| Literature DB >> 27151281 |
Michael Hölzel1, Thomas Tüting2.
Abstract
Phenotype switching contributes to nongenomic heterogeneity in melanoma and other cancers. These dynamic and in part reversible phenotype changes impose diagnostic and therapeutic challenges. Understanding the reciprocal coevolution of melanoma and immune cell phenotypes during disease progression and in response to therapy is a prerequisite to improve current treatment strategies. Here we discuss how proinflammatory signals promote melanoma cell plasticity and govern interactions of melanoma and immune cells in the tumor microenvironment. We examine phenotypic plasticity and heterogeneity in different melanoma mouse models with respect to their utility for translational research and emphasize the interplay between melanoma cells and neutrophils as a critical driver of metastasis.Entities:
Keywords: inflammation; melanoma; metastasis; neutrophils; plasticity; resistance
Mesh:
Substances:
Year: 2016 PMID: 27151281 DOI: 10.1016/j.it.2016.03.009
Source DB: PubMed Journal: Trends Immunol ISSN: 1471-4906 Impact factor: 16.687