The association between Parkinson's disease and melanoma.
Identifieur interne : 000081 ( PubMed/Corpus ); précédent : 000080; suivant : 000082The association between Parkinson's disease and melanoma.
Auteurs : Tianhong Pan ; Xinqun Li ; Joseph JankovicSource :
- International journal of cancer. Journal international du cancer ; 2011.
English descriptors
- KwdEn :
- MESH :
- complications : Melanoma, Parkinson Disease.
- Humans, Incidence, Risk Factors.
Abstract
Parkinson's disease (PD) is a neurodegenerative disorder characterized by a loss of melanin-positive, dopaminergic neurons in the substantia nigra. Although there is convincing epidemiologic evidence of a negative association between PD and most cancers, a notable exception to this is that melanoma, a malignant tumor of melanin-producing cells in skin, occurs with higher-than-expected frequency among subjects with PD and that melanoma patients are more likely to have PD. A clear biological explanation for this epidemiological observation is lacking. Here, we present a comprehensive review of published literature exploring the association between PD and melanoma. On the basis of published findings, we conclude that (i) changes in pigmentation including melanin synthesis and/or melanin synthesis enzymes, such as tyrosinase and tyrosine hydroxylase, play important roles in altered vulnerability for both PD and melanoma; (ii) changes of PD-related genes such as Parkin, LRRK2 and α-synuclein may increase the risk of melanoma; (iii) changes in some low-penetrance genes such as cytochrome p450 debrisoquine hydroxylase locus, glutathione S-transferase M1 and vitamin D receptor could increase the risk for both PD and melanoma and (iv) impaired autophagy in both PD and melanoma could also explain the association between PD and melanoma. Future studies are required to address whether altered pigmentation, PD- or melanoma-related gene changes and/or changes in autophagy function induce oncogenesis or apoptosis. From a clinical point of view, early diagnosis of melanoma in PD patients is critical and can be enhanced by periodic dermatological surveillance, including skin biopsies.
DOI: 10.1002/ijc.25912
PubMed: 21207412
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pubmed:21207412Le document en format XML
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Journal international du cancer</title><idno type="e-ISSN">1097-0215</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Humans</term><term>Incidence</term><term>Melanoma (complications)</term><term>Parkinson Disease (complications)</term><term>Risk Factors</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Melanoma</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term><term>Incidence</term><term>Risk Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a neurodegenerative disorder characterized by a loss of melanin-positive, dopaminergic neurons in the substantia nigra. Although there is convincing epidemiologic evidence of a negative association between PD and most cancers, a notable exception to this is that melanoma, a malignant tumor of melanin-producing cells in skin, occurs with higher-than-expected frequency among subjects with PD and that melanoma patients are more likely to have PD. A clear biological explanation for this epidemiological observation is lacking. Here, we present a comprehensive review of published literature exploring the association between PD and melanoma. On the basis of published findings, we conclude that (i) changes in pigmentation including melanin synthesis and/or melanin synthesis enzymes, such as tyrosinase and tyrosine hydroxylase, play important roles in altered vulnerability for both PD and melanoma; (ii) changes of PD-related genes such as Parkin, LRRK2 and α-synuclein may increase the risk of melanoma; (iii) changes in some low-penetrance genes such as cytochrome p450 debrisoquine hydroxylase locus, glutathione S-transferase M1 and vitamin D receptor could increase the risk for both PD and melanoma and (iv) impaired autophagy in both PD and melanoma could also explain the association between PD and melanoma. Future studies are required to address whether altered pigmentation, PD- or melanoma-related gene changes and/or changes in autophagy function induce oncogenesis or apoptosis. From a clinical point of view, early diagnosis of melanoma in PD patients is critical and can be enhanced by periodic dermatological surveillance, including skin biopsies.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">21207412</PMID><DateCreated><Year>2011</Year><Month>03</Month><Day>28</Day></DateCreated><DateCompleted><Year>2011</Year><Month>05</Month><Day>26</Day></DateCompleted><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1097-0215</ISSN><JournalIssue CitedMedium="Internet"><Volume>128</Volume><Issue>10</Issue><PubDate><Year>2011</Year><Month>May</Month><Day>15</Day></PubDate></JournalIssue><Title>International journal of cancer. Journal international du cancer</Title><ISOAbbreviation>Int. J. Cancer</ISOAbbreviation></Journal><ArticleTitle>The association between Parkinson's disease and melanoma.</ArticleTitle><Pagination><MedlinePgn>2251-60</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/ijc.25912</ELocationID><Abstract><AbstractText>Parkinson's disease (PD) is a neurodegenerative disorder characterized by a loss of melanin-positive, dopaminergic neurons in the substantia nigra. Although there is convincing epidemiologic evidence of a negative association between PD and most cancers, a notable exception to this is that melanoma, a malignant tumor of melanin-producing cells in skin, occurs with higher-than-expected frequency among subjects with PD and that melanoma patients are more likely to have PD. A clear biological explanation for this epidemiological observation is lacking. Here, we present a comprehensive review of published literature exploring the association between PD and melanoma. On the basis of published findings, we conclude that (i) changes in pigmentation including melanin synthesis and/or melanin synthesis enzymes, such as tyrosinase and tyrosine hydroxylase, play important roles in altered vulnerability for both PD and melanoma; (ii) changes of PD-related genes such as Parkin, LRRK2 and α-synuclein may increase the risk of melanoma; (iii) changes in some low-penetrance genes such as cytochrome p450 debrisoquine hydroxylase locus, glutathione S-transferase M1 and vitamin D receptor could increase the risk for both PD and melanoma and (iv) impaired autophagy in both PD and melanoma could also explain the association between PD and melanoma. Future studies are required to address whether altered pigmentation, PD- or melanoma-related gene changes and/or changes in autophagy function induce oncogenesis or apoptosis. From a clinical point of view, early diagnosis of melanoma in PD patients is critical and can be enhanced by periodic dermatological surveillance, including skin biopsies.</AbstractText><CopyrightInformation>Copyright © 2011 UICC.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pan</LastName><ForeName>Tianhong</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Diana Helis Henry Medical Research Foundation, New Orleans, LA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Xinqun</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Jankovic</LastName><ForeName>Joseph</ForeName><Initials>J</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>03</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Int J Cancer</MedlineTA><NlmUniqueID>0042124</NlmUniqueID><ISSNLinking>0020-7136</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015994">Incidence</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008545">Melanoma</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000150">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000150">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012307">Risk Factors</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2010</Year><Month>8</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2010</Year><Month>12</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2011</Year><Month>3</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>1</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2011</Year><Month>1</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>5</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/ijc.25912</ArticleId><ArticleId IdType="pubmed">21207412</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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