The routine use of a molecular testing panel developed at UPMC greatly increases the likelihood of performing the correct initial surgery for patients with thyroid nodules and cancer, report researchers from the University of Pittsburgh Cancer Institute (UPCI), partner with UPMC CancerCenter.

The test improved the chances of patients getting the correct initial surgery by 30 percent, according to the study.

“Before this test, about one in five potential thyroid cancer cases couldn’t be diagnosed without an operation to remove a portion of the thyroid,” said lead author Linwah Yip, M.D., assistant professor of surgery in Pitt’s School of Medicine and UPMC surgical oncologist.  Previously, “if the portion removed during the first surgery came back positive for cancer, a second surgery was needed to remove the rest of the thyroid. The molecular testing panel now bypasses that initial surgery, allowing us to go right to fully removing the cancer with one initial surgery. This reduces risk and stress to the patient, as well as recovery time and costs.”

Cancer in the thyroid, which is located in the “Adam’s apple” area of the neck, is now the fifth most common cancer diagnosed in women.  Thyroid cancer is one of the few cancers that continues to increase in incidence, although the five-year survival rate is 97 percent.

Previously, the most accurate form of testing for thyroid cancer was a fine-needle aspiration biopsy, where a doctor guides a thin needle to the thyroid and removes a small tissue sample for testing. However, in 20 percent of these biopsies, cancer cannot be ruled out. A lobectomy, which is a surgical operation to remove half of the thyroid, is then needed to diagnose or rule-out thyroid cancer. In the case of a postoperative cancer diagnosis, a second surgery is required to remove the rest of the thyroid.

Researchers have identified certain gene mutations that are indicative of an increased likelihood of thyroid cancer, and the molecular testing panel developed at UPMC can be run using the sample collected through the initial, minimally invasive biopsy, rather than a lobectomy. When the panel shows these mutations, a total thyroidectomy is advised.

Dr. Yip and her colleagues followed 671 UPMC patients with suspicious thyroid nodes who received biopsies. Approximately half the biopsy samples were run through the panel, and the other half were not. Patients whose tissue samples were not tested with the panel had a 2.5-fold higher statistically significant likelihood of having an initial lobectomy and then requiring a second operation.

“We’re currently refining the panel by adding tests for more genetic mutations, thereby making it even more accurate,” said co-author Yuri Nikiforov, M.D., Ph.D., professor in the Department of Pathology at Pitt and director of thyroid molecular diagnostics at the UPMC/UPCI Multidisciplinary Thyroid Center. “Thyroid cancer is usually very curable, and we are getting closer to quickly and efficiently identifying and treating all cases of thyroid cancer.” UPMC

It has been some time in the making, but the newly designed Greiner Bio-One website was finally launched at the beginning of July along with our newly designed webshop.

Product and order information for the business divisions Preanalytics (specimen collection), BioScience (products for the biotech industry), Diagnostics (DNA arrays) and OEM (customised developments for the Life Science industry) can be accessed at www.gbo.com.

The innovative design with cool Parallax Scrolling technology at various levels is not the only thing that is new. Alongside the range of improvements, there are also a number of technical innovations, making it even easier to find the information you are looking for.

Features include:

• A download menu divided into product groups, with downloads of flyers, brochures, etc. available in a range of languages
• FAQs for the various products are answered in the "Frequently Asked Questions" section
• The E-learning system "GBO Compass" and social media channels
  can now also be accessed via links
• The latest developments are shown in brief and with an eye-catching layout in Marketing Highlights
• Related content such as print material is shown directly on the various product pages in a separate box.

_{^{Greiner Bio-One International AG
Greiner Bio-One is specialized in the development, production and distribution of high quality laboratory products made from plastic. The company is a technological partner for hospitals, laboratories, universities, research institutes and the diagnostic, pharmaceutical and biotechnology industries. Greiner Bio-One consists of four business units: Preanalytics, BioScience, Diagnostics and OEM. Today the company generates a turnover of 373 Mio. Euro.  Greiner Bio-One is a member of the Greiner Group based in Kremsmünster (Austria).}}

Understanding eye diseases is tricky enough. Knowing what causes them at the molecular level is even more confounding.

Now, University of Iowa researchers have created the most detailed map to date of a region of the human eye long associated with blinding diseases, such as age-related macular degeneration. The high-resolution molecular map catalogues thousands of proteins in the choroid, which supplies blood and oxygen to the outer retina, itself critical in vision. By seeing differences in the abundance of proteins in different areas of the choroid, the researchers can begin to figure out which proteins may be the critical actors in vision loss and eye disease.

“This molecular map now gives us clues why certain areas of the choroid are more sensitive to certain diseases, as well as where to target therapies and why,” says Vinit Mahajan, assistant professor in ophthalmology at the UI and corresponding author on the paper. “Before this, we just didn’t know what was where.”

What vision specialists know is many eye diseases, including age-related macular degeneration (AMD), are caused by inflammation that damages the choroid and the accompanying cellular network known as the retinal pigment epithelium (RPE). Yet they’ve been vexed by the anatomy: Why does it seem that some areas of the choroid-RPE are more susceptible to disease than others, and what is happening at the molecular level? The researchers set about to answer that question with non-diseased eye tissue donated by three deceased older individuals through the Iowa Lions Eye Bank. From there, Mahajan and Jessica Skeie, a post-doctoral researcher in ophthalmology at the UI, created a map that catalogues more than 4,000 unique proteins in each of the three areas of the choroid-RPE: the fovea, macula, and the periphery.

Why that’s important is now the researchers can see which proteins are more abundant in certain areas, and why. One such example is a protein known as CFH, which helps prevent a molecular cascade that can lead to AMD, much like a levee can keep flooding waters at bay. The UI researchers learned, though the map, that CFH is most abundant in the fovea. That helps, because now they know to monitor CFH abundance there; fewer numbers of the protein could mean increased risk for AMD, for instance.

“Now you can see all those differences that you couldn’t see before,” explains Mahajan, whose primary appointment is in the Carver College of Medicine. University of Iowa

Reduced levels of an anti-cancer protein make male brain cells more vulnerable to becoming tumors, according to a new study at Washington University School of Medicine in St. Louis.

New research at Washington University School of Medicine in St. Louis helps explain why brain tumours occur more often in males and frequently are more harmful than similar tumours in females. For example, glioblastomas, the most common malignant brain tumours, are diagnosed twice as often in males, who suffer greater cognitive impairments than females and do not survive as long.

The researchers found that retinoblastoma protein (RB), a protein known to reduce cancer risk, is significantly less active in male brain cells than in female brain cells.

“This is the first time anyone ever has identified a sex-linked difference that affects tumour risk and is intrinsic to cells, and that’s very exciting,” said senior author Joshua Rubin, MD, PhD. “These results suggest we need to go back and look at multiple pathways linked to cancer, checking for sex differences. Sex-based distinctions at the level of the cell may not only influence cancer risk but also the effectiveness of treatments.”

Rubin noted that RB is the target of drugs now being evaluated in clinical trials. Trial organizers hope the drugs trigger the protein’s anti-tumour effects and help cancer patients survive longer.

“In clinical trials, we typically examine data from male and female patients together, and that could be masking positive or negative responses that are limited to one sex,” said Rubin, who is an associate professor of pediatrics, neurology and anatomy and neurobiology. “At the very least, we should think about analysing data for males and females separately in clinical trials.”

Scientists have identified many sex-linked diseases that either occur at different rates in males and females or cause different symptoms based on sex. These distinctions often are linked to sex hormones, which create and maintain many but not all of the biological differences between the sexes.

However, Rubin and his colleagues knew that sex hormones could not account for the differences in brain tumour risk.

“Male brain tumor risk remains higher throughout life despite major age-linked shifts in sex hormone production in males and females,” he said. “If the sex hormones were causing this effect, we’d see major changes in the relative rates of brain tumours in males and females at puberty. But they don’t happen then or later in life when menopause changes female sex hormone production.”

Rubin used a cell model of glioblastoma to prove it is easier to make male brain cells become tumors. After a series of genetic alterations and exposure to a growth factor, male brain cells became cancerous faster and more often than female brain cells. Washington University School of Medicine

A new study suggests uric acid may play a role in causing metabolic syndrome, a cluster of risk factors that increases the risk of heart disease and type 2 diabetes.

Uric acid is a normal waste product removed from the body by the kidneys and intestines and released in urine and stool. Elevated levels of uric acid are known to cause gout, an accumulation of the acid in the joints. High levels also are associated with the markers of metabolic syndrome, which is characterized by obesity, high blood pressure, elevated blood sugar and high cholesterol. But it has been unclear whether uric acid itself is causing damage or is simply a by-product of other processes that lead to dysfunctional metabolism.

New research at Washington University School of Medicine in St. Louis suggests excess uric acid in the blood is no innocent bystander. Rather, it appears to be a culprit in disrupting normal metabolism.

“Uric acid may play a direct, causative role in the development of metabolic syndrome,” said first author Brian J. DeBosch, MD, PhD, an instructor in paediatrics. “Our work showed that the gut is an important clearance mechanism for uric acid, opening the door to new potential therapies for preventing or treating type 2 diabetes and metabolic syndrome.”

Recent research by the paper’s senior author, Kelle H. Moley, MD, the James P. Crane Professor of Obstetrics and Gynecology, and her collaborators has shown that a protein called GLUT9 is an important transporter of uric acid.

DeBosch, a paediatric gastroenterologist who treats patients at St. Louis Children’s Hospital, studied mice to learn what happens when GLUT9 stops working in the gut, essentially blocking the body’s ability to remove uric acid from the intestine. In this study, the kidney’s ability to remove uric acid remained normal.

Eating regular chow, mice missing GLUT9 only in the gut quickly developed elevated uric acid in the blood and urine compared with control mice. And at only 6-8 weeks of age, they developed hallmarks of metabolic syndrome: high blood pressure, elevated cholesterol, high blood insulin and fatty liver deposits, among other symptoms.

The researchers also found that the drug allopurinol, which reduces uric acid production in the body and has long been used to treat gout, improved some, but not all, of the measures of metabolic health. Treatment with the drug lowered blood pressure and total cholesterol levels.

Exposure to uric acid is impossible to avoid because it is a normal by-product of cell turnover in the body. But there is evidence that diet may contribute to uric acid levels. Many foods contain compounds called purines that break down into uric acid. And adding to growing concerns about fructose in the diet, evidence suggests that fructose metabolism in the liver also drives uric acid production.

“Switching so heavily to fructose in foods over the past 30 years has been devastating,” Moley said. “There’s a growing feeling that uric acid is a cause, not a consequence, of metabolic syndrome. And now we know fructose directly makes uric acid in the liver. With that in mind, we are doing further research to study what happens to these mice on a high-fructose diet.” University of Washington at St. Louis