Are Parkinson disease patients protected from some but not all cancers?
Identifieur interne : 000154 ( PubMed/Curation ); précédent : 000153; suivant : 000155Are Parkinson disease patients protected from some but not all cancers?
Auteurs : Rivka Inzelberg [Israël] ; Joseph JankovicSource :
- Neurology ; 2007.
English descriptors
- KwdEn :
- Cell Death (genetics), Cell Survival (genetics), Comorbidity, Gene Expression Regulation, Neoplastic (genetics), Genes, Tumor Suppressor (physiology), Genetic Predisposition to Disease (genetics), Humans, Neoplasms (epidemiology), Neoplasms (genetics), Neoplasms (physiopathology), Oncogenes (genetics), Parkinson Disease (epidemiology), Parkinson Disease (genetics), Parkinson Disease (physiopathology), Risk Factors.
- MESH :
- epidemiology : Neoplasms, Parkinson Disease.
- genetics : Cell Death, Cell Survival, Gene Expression Regulation, Neoplastic, Genetic Predisposition to Disease, Neoplasms, Oncogenes, Parkinson Disease.
- physiology : Genes, Tumor Suppressor.
- physiopathology : Neoplasms, Parkinson Disease.
- Comorbidity, Humans, Risk Factors.
Abstract
There is substantial evidence based on well designed epidemiologic studies for low cancer rates in patients with Parkinson disease (PD). This risk reduction cannot be attributed to the recognized low life-long incidence of smoking in patients with PD, as not only smoking-related cancers but also non-smoking-related ones are less common in PD. Whereas the risk for most cancers appears to be relatively low in patients with PD, breast cancer and melanomas occur more frequently in the PD population as compared with controls. The relationship between this peculiar pattern of cancer rates and PD might be related to the involvement of common genes in both diseases. Mutations in parkin gene, for example, have been reported in several types of cancer. Furthermore, genes involved in familial forms of PD appear to be abnormally expressed in cancers. Thus, parkin and PINK1 might be tumor suppressor genes, whereas DJ-1 is an oncogene. Cell survival signals may differ owing to mutated genes and represent two opposite extremes such as cell proliferation in cancer and cell death due to apoptosis in PD. Unraveling the link between PD and cancer may open a therapeutic window for both diseases.
DOI: 10.1212/01.wnl.0000277638.63767.b8
PubMed: 17699801
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This risk reduction cannot be attributed to the recognized low life-long incidence of smoking in patients with PD, as not only smoking-related cancers but also non-smoking-related ones are less common in PD. Whereas the risk for most cancers appears to be relatively low in patients with PD, breast cancer and melanomas occur more frequently in the PD population as compared with controls. The relationship between this peculiar pattern of cancer rates and PD might be related to the involvement of common genes in both diseases. Mutations in parkin gene, for example, have been reported in several types of cancer. Furthermore, genes involved in familial forms of PD appear to be abnormally expressed in cancers. Thus, parkin and PINK1 might be tumor suppressor genes, whereas DJ-1 is an oncogene. Cell survival signals may differ owing to mutated genes and represent two opposite extremes such as cell proliferation in cancer and cell death due to apoptosis in PD. Unraveling the link between PD and cancer may open a therapeutic window for both diseases.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">17699801</PMID><DateCreated><Year>2007</Year><Month>10</Month><Day>09</Day></DateCreated><DateCompleted><Year>2007</Year><Month>11</Month><Day>26</Day></DateCompleted><DateRevised><Year>2009</Year><Month>01</Month><Day>08</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1526-632X</ISSN><JournalIssue CitedMedium="Internet"><Volume>69</Volume><Issue>15</Issue><PubDate><Year>2007</Year><Month>Oct</Month><Day>9</Day></PubDate></JournalIssue><Title>Neurology</Title><ISOAbbreviation>Neurology</ISOAbbreviation></Journal><ArticleTitle>Are Parkinson disease patients protected from some but not all cancers?</ArticleTitle><Pagination><MedlinePgn>1542-50</MedlinePgn></Pagination><Abstract><AbstractText>There is substantial evidence based on well designed epidemiologic studies for low cancer rates in patients with Parkinson disease (PD). This risk reduction cannot be attributed to the recognized low life-long incidence of smoking in patients with PD, as not only smoking-related cancers but also non-smoking-related ones are less common in PD. Whereas the risk for most cancers appears to be relatively low in patients with PD, breast cancer and melanomas occur more frequently in the PD population as compared with controls. The relationship between this peculiar pattern of cancer rates and PD might be related to the involvement of common genes in both diseases. Mutations in parkin gene, for example, have been reported in several types of cancer. Furthermore, genes involved in familial forms of PD appear to be abnormally expressed in cancers. Thus, parkin and PINK1 might be tumor suppressor genes, whereas DJ-1 is an oncogene. Cell survival signals may differ owing to mutated genes and represent two opposite extremes such as cell proliferation in cancer and cell death due to apoptosis in PD. Unraveling the link between PD and cancer may open a therapeutic window for both diseases.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Inzelberg</LastName><ForeName>Rivka</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Neurology, Meir Hospital, Kfar Saba, Tchernikovsky Street, Israel. rivka.inzelberg@clalit.org.il</Affiliation></AffiliationInfo></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>2007</Year><Month>08</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurology</MedlineTA><NlmUniqueID>0401060</NlmUniqueID><ISSNLinking>0028-3878</ISSNLinking></MedlineJournalInfo><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Neurology. 2008 Nov 11;71(20):1650; author reply 1650-1</RefSource><PMID Version="1">19001259</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016923">Cell Death</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002470">Cell Survival</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015897">Comorbidity</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015972">Gene Expression Regulation, Neoplastic</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016147">Genes, Tumor Suppressor</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020022">Genetic Predisposition to Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009369">Neoplasms</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000453">epidemiology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009857">Oncogenes</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000453">epidemiology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012307">Risk Factors</DescriptorName></MeshHeading></MeshHeadingList><NumberOfReferences>89</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="aheadofprint"><Year>2007</Year><Month>8</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>8</Month><Day>19</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>12</Month><Day>6</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>8</Month><Day>19</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pii">01.wnl.0000277638.63767.b8</ArticleId><ArticleId IdType="doi">10.1212/01.wnl.0000277638.63767.b8</ArticleId><ArticleId IdType="pubmed">17699801</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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