(RxWiki News) Past studies have suggested there is a link between Parkinson’s disease (PD) and cancer. A shared genetic predisposition is not only important for the patient, but also could have an affect on their relatives.
This study demonstrates a need for a genetic link to be better understood.
A recent Utah wide population based database was investigated for a link between PD and cancer. The study suggests that PD patients and their relatives are at an increased risk for melanoma and prostate cancer.
"Tell a doctor about your family medical history."
Seth A. Kareus, M.D., and colleagues from the University of Utah in Salt Lake City searched the Utah Population Database of 2.3 million individuals for incidents of cancer in people with Parkinson’s disease as their cause of death.
The database contained 2,998 people who had PD listed as a primary or contributing cause of death and 100,817 who were diagnosed with cancer between 1904 and 2008.
Individuals with at least three generations of genealogy in the database were classified by their birth year, sex and place of birth. Researchers estimated the rates for different types of cancer and number of relatives with cancer for patients who died of PD.
In individuals who died of PD, 48 also had melanoma. This is significantly larger than the 24.6 expected.
Prostate cancer was the only other cancer with higher rates among PD patients. In individuals who died of PD, 212 had prostate cancer, while only 124.1 were expected to have the disease.
The increased risk of melanoma and prostate cancer was also seen in relatives of those who died of PD.
Lung, pancreas and stomach cancers in men were associated with PD at a much lower rate than expected, while women who died of PD experienced colorectal cancer at a lower rate than expected.
This possible genetic predisposition could lead to better screening processes for the diseases and supports the need for further investigation into the nature of the link.
The study was published in September in Archives of Neurology.
Some authors receive grants from the Huntsman Cancer Foundation, the National Library of Medicine, the National Institutes of Health’s National Cancer Institute, the Noorda Foundation, the National Institute of Neurological Disorders and Stroke. Other author financial support comes from Athena Diagnostics.
The research was funded by the Utah Cancer Registry and the Utah State Department of Health and the University of Utah.
Partial support was provided by the Huntsman Cancer Institute, the University of Utah and the National Cancer Institute.