Differential risks of cancer types in people with Parkinson’s disease: A national record-linkage study

2014 ◽  
Vol 50 (14) ◽  
pp. 2456-2462 ◽  
Author(s):  
E.L. Ong ◽  
Raph Goldacre ◽  
Michael Goldacre
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Record Linkage ◽  
Linkage Study ◽  
Cancer Types

scholarly journals Genomewide linkage study of modifiers of LRRK2 -related Parkinson's disease

2011 ◽  
Vol 26 (11) ◽  
pp. 2039-2044 ◽  
Author(s):  
Jeanne C. Latourelle ◽  
Audrey E. Hendricks ◽  
Nathan Pankratz ◽  
Jemma B. Wilk ◽  
Cheryl Halter ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Linkage Study ◽  
Genomewide Linkage

scholarly journals A linkage study of candidate loci in familial Parkinson's Disease

BMC Neurology ◽  
2003 ◽  
Vol 3 (1) ◽  
Author(s):  
Karin Wirdefeldt ◽  
Catherine E Burgess ◽  
Lisa Westerberg ◽  
Haydeh Payami ◽  
Martin Schalling
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Linkage Study ◽  
Candidate Loci ◽  
Familial Parkinson’S Disease

scholarly journals The Links between Parkinson’s Disease and Cancer

Biomedicines ◽  
2020 ◽  
Vol 8 (10) ◽  
pp. 416
Author(s):  
Maria Ejma ◽  
Natalia Madetko ◽  
Anna Brzecka ◽  
Konstanty Guranski ◽  
Piotr Alster ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mitochondrial Dysfunction ◽  
Epidemiologic Studies ◽  
The Other ◽  
Cancer Proliferation ◽  
Cancer Types ◽  
Cancer Suppression ◽  
And Oxidative Stress

Epidemiologic studies indicate a decreased incidence of most cancer types in Parkinson’s disease (PD) patients. However, some neoplasms are associated with a higher risk of occurrence in PD patients. Both pathologies share some common biological pathways. Although the etiologies of PD and cancer are multifactorial, some factors associated with PD, such as α-synuclein aggregation; mutations of PINK1, PARKIN, and DJ-1; mitochondrial dysfunction; and oxidative stress can also be involved in cancer proliferation or cancer suppression. The main protein associated with PD, i.e., α-synuclein, can be involved in some types of neoplastic formations. On the other hand, however, its downregulation has been found in the other cancers. PINK1 can act as oncogenic or a tumor suppressor. PARKIN dysfunction may lead to some cancers’ growth, and its expression may be associated with some tumors’ suppression. DJ-1 mutation is involved in PD pathogenesis, but its increased expression was found in some neoplasms, such as melanoma or breast, lung, colorectal, uterine, hepatocellular, and nasopharyngeal cancers. Both mitochondrial dysfunction and oxidative stress are involved in PD and cancer development. The aim of this review is to summarize the possible associations between PD and carcinogenesis.

scholarly journals Identification of TMEM230 mutations in familial Parkinson’s disease (response to comments)

2017 ◽  
Author(s):  
Han-Xiang Deng ◽  
Teepu Siddique
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Clinical Information ◽  
Genetic Data ◽  
Linkage Study ◽  
Sequencing Data ◽  
Disease Response ◽  
Whole Exome Sequencing Data ◽  
Family Based ◽  
Familial Parkinson’S Disease

We recently reported mutations in TMEM230 in familial Parkinson’s disease (PD). Farrer et al raised the concern that mutations in TMEM230 may not be pathogenic to PD. We seriously evaluated Dr. Farrer’s assertions. We obtained updated clinical information and performed several new experiments, including MegaEx chip screening of the family DNA samples with ∼2 million SNPs for whole-genome linkage study and re-analysis of whole-exome sequencing data. We did not find any other locus more robust than the chromosome 20p (TMEM230), nor any other variants with better segregation than TMEM230-R141L to explain the inheritance of PD in the large Mennonite family. Based on the new genetic data from the Mennonite PD family, and the robust genetic data showing additional TMEM230 mutations in multiple PD families, we are confident to conclude that TMEM230 is a new PD-causing gene. Further studies of TMEM230 should provide important mechanistic insights into understanding the vesicle/endosome trafficking/recycling defects in the pathogenesis of PD.

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