| Literature DB >> 27761938 |
Rivka Inzelberg1,2, Shira Flash3, Eitan Friedman4,5, Esther Azizi6.
Abstract
The mechanisms underlying the high prevalence of cutaneous malignant melanoma (CMM) in Parkinson disease (PD) are unclear, but plausibly involve common pathways. 129Ser-phosphorylated α-synuclein, a pathological PD hallmark, is abundantly expressed in CMM, but not in normal skin. In inherited PD, PARK genes harbor germline mutations; the same genes are somatically mutated in CMM, or their encoded proteins are involved in melanomagenesis. Conversely, genes associated with CMM affect PD risk. PD/CMM-targeted cells share neural crest origin and melanogenesis capability. Pigmentation gene variants may underlie their susceptibility. We review putative genetic intersections that may be suggestive of shared pathways in neurodegeneration/melanomagenesis. Ann Neurol 2016;80:811-820.Entities:
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Year: 2016 PMID: 27761938 DOI: 10.1002/ana.24802
Source DB: PubMed Journal: Ann Neurol ISSN: 0364-5134 Impact factor: 10.422