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Top ten research priorities for the management of Parkinson’s

The top ten research priorities for the management of Parkinson’s:

  1. What treatments are helpful for reducing balance problems and falls in people with Parkinson’s?
  2. What approaches are helpful for reducing stress and anxiety in people with Parkinson’s?
  3. What treatments are helpful for reducing dyskinesias (involuntary movements, which are a side effect of some medications) in people with Parkinson’s?
  4. Is it possible to identify different types of Parkinson’s, eg, tremor dominant? And can we develop treatments to address these different types?
  5. What best treats dementia in people with Parkinson’s?
  6. What best treats mild cognitive problems such as memory loss, lack of concentration, indecision and slowed thinking in people with Parkinson’s?
  7. What is the best method of monitoring a person with Parkinson’s response to treatments?
  8. What is helpful for improving the quality of sleep in people with Parkinson’s?
  9. What helps improve the dexterity (fine motor skills or coordination of small muscle movements) of people with Parkinson’s so they can do up buttons, use computers, phones, remote controls etc?
  10. What treatments are helpful in reducing urinary problems (urgency, irritable bladder, incontinence) in people with Parkinson’s?

 Source:

University of East Anglia

Telemedicine Improves Access to Specialty Parkinson’s Care

An additional Penn study being presented at the AAN meeting examined use of telemedicine visits to increase access to specialty care for Parkinson’s patients, in an effort to help remove barriers to specialty care experienced by many patients who live far from care or have disabilities that make it difficult to travel. A Penn Medicine team led by Jayne Wilkinson, MD, and Meredith Spindler, MD, conducted a randomized controlled trial using video telemedicine in the patient’s home or at a facility near the patient (in this case, VA Community Based Outpatient Clinics (CBOCs), connecting them to a neurologist specializing in movement disorders and Parkinson’s disease, based at the Parkinson’s Disease Research, Education, and Clinical Center (PADRECC) at the Philadelphia VA Medical Center. Early results demonstrate that the process of using telemedicine for Parkinson’s specialty care is feasible, provided similar quality of life, care and communication, and significantly decreased travel. This is the largest study to evaluate telemedicine in this Parkinson’s patient population.

Dr. Wilkinson and Spindler

Source:

University of Pennsylvania School of Medicine

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Research findings underscore striking heterogeneity of depression

Depression is generally considered to be a specific and consistent disorder characterised by a fixed set of symptoms and often treated with a combination of psychotherapy and medication. However, the standard rating scales used by healthcare professionals and researchers to diagnose this disease often differ in the symptoms they list, perhaps explaining why a one-size-fits-all treatment has to date been so ineffective. This is the finding of research conducted by psychologist Eiko Fried from the University of Amsterdam (UvA). His results are published in the latest edition of the Journal of Affective Disorders.

Depression is often viewed as a common medical disorder like measles – one either has it or one doesn’t. As a result, diagnosis is generally followed by assigning specific treatment options. But unlike physical disorders where blood tests or other objective tests enable a reliable diagnosis, there are no such measures to determine whether someone is depressed. Instead, researchers and clinicians query patients about symptoms that are indicative of depression, such as sadness, suicidal ideation and sleep problems. If a person has many depression symptoms, she is considered depressed.

Heterogeneity

In his study, Fried used a content analysis to investigate the symptom overlap of 7 rating scales of symptoms that are commonly used in depression research. One of the scales is the Hamilton Rating Scale of Depression, which contains 17 predominantly physical depression symptoms like paralysis, weight loss and psychomotor retardation. Another is the Beck Depression Inventory, which includes 21 mostly cognitive-affective symptoms such as feelings like worthlessness, guilt, crying and self-dislike.

What he found was that these and other rating scales show surprisingly little symptom overlap. Moreover, together they feature a total of 52 different depression symptoms ranging from sadness, lack of interest and suicidal ideation to genital problems, irritability and anxiety. These findings underline the striking heterogeneity of depression, a disorder mostly viewed as one consistent syndrome, says Fried. ‘Patients diagnosed with depression are often thought to have similar kinds of problems and therefore receive very similar treatment. However, the fact that 7 common rating scales of depression contain over 50 different symptoms shows how strikingly different depressed patients can be in terms of the problems they experience. This seems to indicate the need for more personalized treatment and might explain why current “one-size-fits-all” solutions like antidepressants show so little efficacy.’

Predetermined outcome

Fried believes his findings could also pose a major problem for depression research because the type of scale used by researchers might determine the outcome of a scientific study. Fried: ‘For example, imagine you are a researcher and want to study the brain structure of depressed patients. This is usually done by giving a large group of people one specific depression scale, and if these people have a certain number of symptoms they are enrolled into the study as depressed.’ According to Fried, his findings suggest that the type of scale a researcher uses might dictate the kind of people who are enrolled in the study. ‘For instance, if a researcher uses Hamilton’s scale, which is focused on physical symptoms, the kinds of participants she examines in her brain study will differ dramatically from those who would be enrolled if she were to use Beck’s cognitive-affective scale. And these different groups of people will likely differ in their brain structures. As this and prior studies show, depressed people differ considerably in the problems they experience and symptoms they exhibit. This likely explains why so many different depression studies come to very different conclusions.’

Source:

Universiteit van Amsterdam (UVA)

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Frequent nighttime hot flashes may trigger mild depression symptoms during menopause

A woman’s perception that she is experiencing a high number of nighttime hot flashes can trigger mild symptoms of depression during menopause, according to a new study published in the Endocr…

Source: Frequent nighttime hot flashes may trigger mild depression symptoms during menopause

Frequent nighttime hot flashes may trigger mild depression symptoms during menopause

A woman’s perception that she is experiencing a high number of nighttime hot flashes can trigger mild symptoms of depression during menopause, according to a new study published in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism.

Menopause occurs when a woman’s ovaries stop producing estrogen and other hormones, and her menstrual periods stop, according to the Hormone Health Network. The transition takes place gradually, usually over four or five years. Among American women, the average age for menopause to occur is 51 years old. The Hormone Health Network’s interactive Menopause Map™ helps women learn more about the stages of menopause and where they are in the journey.

Using a medication to simulate the decline in a woman’s estrogen levels during menopause, the researchers found both interruption of sleep and greater frequency of perceived nighttime hot flashes were associated with mood disturbance.

“When women were awake long enough to later recall nighttime hot flashes, that perception contributed to mood disturbance in women whose estrogen levels had fallen,” said the study’s first author, Hadine Joffe, MD, MSc, of Brigham and Women’s Hospital and Dana Farber Cancer Institute at Harvard Medical School in Boston, MA. “The association was independent of sleep disruption that the women experienced.”

Twenty-nine healthy, premenopausal women between the ages of 18 and 45 took part in the study. The women took a medication to suppress estrogen production in the ovaries for a four-week period, a treatment that mimics menopause and induces menopausal symptoms to varying degrees of intensity. Before and after the four-week timeframe, researchers monitored the participants’ sleep and hormone levels. The participants completed mental health questionnaires at the beginning and end of the study.

The study found that women who reported experiencing frequent nighttime hot flashes were more likely to experience mild symptoms of depression than those who reported fewer or no nighttime hot flashes. Although researchers also monitored the women for physiologic signs of nighttime hot flashes during the sleep study, they found only the women’s perception of hot flash frequency—not the measured number of hot flashes—was linked to changes in mood.

Women who experienced sleep interruption also were more likely to exhibit symptoms of depression than women who got more sleep. Daytime hot flashes had no effect on the participants’ mood.

“The results of our research suggest menopausal women who report experiencing nighttime hot flashes and sleep disruption should be screened for mood disturbances,” Joffe said. “Any treatment of mood symptoms in this population also should incorporate efforts to address sleep and nighttime hot flashes.”

Source:

Endocrine Society

Connie’s comments: Take dietary supplements for menopause together with whole foods.

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Big data analytical methods reveal ‘social character’ of genes

A new study at the University of Haifa has used “big data” analytical methods to reveal the “social character” of genes – a phenomenon in certain diseases whereby genes operate jointly rather than independently. “The problem is that the possible number of combinations of different genes is enormous, and it is almost impossible to examine them all effectively and reliably,” the researchers explain. “Our study offers a solution to this problem.” The study, which was undertaken as part of a master’s thesis by Pavel Goldstein from the Department of Statistics, and was headed by Dr. Anat Reiner-Benaim from the department in cooperation with Professor Abraham B. Korol from the Department of Evolution and Environmental Biology, proposes a new method for discovering complex and rare genetic effects that form part of the mechanism of creation of complex diseases, such as autoimmune diseases.

One of the most active fields of genetic research at present focuses on the connection between genetic markers – DNA segments situated along the genome that effectively represent genes – and the expression of different genes – the creation of the proteins they encode. Various studies over recent years have shown that in complex biological mechanisms, such as those in most diseases, the genetic expression is not the product of the action of a single marker, but rather of a combination of several markers, some close to the location of the gene on the DNA chain and others more distant. In the Human Genome Project, for example, the researchers initially found that some 98 percent of the human genome contains genes that do not “do” anything. However, it later emerged that some of these genes are in fact active – not independently, but as part of a network of genes. Thus the influence of a given genetic marker may be dependent on the influence of other markers – a phenomenon known as epistasis.

The problem is that the theoretical number of combinations in which different genes could cooperate is almost infinite – equivalent to the product of the enormous number of potential connections between markers and the potential list of genetic expression. Accordingly, it is difficult even to decide where to look for these connections.

In the new study, published in the journal PLOS ONE, the researchers from the University of Haifa propose a new method of calculation that significantly reduces the number of possibilities, thereby making the identification of the interactions between genes a feasible task. Their method is based on innovative statistical tools from the “big data” field of analysis, and the preliminary goal is to reduce significantly the dimension dimension of genetic markers and the number of genetic expressions. The method shrinks the number of testing markers by applying a hierarchical filter to DNA areas containing at least one epistatic phenomenon, thereby enabling research to focus solely on genetic markers within these areas. The method reduces the number of genetic expressions by clustering together similar expressions.

The researchers used a study into simulative data to illustrate the advantages of their proposed method for the discovery of epistasis over two other methods. The use of genetic expression clusters and the hierarchical search of DNA areas with the potential presence of epistasis significantly increased the changes of discovering the phenomenon of epistasis, while reducing the rate of false discoveries to a very low level. The proposed method was applied for the purpose of analyzing the genome of the thale cress plant (Arabidopsis thaliana). The genetic mapping of this plant and data for its genetic expression are stored in The Arabidopsis Information Resource (TAIR), and as is customary in the field are accessible to the entire research community. The analysis addressed some 7,200 non-zero genetic expressions and 500 molecular markers situated along the five chromosomes of the plant genome. A search for epistasis based on marker pairs yields a total of nine million connections to be examined.

In the present study, the genetic expressions were grouped into some 300 clusters based on their mutual correlation. The 500 genetic markers were represented by 47 “regional” markers. As a result, the nine million possibilities for epistasis were reduced to just 340,000.

The researchers explain that the proposed method was successful in the challenging task of discovering weak effects, that is, effects relating to a group or network of genetic expressions in which each gene makes only a small contribution to the overall effect.

An analysis of the expressions of individual genes that were not included in the clusters enabled only the discovery of strong effects. This suggests that strong epistatic effects exist in the expression of single genes, while weak effects exist across groups of genes.

“The fact that we also observed that genetic traits involved in a strong effect showed low connectivity with other traits, and accordingly were not identified as part of the clusters, raises a hypothesis regarding the ‘social’ character of gene behavior, namely that a strong gene does not require cooperation with additional genes in order for an effect to be present, whereas a weak gene must create some type of associative mechanism, such as genetic networks, in order for an effect to be present,” the researchers concluded.

It is interesting to note that similar phenomena have also been found in the social sciences; for further discussion of this aspect, see Briñol et al., 2007 and Galinsky et al., 2008.

Source:

University of Haifa

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Proteins in the blood could improve detection of pancreatic cancer

Pancreatic cancer is one of the most lethal forms of cancer because early stage symptoms are relatively light, often resulting in it being discovered only after spreading to other organs. In order to improve the prognosis of pancreatic cancer, the development of methods for early detection of pancreatic cancer with a blood test is important. Working toward that goal, a research collaboration between Kumamoto University, Tohoku University and the National Cancer Center of Japan has discovered proteins in the blood which improve the detection of pancreatic cancer. When used in combination with conventional biomarkers, they enable the diagnosis of early stage pancreatic cancer, which was previously difficult.

To discover biomarkers useful in detecting pancreatic cancer, the researchers decided to analyze the genes of proteins which were reported to have higher expression in pancreatic cancer tissues, as candidates. They then tested a number of clinical specimens using two types of proteomics (large-scale protein analysis techniques) technologies and analyzed the changes of candidate proteins in the blood of both pancreatic cancer patients and healthy subjects. The blood samples were collected from 10 medical institutions around Japan.

“We selected 130 proteins and their expression levels were comprehensively measured in the blood plasma of 106 healthy subjects and 164 pancreatic cancer patients using antibody-based proteomics,” said lead researcher Professor Sumio Ohtsuki. “As a result, we found 23 proteins that had significantly changed in the plasma between the two groups.”

The researchers used a mass spectrometer and quantitative proteomics techniques to verify the pancreatic cancer biomarker candidates through accurate and specific measurements. In order to efficiently analyze a large number of clinical samples, they developed a technique using an automated sample preparation robot, a high-throughput liquid chromatography-mass spectrometer (LC-MS/MS), and auto-analysis software. The newly developed system can accurately analyze approximately 1000 samples per week while a conventional system could only assess around 80 samples.

With their new analysis system, they compared amount of candidate proteins in the plasma of 65 healthy and 38 early pancreatic cancer subjects and were able to show that the amount of insulin like growth factor binding protein 2 (IGFBP2) and IGFBP3 changed in pancreatic cancer patients at early stages. Additionally, the IGFBP2 and IGFBP3 diagnosed 12 early pancreatic cancer patients out of 15 cases (80%), who were negative for CA19-9, an existing diagnostic marker.

Furthermore, researchers analyzed approximately 600 more samples which included various other forms of cancer. They revealed the potential of IGFBP2 and IGFBP3 to also be effective in screening for cancers such as stomach, gallbladder, colorectal, duodenal, and hepatocellular carcinoma.

“These diagnostic markers are expected to contribute to the improvement of cancer prognosis, because early detection provides patients with a better chance of complete cure through surgery.” said Professor Ohtsuki. “Additionally, the new mass spectrometry system that we developed in this study is expected to make the analysis of a much large number of specimens possible in future clinical practice.”

Source:

Kumamoto University

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IU scientists find evidence for link between prostate cancer and Ewing’s sarcoma

Medical researchers at Indiana University Bloomington have found evidence for a link between prostate cancer, which affects millions of men age 50 and older, and Ewing’s sarcoma, a rare form …

Source: IU scientists find evidence for link between prostate cancer and Ewing’s sarcoma

IU scientists find evidence for link between prostate cancer and Ewing’s sarcoma

Medical researchers at Indiana University Bloomington have found evidence for a link between prostate cancer, which affects millions of men age 50 and older, and Ewing’s sarcoma, a rare form of cancer that affects children and young adults.

The results of the study, reported today in the journal Cell Reports, suggest that the molecular mechanism that triggers the rare disease Ewing’s sarcoma could act as a potential new direction for the treatment of more than half of patients with prostate cancer.

A form of bone and soft tissue cancer that affects about one in 1 million children and young adults age 10 to 19, Ewing’s sarcoma is terminal in 44 percent of teens age 15 to 19 and 30 percent of children. Over 100,000 men are diagnosed with prostate cancer each year in the U.S, with more than 99 percent of cases occurring after age 50.

“This research shows that the molecular mechanism involved in the development of most prostate cancers is very similar to the molecular mechanism known to cause Ewing’s sarcoma,” said Peter Hollenhorst, an associate professor in the Medical Sciences Program at IU Bloomington, a part of the IU School of Medicine. “It also suggests that this mechanism might be used to explore a common treatment for both diseases, one of which is not often pursued by drug companies due to its rarity.”

Hollenhorst is also a member of the Indiana University Melvin and Bren Simon Cancer Center in Indianapolis.

Other authors on the paper include Vivekananda Kedage, a graduate student in the IU Bloomington College of Arts and Sciences’ Department of Molecular and Cellular Biochemistry, and Travis J. Jerde, an associate professor in the Department of Pharmacology and Toxicology at the IU School of Medicine in Indianapolis. Kedage is the first author on the study.

There are 28 genes in the human body known as ETS genes, four of which are known to produce proteins that cause prostate cancer. These four cancer-causing genes, or “oncogenes,” are called ETV1, ETV4, ETV5 and ERG, the last of which has been implicated in over 50 percent of all prostate cancers. The other three combined play a role in about 7 percent of prostate cancers.

Ewing’s sarcoma results from errors in the chromosome repair process that causes the merger of two separate gene segments into a mutant hybrid gene, also known as a chimeric or fusion gene. One of these genes is called EWS, the other is a gene that produces ETS proteins.

Hollenhorst’s study is the first to show that the proteins produced by the EWS gene interact with all four ETS proteins known to trigger prostate cancer. Moreover, the EWS protein only interacts with proteins from these four harmful ETS genes, not the other 24 ETS genes not found to play a role in prostate cancer.

“A molecular mechanism that sets these four genes apart from the ones that don’t trigger cancer has never been identified until now,” Hollenhorst said. “This is significant because it suggests that any compound that disrupts EWS-ETS interaction would specifically inhibit the function of the four oncogenes and not the others, which play important roles in the healthy function of the body.”

The team also found the ETS genes implicated in prostate cancer interact with the un-mutated form of the EWS gene. In Ewing’s sarcoma, the small blue tumors that characterize the disease do not occur unless mutation occurs.

IU scientists used a combination of laboratory experiments and mouse models to observe the interaction of EWS and ETS proteins in prostate cells. The majority of the experiments involved observing the behavior of ETS oncogenes in prostate cancer cell cultures to reveal interaction with EWS proteins.

In experiments at the IU School of Medicine, they also introduced the ERG gene into normal human prostate cells in mice, which triggered the formation of tumors. The scientists then introduced an artificial mutation in the ERG gene to disrupt interaction with the proteins produced by the EWS gene. In these mice, the tumors failed to form.

“Together, the results indicated that the interaction between ERG and EWS is important for tumor formation,” Hollenhorst said. “We chose to focus our greatest efforts on the ERG protein since it is responsible for over 50 percent of all prostate cancers, and therefore the potential to benefit the greatest number of people.”

Source:

Indiana University

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New oncogene may contribute to high incidence of prostate cancer among African American men

A team of scientists has identified MNX1 as a new oncogene – a gene than can cause cancer – that is more active in African American prostate cancer than in European American prostate ca…

Source: New oncogene may contribute to high incidence of prostate cancer among African American men

New oncogene may contribute to high incidence of prostate cancer among African American men

A team of scientists has identified MNX1 as a new oncogene – a gene than can cause cancer – that is more active in African American prostate cancer than in European American prostate cancer. The finding suggests that genetic factors can contribute, at last in part, to the higher incidence of prostate cancer among African American men compared with men of other ethnic groups. The team includes scientists at Baylor College of Medicine, Third Military Medical University in China, the Michael E. DeBakey VA Medical Center, and Agilent Technologies India Pvt. Ltd. The study appeared Aug. 31 in Cancer Research.

“African Americans have about one-and-a-half times the incidence and twice the mortality associated with prostate cancer of European Americans, and the reasons for this are not clear,” said senior author Dr. Michael Ittmann, professor of pathology & immunology at Baylor and the Michael E. DeBakey Department of VA Medical Center.

Most scientists think that some of the health disparities among ethnic groups can be explained by differences in biology. Socio-economic factors, such as unequal access to healthcare services that make African American men less likely to receive regular physical examinations and screening for prostate cancer, may also be involved.

To study the genetic differences between African American prostate cancer and European American prostate cancer, the scientists took advantage of the tremendously diverse resources available at the Dan L Duncan Comprehensive Cancer Center at Baylor, which include one of the most extensive African American prostate tissue banks.

“We determined the gene expression profiling of African American prostate cancers,” said Ittmann, “and compared it with that of normal prostate tissue. Then, in collaboration with Dr. Chad Creighton, associate professor of medicine at Baylor and member of the Dan L Duncan Comprehensive Cancer Center Division of Biostatistics, we compared the gene expression profiling of African American prostate cancers with that of European American prostate cancers, which is available in published datasets.”

“We found 24 genes that were different between the African American and the European American prostate cancer datasets,” said Ittmann. “Some of the genes were less active in African American prostate cancer, but we concentrated on those that were more active as they could potentially be oncogenes. MNX1 was at the top of the list.”

MNX1 had been previously described as an oncogene linked to infantile acute myeloid leukemia, a rare cancer of the bone marrow and lymph nodes.

“Our study so far suggested that MNX1 was likely an oncogene in prostate cancer. The protein the MNX1 gene produces is a transcription factor; it can turn on gene transcription in other genes, which results in those genes producing more of their proteins. So we went on and studied MNX1 more extensively,” said Ittmann.

The scientists discovered that, compared with normal prostate tissues, both African American and European American prostate cancer have MNX1 genes that are more active and produce more of the MNX1 protein. However, MNX1 is significantly more active in African American prostate cancer than in European American prostate cancer.

Further research shed light on what can increase MNX1 activity in prostate cancer and strengthened MNX1’s ties to the disease.

“Interestingly, we found that both androgens, such as testosterone, and AKT, a signaling pathway, increase MNX1 activity. It’s been known for quite some time that androgens and the AKT pathway play a central role in prostate cancer,” said Ittmann.

The scientists then determined whether increased MNX1 activity affected a metabolic pathway prostate cancer uses to grow. Dr. Arun Sreekumar, professor of molecular and cellular biology, who also is with the Alkek Center for Molecular Discovery and the Verna and Marrs McLean department of biochemistry and molecular biology at Baylor, performed lipid analysis in African American prostate cancer tissues and showed that products of lipid metabolism increased when compared with those of normal prostate tissues.

“I am excited that these data highlight the existence of a biological basis in health disparity in prostate cancer,” said Sreekumar.

In summary, in African American prostate cancer androgen and the AKT signaling pathway can increase the activity of MNX1, which in turn increases lipid metabolism. Increased lipid metabolism is a hallmark of aggressive prostate cancer, which is more common on African American men.

These results can potentially lead to new approaches to treat and diagnose prostate cancer. For instance, currently, there are medications available to control lipid synthesis, which allows for exploring the effect of targeting lipid synthesis on prostate cancer growth. The scientists will also explore whether MNX1 can help predict cases of aggressive prostate cancer in the clinic.

“The better we can understand different subsets of prostate cancer, for instance, prostate cancer from African American men, the better we can treat them. A “one-size-fits-all” approach to treatment may not work for all patients,” said Creighton.

Source:

Baylor College of Medicine

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WSU researchers identify potential new diagnostic tool for early detection of colorectal cancer

Scientists at Washington State University and Johns Hopkins Medical School have discovered a fast, noninvasive method that could lead to the early diagnosis of colorectal cancer. Using ultrasensiti…

Source: WSU researchers identify potential new diagnostic tool for early detection of colorectal cancer

WSU researchers identify potential new diagnostic tool for early detection of colorectal cancer

Scientists at Washington State University and Johns Hopkins Medical School have discovered a fast, noninvasive method that could lead to the early diagnosis of colorectal cancer.

Using ultrasensitive, high-speed technology, the researchers identified a suite of molecules in the feces of mice that signifies the presence of precancerous polyps.

This “metabolic fingerprint” matches changes in both mouse and human colon tumor tissues and suggests a potential new diagnostic tool for early detection of colorectal cancer in a clinical setting.

Herbert Hill, WSU Regents professor, and graduate student Michael Williams conducted the study in collaboration with Raymond Reeves, WSU School of Molecular Biosciences, and Linda Resar, Johns Hopkins University School of Medicine.

The findings were reported this month in the Journal of Proteome Research.

Better screening tools needed

Colorectal cancer is the second most common cancer worldwide. Nearly 1.4 million new cases were diagnosed in 2012, according to the World Cancer Research Fund International. It is the second leading cause of cancer-related deaths in the U.S.

Though early detection is key to successful treatment, most screening tests are limited in diagnostic capability or ease of application. Colonoscopy, for example, is a known lifesaver but is costly and unappealing to many people who might otherwise undergo testing.

Decreasing the invasiveness of the procedure could help. Williams said more people would be willing to provide a stool sample than undergo a biopsy through a colonoscope. In addition, colonoscopes can only extend a limited distance into the large intestine, potentially missing some polyps.

“With our new test, it could be possible to diagnose cancer occurring throughout the entire colon,” he said.

‘Sniffing’ out cancer

Hill and Williams discovered the molecular fingerprint for colon cancer using a technology called ion mobility-mass spectrometry. IMMS is found in sensor devices worldwide that sniff out illicit drugs, chemical warfare agents and explosives in airports. Hill has been an innovator in the field for nearly 40 years.

In this case, IMMS was coupled with ultraperformance liquid chromatography.

The researchers first identified metabolic products from normal colon tissue in both humans and mice. IMMS can measure hundreds of metabolites simultaneously, such as enzymes, fats, glucose and amino acids.

The scientists then compared this normal profile to that found in cancerous colon tissues from humans and research mice with polyps in their colons that mimic those in humans.

In both cases, the scientists found that colon cancer caused significant changes in fat metabolism, especially for lipids and fatty acids. These abnormalities created a molecular fingerprint that was similar in humans and mice, said Hill.

Diagnostic changes in the feces

Next, Hill and Williams examined droppings from transgenic and control mice to see if the molecular fingerprint could be found in feces as well.

Indeed IMMS detected many of the same metabolic abnormalities seen in the previous study and could clearly distinguish between healthy mice and those with colorectal cancer.

“The feces was not exactly the same as the tissue samples, but it had a lot of similarities to the tissue,” said Hill. “We found the lipids and fatty acids were changing — and there were also changes in the amino acids.”

Specifically, an important class of fats called lysophospholipids changed dramatically, said Williams.

“These types of lipids are known to be important in the development of cancer and are particularly tied to colorectal cancer.”

All of which is encouraging to Hill and Williams as they search for a more user-friendly method to diagnose colorectal cancer in the early stages.

Early warning system

“The benefit of early detection is that we can catch cancer before it metastasizes to other parts of the body,” said Williams. “Our results represent the zero stage of cancer, the polyp stage – as early as colon cancer can be detected.”

“The exciting part is being able to see differences in the stool,” said Hill. “This could lead to a noninvasive, more comprehensive early-warning detection method for colorectal cancer, but a lot of research needs to be done before it can be actually realized.”

Their next step, if funded, is to evaluate human stool samples to see if the molecular fingerprint is present with colorectal cancer in people.

Hill said the laboratory equipment needed to run these diagnostic tests is already commercially available.

Source:

Washington State University

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