Year: 2012
Type: review
Abstract: In 1999, The American Journal of Pathology published an article entitled "Vascular channel formation by human melanoma cells in vivo and in vitro: vasculogenic mimicry," by Maniotis and colleagues, which ignited a spirited debate for several years and earned distinction as a citation classic. Tumor cell vasculogenic mimicry (VM) refers to the plasticity of aggressive cancer cells forming de novo vascular networks, which thereby contribute to perfusion of rapidly growing tumors, transporting fluid from leaky vessels, and/or connecting with the constitutional endothelial-lined vasculature. The tumor cells capable of VM share a plastic, transendothelial phenotype, which may be induced by hypoxia. Since VM was introduced as a novel paradigm for melanoma tumor perfusion, many studies have contributed new findings illuminating the underlying molecular pathways supporting VM in a variety of tumors, including carcinomas, sarcomas, glioblastomas, astrocytomas, and melanomas. Facilitating the functional plasticity of tumor cell VM are key proteins associated with vascular, stem cell, and hypoxia-related signaling pathways, each deserving serious consideration as potential therapeutic targets and diagnostic indicators of the aggressive, metastatic phenotype.
Source: American Journal Of Pathology
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: hybrid
Estimated APC paid: $2,800
Awards: REGULATION OF UVEAL MELANOMA INTERCONVERTED PHENOTYPE, PROSTATIC VASCULOGENIC MIMICRY: A NEW METASTATIC PATHWAY, Epigenetic Effect of the Microenvironment on Stem Cell Plasticity and Function, Endothelial Transdifferentiation of Invasive Tumor Cells, The Coding, Decoding, Transfer, and Translation of Information in Cancer, G5962862063
OpenAlex ID: W155717428