. This review focuses on the adhesion molecules and chemokines which control the homing of CD8+ cytotoxic T-cells, monocytes and neutrophils to peripheral tissues, including tumours. We discuss the role of these leukocyte subsets in regulating melanoma growth, and detail the mechanisms used by tumours to selectively recruit or exclude these leukocytes for their own advantage. In doing so, we bring to light an underappreciated component of tumour biology which should be considered in combination with current treatments to selectively alter the leukocyte composition of tumours and ultimately enhance treatment outcome.

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Section: Vasculogenic Mimicry Channels: An Alternative Route Of Leukomentioning

confidence: 99%

Control of immune cell entry through the tumour vasculature: a missing link in optimising melanoma immunotherapy?

et al. 2017

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“…It is intriguing to find that both tumors in this series were monosomy 3 and exhibited vasculogenic mimicry patterns: genetic and histopathological findings that have been associated with an aggressive clinical course [15,16]. However, it should be emphasized that both patients in this study are alive and metastasis free 9 years following enucleation.…”

Section: Discussionmentioning

confidence: 74%

Growth of Uveal Melanoma following Intravitreal Bevacizumab

et al. 2016

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Purpose: Typically treatment of large melanomas (by Collaborative Ocular Melanoma Study criteria) is restricted to enucleation, due to size constraints for plaque brachytherapy. Because primary and metastatic uveal melanoma cells are inhibited by bevacizumab (an anti-vascular endothelial growth factor), this prospective study evaluated the impact of intravitreal bevacizumab on large uveal melanomas that were destined for enucleation. Size reduction by bevacizumab would potentially salvage these eyes by making them eligible for treatment with plaque brachytherapy. Procedures: Two patients with large uveal melanoma were each treated with one intravitreous injection of bevacizumab (1.25 mg/0.05 mL). Results: Both tumors displayed paradoxical growth 1 week following the injection, with confirmed growth 1 week later (increase from baseline of 1.1 mm in one eye and 3.1 mm in the other eye). Both eyes were enucleated and monosomy 3 and vasculogenic mimicry patterns were identified in both tumors. At 9 years follow-up, both patients were alive and metastasis free. Conclusion: These patients demonstrate that neoadjuvant intravitreous bevacizumab does not decrease the size of large uveal melanomas and may, in fact, result in their paradoxical growth. This observation supports a cautious approach in the use of intravitreous bevacizumab for uveal melanoma, particularly in the neoadjuvant setting.

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“…In tumor cellformed vessels, blood passes through basement membrane-lined vascular networks with tumor cells sitting exterior to the membrane matrix, while traditional vessels support blood flowing through endothelial cells lining the vasculature with the basement membrane exterior to the cells. The light microscopic morphological characterization of VM in patient tumors showed matrix-rich channels containing plasma and RBCs lined by melanoma cells, and noteworthy poor clinical outcome in patients where VM was identified (14). Because VM is associated with the aggressive tumor cell phenotype and advanced stage disease, it is hypothesized that this extravascular perfusion pathway serves as a growth advantage and escape route for rapidly growing tumor cells.…”

Section: Melanoma Vascular Phenotypementioning

confidence: 99%

Heterogeneity and Plasticity of Melanoma: Challenges of Current Therapies

Hendrix

Seftor

Margaryan

et al. 2017

Cutaneous Melanoma: Etiology and Therapy

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Abstract:The heterogeneity and plasticity of aggressive melanoma presents formidable challenges in the design of current therapies. Plasticity is defined as the phenotype of cancer cells expressing properties normally related to stem cells, including the expression of genes associated with multiple cellular phenotypes and appearing as undifferentiated, embryonic-like cells. The multipotent phenotype of these tumor cells, expressing vascular, embryonic, and cancer stem cell (CSC) capabilities, offers new insights into their functional adaptation and resistance to current therapies. This chapter highlights major advances in research that (i) help clarify the underlying challenges associated with angiogenesis inhibitor therapy; (ii) discuss important implications of the discovery of reactivation of the normally dormant Nodal embryonic signaling pathway that underlies the CSC phenotype, unregulated tumor growth and metastasis, and resistance to current therapies; and (iii) demonstrate the advantage of using combinatorial strategies to effectively target heterogeneous melanoma subpopulations to eliminate relapse and disease progression.

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Tumor vasculogenic mimicry predicts poor prognosis in cancer patients: a meta-analysis

Abstract: The presence of VM predicts poorer survival outcomes in cancer patients.

Cited by 109 publications

References 63 publications

Control of immune cell entry through the tumour vasculature: a missing link in optimising melanoma immunotherapy?

Control of immune cell entry through the tumour vasculature: a missing link in optimising melanoma immunotherapy?

Growth of Uveal Melanoma following Intravitreal Bevacizumab

Heterogeneity and Plasticity of Melanoma: Challenges of Current Therapies

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