Molecular Determinants of Melanoma Vasculogenic Mimicry


Amalia Vartanian and Anatoly Baryshnikov

Series: Cancer Etiology, Diagnosis and Treatments
BISAC: MED062000

The rising incidence of melanoma makes this tumor an important public health problem. Standard systemic therapies have not been adequately effective in the management of melanoma. Moreover, melanoma is resistant to antiangiogenesis therapy suggesting the existence of an alternative blood circulation system. For years sprouting angiogenesis has been considered as exclusive mechanism of tumor vascularization. However, in recent years another mechanism of tumor vascularization has been identified that does not involve endothelial cells, a process called vasculogenic mimicry (VM). VM describes the unique ability of highly aggressive tumor cells to express a multipotent, stem cell-like phenotype, and form capillary-like structures (CLS) and a matrix-rich patterned network in three-dimentional culture that mimic embryonic vasculogenic networks. VM occurrence is in tumors strongly associated with poor prognosis.

This book will focus on the molecular determinants and signaling pathways involved in melanoma VM. We will discuss the mechanisms that operate at the initial phase of CLS formation by melanoma cells. We will provide the experimental evidence that CLS formation requires apoptotic cell death through activation of a caspase-dependent mechanism. In addition, we will describe the status of VM under the condition of angiogenesis blockage. (Imprint: Nova Biomedical )



Table of Contents




Functional Relevance of VM

Key VM Signaling Molecules

Signaling Cascades Involved in Melanoma VM

Notch Signalling Pathway and Melanoma VM

Prognostic Significance of Pas-Positive Patterns in Melanoma

Clinical Significance of VM




Additional information