Researchers have identified a way in which men can develop prostate cancer after contracting trichomoniasis, a curable but often overlooked sexually transmitted disease.
Previous studies have teased out a casual, epidemiological correlation between the two diseases, but this latest study suggests a more tangible biological mechanism.
John Alderete, a professor at Washington State University’s School of Molecular Biosciences, says the trichomoniasis parasite activates a suite of proteins, the last of which makes sure the proteins stay active.
‘It’s like switching a light switch on,’ he says. ‘Then, if you don’t control the brightness of that light, you can go blind. That’s the problem.’
Caused by a protozoan parasite, trichomoniasis is often referred to as the most common curable sexually transmitted infection. However, most infected people have no symptoms, so it often goes untreated.
‘Most women, it’s the Number One sexually transmitted infection,’ says Alderete. ‘We’re going to have at least 10 million women infected this year and an equal number of men because they all get infected if they come into contact with an infected partner.’
Infected women have a greater risk of pregnancy complications and HIV. Infected men have a 40 percent greater chance of developing prostate cancer, according to a 2006 study led by Siobhan Sutcliffe, a Washington University epidemiologist and co-author of the recent paper.
Sutcliffe cautions that the epidemiological link she found is not conclusive and compares the science to the early connections drawn between smoking and lung cancer.
‘It’s still in a really exploratory phase,’ she says.
A study after her 2006 research found no connection between trichomoniasis and prostate cancer, while a third out of Harvard found an even greater likelihood of cancer in infected men.
This latest study, she says, ‘is providing a molecular mechanism that might explain that association.’
Much of the study was done in a single building, WSU’s Biotechnology and Life Sciences Building, and involved two of the more accomplished researchers on the Pullman campus.
WSU cancer researcher Nancy Magnuson is an expert on the protein PIM1, a promoter of cancer cell growth, and identified the protein in the cascade of proteins leading from trichomoniasis to prostate cancer. WSU molecular biologist Ray Reeves brought to bear his expertise in HMGA1. The protein turns genes on and off and ended up being the actor making sure other proteins in the trichomoniasis-to-cancer sequence stay on.
Alderete hopes knowledge of the mechanism will lead to better diagnosis and treatment.
‘What this is also doing is telling the world, ‘People, this is a latent infection,” he says. ”You guys out there, if you’ve been exposed to it, you’ve got it in there, and we need now a diagnostic for you.” EurekAlert

Johns Hopkins researchers have created a synthetic protein that, when activated by ultraviolet light, can guide doctors to places within the body where cancer, arthritis and other serious medical disorders can be detected.
The technique could lead to a new type of diagnostic imaging technology and may someday serve as a way to move medications to parts of the body where signs of disease have been found. In a study the researchers reported success in using the synthetic protein in mouse models to locate prostate and pancreatic cancers, as well as to detect abnormal bone growth activity associated with Marfan syndrome.
The synthetic protein developed by the Johns Hopkins team does not zero in directly on the diseased cells. Instead, it binds to nearby collagen that has been degraded by various health disorders. Collagen, the body’s most abundant protein, provides structure and creates a sturdy framework upon which cells build nerves, bone and skin. Some buildup and degradation of collagen is normal, but disease cells such as cancer can send out enzymes that break down collagen at an accelerated pace. It is this excessive damage, caused by disease, that the new synthetic protein can detect, the researchers said.
‘These disease cells are like burglars who break into a house and do lots of damage but who are not there when the police arrive,’ said S. Michael Yu, a faculty member in the Whiting School of Engineering’s Department of Materials Science and Engineering. ‘Instead of looking for the burglars, our synthetic protein is reacting to evidence left at the scene of the crime,’ said Yu, who was principal investigator in the study.
A key collaborator was Martin Pomper, a School of Medicine professor of radiology and co-principal investigator of the Johns Hopkins Center of Cancer Nanotechnology Excellence. Pomper and Yu met as fellow affiliates of the Johns Hopkins Institute for NanoBioTechnology. ‘A major unmet medical need is for a better non-invasive characterisation of disrupted collagen, which occurs in a wide variety of disorders,’ Pomper said. ‘Michael has found what could be a very elegant and practical solution, which we are converting into a suite of imaging and potential agents for diagnosis and treatment.’
The synthetic proteins used in the study are called collagen mimetic peptides or CMPs. These tiny bits of protein are attracted to and physically bind to degraded strands of collagen, particularly those damaged by disease. Fluorescent tags are placed on each CMP so that it will show up when doctors scan tissue with fluorescent imaging equipment. The glowing areas indicate the location of damaged collagen that is likely to be associated with disease.
In developing the technique, the researchers faced a challenge because CMPs tend to bind with one another and form their own structures, similar to DNA, in a way that would cause them to ignore the disease-linked collagen targeted by the researchers.
To remedy this, the study’s lead author, Yang Li, synthesized CMPs that possess a chemical ‘cage’ to keep the proteins from binding with one another. Just prior to entering the bloodstream to search for damaged collagen, a powerful ultraviolet light is used to ‘unlock’ the cage and allow the CMPs to initiate their disease-tracking mission. Li is a doctoral student from the Department of Chemistry in the Krieger School of Arts and Sciences at Johns Hopkins. Yu, who holds a joint appointment in that department, is his doctoral adviser.
Yu’s team tested Li’s fluorescently tagged and caged peptides by injecting them into lab mice that possessed both prostate and pancreatic human cancer cells. Through a series of fluorescent images taken over four days, researchers tracked single strands of the synthetic protein spreading throughout the tumour sites via blood vessels and binding to collagen that had been damaged by cancer.
Similar in vivo tests showed that the CMP can target bones and cartilage that contain large amounts of degraded collagen. Therefore, the new protein could be used for diagnosis and treatment related to bone and cartilage damage. John Hhopkins University

A team of Australian researchers, led by University of Melbourne has developed a genetic test that is able to predict the risk of developing Autism Spectrum Disorder, ASD.
Lead researcher Professor Stan Skafidas, Director of the Centre for Neural Engineering at the University of Melbourne said the test could be used to assess the risk for developing the disorder.
‘This test could assist in the early detection of the condition in babies and children and help in the early management of those who become diagnosed,’ he said.
‘It would be particularly relevant for families who have a history of Autism or related conditions such as Asperger’s Syndrome,’ he said.
Autism affects around one in 150 births and is characterised by abnormal social interaction, impaired communication and repetitive behaviours.
The test correctly predicted ASD with more than 70 per cent accuracy in people of central European descent. Ongoing validation tests are continuing including the development of accurate testing for other ethnic groups.
Clinical neuropsychologist, Dr Renee Testa from the University of Melbourne and Monash University, said the test would allow clinicians to provide early interventions that may reduce behavioural and cognitive difficulties that children and adults with ASD experience.
‘Early identification of risk means we can provide interventions to improve overall functioning for those affected, including families,’ she said.
A genetic cause has been long sought with many genes implicated in the condition, but no single gene has been adequate for determining risk.
Using US data from 3,346 individuals with ASD and 4,165 of their relatives from Autism Genetic Resource Exchange (AGRE) and Simons Foundation Autism Research Initiative (SFARI), the researchers identified 237 genetic markers (SNPs) in 146 genes and related cellular pathways that either contribute to or protect an individual from developing ASD.
Senior author Professor Christos Pantelis of the Melbourne Neuropsychiatry Centre at the University of Melbourne and Melbourne Health said the discovery of the combination of contributing and protective gene markers and their interaction had helped to develop a very promising predictive ASD test.
The test is based on measuring both genetic markers of risk and protection for ASD. The risk markers increase the score on the genetic test, while the protective markers decrease the score. The higher the overall score, the higher the individual risk.
‘This has been a multidisciplinary team effort with expertise across fields providing new ways of investigating this complex condition,’ Professor Pantelis said. EurekAlert

The cellular cause of birth defects like cleft palates, missing teeth and problems with fingers and toes has been a tricky puzzle for scientists.
Now Professor Emily Bates and her biochemistry students at Brigham Young University have placed an important piece of the developmental puzzle. They studied an ion channel that regulates the electrical charge of a cell. In a new study they show that blocking this channel disrupts the work of a protein that is supposed to carry marching orders to the nucleus.
Without those instructions, cells don’t become what they were supposed to become – be that part of a palate, a tooth or a finger. Though there are various disorders that lead to birth defects, this newly discovered mechanism may be what some syndromes have in common.
Bates and her graduate student, Giri Dahal, now want to apply the findings toward the prevention of birth defects – particularly those caused by fetal alcohol syndrome and fetal alcohol spectrum disorder.
‘What we think might be the case is that this is the target for a few similar disorders,’ Bates said. ‘The big thing that we have right now is that this ion channel is required for protein signalling, which means that developmental signalling pathways can sense the charge of a cell. And that’s exciting for a lot of different reasons.’
For example, the new study might also have implications for the battle against cancer. With cancer, the problem is that cells are receiving a bad set of instructions that tells them to multiply and spread. If they can devise a way to block the ion channel, it may stop those cancerous instructions from getting through.
‘This protein signalling pathway is the same one that tells cancer cells to metastasise,’ Bates said. ‘We’re planning to test a therapy to specifically block this channel in just the cells that we want to stop.’ Brigham Young University

Researchers from Sainte-Justine University Hospital Center and University of Montreal have identified several novel genes that make some children more efficient than others in the way their immune system responds to malaria infection. This world-first in integrative efforts to track down genes predisposing to specific immune responses to malaria and ultimately to identify the most suitable targets for vaccines or treatments was published by lead author Dr. Youssef Idaghdour and senior author Pr. Philip Awadalla, whose laboratory has been performing world-wide malaria research for the past 13 years.
‘Malaria is a major health problem world-wide, with over 3 billion individuals at risk and hundreds of thousands of deaths annually, a majority of which are African children under the age of 5. Why are some children prone to infection, while others are resistant and efficiently fight the disease? These are the questions we sought to answer with our study’, Idaghdour says.
However, to succeed where many other studies have failed, the team used an approach different from the classic in vitro one, where the genome is analysed using cells grown in a laboratory. Instead, they used an in vivo approach, analysing blood samples of children from the Republic of Benin, West Africa, collected with the help of collaborators in the city of Cotonou and the nearby village of Zinvié. ‘This approach allowed us to identify how the ‘environment’ engages in an arms race to define the clinical course of the disease, in this case the environment being the number of parasites detected in the child’s blood running against the genetic make-up of the infected child’, Idaghdour explains.
‘We used an innovative combination of technologies that assessed both genetic variation among children and the conditions in which their genes are ‘expressed’. By doing so, we increased the power of our analysis by permitting us not only to detect the mutations, but also to capture their effect depending on how they affect genes being turned ‘on’ or ‘off’ in presence of the parasite’, Awadalla explains. ‘Our approach made us successful, where million-dollar studies have failed in the past. There has never been this many genes associated with malaria discovered in one study.’
This major milestone in understanding how the genetic profile affects the ability of children to cope with infection could pave the way to the development of low-cost genetic profiling tests in a not so far future. ‘Accurate diagnosis of the infectious agent is critical for appropriate treatment, of course. However, determining a patient’s genetic predisposition to infection would allow us to be more aggressive in our treatment of patients, whether we are speaking of vaccines or preventive drugs’, Awadalla says. EurekAlert