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Dev Biol. 2018 Apr 13. pii: S0012-1606(18)30137-4. doi: 10.1016/j.ydbio.2018.04.008. [Epub ahead of print]

The convergent roles of CD271/p75 in neural crest-derived melanoma plasticity.

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Stowers Institute for Medical Research, Kansas City, MO 64110, USA.
Stowers Institute for Medical Research, Kansas City, MO 64110, USA; Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, KS 66160, USA. Electronic address:


The embryonic microenvironment is an important source of signals that promote multipotent cells to adopt a specific fate and direct cells along distinct migratory pathways. Yet, the ability of the embryonic microenvironment to retain multipotent progenitors or reprogram de-differentiated cells is less clear. Mistakes in cell differentiation or migration often result in developmental defects and tumorigenesis, including aggressive cancers that share many characteristics with embryonic progenitor cells. This is a striking feature of the vertebrate neural crest, a multipotent and highly migratory cell population first identified by His (1868) with the potential to metamorphose into aggressive melanoma cancer. In this perspective, we address the roles of CD271/p75 in tumor initiation, phenotype switching and reprogramming of metastatic melanoma and discuss the convergence of these roles in melanoma plasticity.


CD271; Melanoma; Microenvironment; NGF; Neural crest; p75

[Available on 2019-10-13]

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