Severe influenza doubles the odds that a person will develop Parkinson’s disease later in life, according to University of British Columbia researchers.
However, the opposite is true for people who contracted a typical case of red measles as children – they are 35 per cent less likely to develop Parkinson’s, a nervous system disorder marked by slowness of movement, shaking, stiffness, and in the later stages, loss of balance.
The findings by researchers at UBC’s School of Population and Public Health and the Pacific Parkinson’s Research Centre are based on interviews with 403 Parkinson’s patients and 405 healthy people in British Columbia, Canada.
Lead author Anne Harris also examined whether occupational exposure to vibrations – such as operating construction equipment – had any effect on the risk of Parkinson’s. In another study she and her collaborators reported that occupational exposure actually decreased the risk of developing the disease by 33 percent, compared to people whose jobs involved no exposure.
Meanwhile, Harris found that those exposed to high-intensity vibrations – for example, by driving snowmobiles, military tanks or high-speed boats – had a consistently higher risk of developing Parkinson’s than people whose jobs involved lower-intensity vibrations (for example, operating road vehicles). The elevated risk fell short of the statistical significance typically used to establish a correlation, but was strong and consistent enough to suggest an avenue for further study, Harris says.
‘There are no cures or prevention programs for Parkinson’s, in part because we still don’t understand what triggers it in some people and not others,’ says Harris, who conducted the research while earning her doctorate at UBC. ‘This kind of painstaking epidemiological detective work is crucial in identifying the mechanisms that might be at work, allowing the development of effective prevention strategies.’ University of British Columbia

Men whose testosterone drops following radiation therapy for prostate cancer are more likely to experience a change in PSA levels that signals their cancer has returned, according to new research from Fox Chase Cancer Center.
Specifically, men whose testosterone fell following various forms of radiation therapy were more likely to experience an increase in prostate-specific antigen (PSA)—often the first indication the cancer has recurred.
‘The men who had a decrease in testosterone also appear to be the men more likely to see an increase in PSA after treatment,’ says study author Jeffrey Martin, MD, resident physician in the Department of Radiation Oncology at Fox Chase.
In theory, doctors may one day be able to use testosterone levels to guide treatment decisions, says Martin. ‘For men with a decrease in testosterone, doctors might intervene earlier with other medications, or follow their PSA more closely than they would otherwise, to spot recurrences at an earlier time.’
Martin and his colleagues decided to conduct the study because there is limited information regarding testosterone levels after radiation treatment and what it means for prognosis. To investigate whether a decrease in testosterone has any clinical effects, Martin and his colleagues reviewed medical records from nearly 260 men who received radiation therapy for prostate cancer between 2002 and 2008. The men were treated with either brachytherapy, in which doctors insert radioactive seeds in the prostate, or intensity modulated radiation therapy (IMRT), in which an external beam of radiation is directed at the prostate.
The researchers found that testosterone levels tended to decrease following both forms of radiation therapy. And men who experienced a post-radiation drop in testosterone— particularly a significant drop—were more likely to see their PSA levels rise during the follow-up period.
Still, an increase in PSA—known as biochemical failure—was relatively rare, the authors found. ‘Only 4% of patients with low-risk prostate cancer had biochemical failure at five years,’ says Martin.
Even though researchers have seen testosterone decrease following another form of radiation, these latest findings are still somewhat surprising, says Martin, because testosterone is believed to drive prostate cancer. In fact, some patients with advanced forms are prescribed hormone therapy that attempts to knock down testosterone.
‘Seeing that a drop in testosterone is tied to recurrence is kind of a surprising result,’ says Martin. ‘We don’t necessarily know what this means yet. I think the relationship between testosterone levels following radiation therapy and prognosis needs more study, and until then it’s premature to say this is something patients should ask their doctors about.’
This was a small study that needs to be validated in a larger group of men before doctors begin basing their predictions of recurrence on patients’ testosterone levels, he cautions. ‘I think the link between testosterone and PSA needs more study, in a larger set of patients.’ EurekAlert

Scientists say they have developed a breath-test that can accurately tell if a person has bowel cancer. The test, which looks for exhaled chemicals linked to tumour activity, was able to identify a majority of patients with the disease.
The British Journal of Surgery reported an overall accuracy of 76%.
However, another scientist said it was unlikely a fully functioning and reliable breath-test would be available soon for the general public. Scientists are working on breath-tests for a host of other diseases, including several types of cancer, TB and diabetes.
If diagnosed and treated early, the chances of stopping cancer can be good, but there is often little or no outward sign of the disease until it has progressed significantly.
The current screening test for bowel cancer looks for signs of blood in the faeces, but only a small proportion of those who test positive actually have colorectal cancer, which means unnecessary and invasive further testing for many people.
The breath-test technology relies on the idea that the biology of tumours can lead to the production of specific ‘volatile organic compounds’, combinations of chemicals unlikely in a healthy person.
These can be found in small amounts in the breath of the patient, and early studies found dogs could be trained to identify them – although the latest study relies an electronic device to analyse breath gases.
The team from a hospital in Bari, southern Italy, compared the breath of 37 patients known to have bowel cancer with that of 41 ‘controls’ who were thought to be healthy.
The initial test identified the cancer patients with 85% accuracy, and although, when combined with a follow-up test, the overall result fell to 76%, the researchers were upbeat about its potential.
‘The present findings further support the value of breath-testing as a screening tool,’ they say.
It might be possible that the technique could help identify patients whose cancer was returning after treatment.
Bigger studies with a greater number of patients were now needed to fine-tune the test and confirm it worked, said Dr Donato Altomare and colleagues. BBC

Genetics researchers have identified a key gene that, when mutated, causes the rare multisystem disorder Cornelia deLange syndrome (CdLS). By revealing how mutations in the HDAC8 gene disrupt the biology of proteins that control both gene expression and cell division, the research sheds light on this disease, which causes intellectual disability, limb deformations and other disabilities resulting from impairments in early development.
‘As we better understand how CdLS operates at the level of cell biology, we will be better able to define strategies for devising treatments for CdLS, and possibly for related disorders,’ said study leader Matthew A. Deardorff, M.D., Ph.D., a pediatric genetics clinician and scientist at The Children’s Hospital of Philadelphia. Deardorff also is in the Perelman School of Medicine at the University of Pennsylvania.
The current findings add to previous discoveries by researchers at The Children’s Hospital of Philadelphia. A group led by Ian Krantz, M.D., and Laird Jackson, M.D., announced in 2004 that mutations in the NIPBL gene are the primary cause of CdLS, accounting for roughly 60 percent of the ‘classical’ cases of the disease. In 2007, Deardorff joined them to describe mutations in two additional genes, SMC1A and SMC3. First described in 1933, CdLS affects an estimated 1 in 10,000 children.
The CdLS research team at Children’s Hospital has focused on the cohesin complex, a group of proteins that form a bracelet-like structure that encircles pairs of chromosomes, called sister chromatids. ‘Cohesin has two roles,’ said Deardorff. ‘It keeps sister chromatids together during cell division, and it allows normal transcription—the transmission of information from DNA to RNA.’
Deardorff added that mutations that perturb normal cohesin function can interfere with normal human development. Such is the case in CdLS, which exemplifies a newly recognised class of diseases called cohesinopathies.
In the current study, the scientists investigated both acetylation—how an acetyl molecule is attached to part of the cohesin complex—and deactylation, the removal of that molecule. Normally, deactylation helps recycle cohesin to make it available during successive rounds of cell division. The study team found that mutations in the HDAC8 gene threw off normal cellular recycling of cohesin.
Mutations in the gene cause loss of HDAC8 protein activity, and consequently decrease the amount of ‘recharged’ cohesin available to properly regulate gene transcription. This, in turn, the researchers suggest, impairs normal embryonic development and gives rise to CdLS.
The researchers showed in cell cultures that mutations in HDAC8 lead to a decrease in cohesin binding to genes, similar to that seen for cells deficient in the NIPBL gene. They also identified HDAC8 mutations in approximately 5 percent of patients with CdLS.
Because mothers of children with CdLS may carry mutations in the HDAC8 gene, identifying these mutations will be very useful in accurately counseling families of their recurrence risk—the likelihood of having a subsequent child with CdLS.
Furthermore, added Deardorff, by providing biological details of the underlying defect in CdLS, the current research suggests future approaches to treating the genetic disease. ‘By concentrating downstream on the biological pathway in the cohesin cycle rather than focusing on the defective gene, we may be able to eventually screen for small-molecule drugs that could be used to intervene in CdLS.’ Children’s Hospital of Philadelphia

In the first broad genetic landscape mapped of a Burkitt lymphoma tumour, scientists at Duke Medicine and their collaborators identified 70 mutations, including several that had not previously been associated with cancer and a new one that was unique to the disease.

Findings from the genetic sequencing of Burkitt lymphoma, an aggressive form of lymphoma, could be used to develop new drugs or aim existing therapies at mutations known to be susceptible

‘This study lays out the most common genetic alterations in the disease, and allows us to understand the biology of the disease so we can design better therapies,’ said Sandeep S. Dave, M.D., MBA, MS, associate professor at Duke and senior author of the study.

Dave and colleagues sequenced the first complete Burkitt lymphoma genome, plus the genes from 59 additional Burkitt cases and 94 diffuse large B cell lymphomas, which share many of the same characteristics of Burkitt lymphoma. Similarities between the malignancies can often lead to mistaken diagnoses and failed treatments.

The researchers reported striking differences in the gene mutation patterns of Burkitt lymphomas vs. the diffuse large B cell lymphomas.

‘It’s important that doctors make the right diagnosis for Burkitt lymphoma, which can be cured with the correct therapies,’ Dave said. ‘But if misdiagnosed and given the standard chemotherapy regimes for diffuse large B cell lymphomas, Burkitt lymphoma patients invariably relapse.’

The analysis identified 70 genes that were frequently mutated in the Burkitt lymphomas, including a number of genes that were identified in cancer for the first time. One of the newly identified gene mutations, ID3, appeared in 34 percent of the Burkitt cases, but was not evident in any of the diffuse large B cell lymphomas.

The mutation has a silencing effect on a gene that suppresses cell growth, enabling cells to multiply. Dave said this alteration alone may not cause cancer, but when it occurs along with the MYC gene mutations that are common in Burkitt lymphoma and other malignancies, it works like an accelerant to fuel tumour growth.

That finding could prove helpful for developing a new drug to function like a normal ID3 gene and suppress cancer cell proliferation in lymphomas as well as numerous other cancers.

‘If we can find a way to mimic ID3, restoring the function of the gene to slow the growth of tumours, this could provide a new treatment approach,’ Dave said. ‘We have experiments that suggest this is the case, but much more research is needed. This work provides a starting point.’ Duke Medicine