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Whole-exome sequencing: Rational approach for ‘diagnostic odyssey’ patients

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A new clinical study from the Mayo Clinic Center for Individualized Medicine shows that whole-exome sequencing (WES) could serve as a viable diagnostic approach for identifying rare inherited diseases and providing a resolution for patients on a diagnostic odyssey. WES is a laboratory process that determines, all at once, the entire unique DNA sequence (i.e., the inherited genetic material) of an organism’s genome. WES provides patients with rare genetic conditions who have been evaluated by multiple providers over, sometimes, years, without a diagnosis (i.e., a diagnostic odyssey) an opportunity to get answers.

“The significant diagnostic yield, moderate cost and notable health marketplace acceptance of whole-exome sequencing for clinical purposes, compared with conventional genetic testing, make it a rational diagnostic approach for patients on a diagnostic odyssey,” says lead author Konstantinos Lazaridis, M.D., director of the Mayo Individualized Medicine Clinic and primary investigator of the multisite study published in Mayo Clinic Proceedings.

During the study, WES testing was provided by Mayo Clinic physicians to patients on a diagnostic odyssey. DNA specimens of the person seeking medical attention and other affected or unaffected relatives were submitted to clinical WES laboratories. Researchers aimed at discovering genetic variant(s) that cause or contribute to the patient’s disease, permitting resolution of the diagnostic odyssey and potentially leading to better patient management through disease-specific treatments.

In the first 18 consecutive months, the Individualized Medicine Clinic received 82 consult requests for patients on a diagnostic odyssey. Seven of the cases were deferred, and 75 cases were approved to proceed with WES. Individualized Medicine Clinic genomic counselors met with 71 patients; 51 patients submitted specimens for clinical WES testing and received the results. Ultimately, 15 patients or 29 percent resulted in a diagnosis based on WES findings.

“The success rate of 29 percent, which is about twofold higher of conventional genetic evaluations for such patients, makes WES a reasonable diagnostic approach for patients on a diagnostic odyssey” says Dr. Lazaridis.

The health care marketplace also appears to be accepting WES as a valued diagnostic approach for these patients– a concern of any new genetic test. Despite the slightly higher cost of testing ($8,000 average cost per patient), WES is poised to show increasing value due to the continued decline in sequencing costs. Of interest, the study reported that Medicaid supported 27 percent of the patients, and 38 percent of patients received complete or partial insurance coverage. There was a relatively low rate (15 percent) of known insurance denial for WES testing. Six patients or 12 percent were fully covered by commercial insurance, and the average out-of-pocket expense of the 4 out of 18 patients with partial insurance coverage for which data was provided was approximately 13 percent of the cost of testing. These findings support that insurance coverage exists for clinical WES testing and is similar to that of established genetic tests.

“With several million patients in the U.S. suffering from a rare or an undiagnosed disease, WES is emerging as a promising, affordable test that could enhance clinical care by improving diagnosis of such patients. I envision, one day WES will be performed on every newborn and every patient who needs medical care” says Dr. Lazaridis.

The research was funded by the Mayo Clinic Center for Individualized Medicine, James L. and Donna K. Barksdale, Everett J. and Jane M. Hauck, William O. Lund Jr., and the Natalie C. Lund Charitable Foundation.

Additional authors on the research team are: Kimberly Schahl, CGC, Informed DNA; Margot Cousin, Ph.D., Mayo Clinic; Dusica Babovic-Vuksanovic, M.D., Mayo Clinic; Douglas Riegert-Johnson, M.D., Mayo Clinic; Ralitza Gavrilova, M.D., Mayo Clinic; Tammy McAllister, M.A., Mayo Clinic; Noralane Lindor, M.D., Mayo Clinic; Roshini Abraham, Ph.D., Mayo Clinic; Michael Ackerman, M.D., Ph.D., Mayo Clinic; Pavel Pichurin, M.D., Mayo Clinic; David Deyle, M.D., Mayo Clinic; Dimitar Gavrilov, M.D., Ph.D., Mayo Clinic; Jennifer Hand, M.D., Mayo Clinic; Eric Klee, Ph.D., Mayo Clinic; Michael Stephens, M.D., Mayo Clinic; Myra Wick, M.D., Ph.D., Mayo Clinic; Elizabeth Atkinson, M.S., Mayo Clinic; David Linden, Ph.D., Mayo Clinic; Matthew Ferber, Ph.D., Mayo Clinic; Eric Wieben, Ph.D., Mayo Clinic; Gianrico Farrugia, M.D. , Mayo Clinic

About Mayo Clinic

Mayo Clinic is a nonprofit organization committed to medical research and education, and providing expert, whole-person care to everyone who needs healing. For more information, visit http://www.mayoclinic.org/about-mayo-clinic or http://newsnetwork.mayoclinic.org/.

About Mayo Clinic Proceedings

Mayo Clinic Proceedings is a monthly peer-reviewed medical journal that publishes original articles and reviews dealing with clinical and laboratory medicine, clinical research, basic science research and clinical epidemiology. Proceedings is sponsored by the Mayo Foundation for Medical Education and Research as part of its commitment to physician education. It publishes submissions from authors worldwide. The journal has been published for more than 80 years and has a circulation of 130,000. Articles are available at http://www.mayoclinicproceedings.org.

MEDIA CONTACT: Colette Gallagher, Mayo Clinic Public Affairs, 507-284-5005, newsbureau@mayo.edu

Source: Mayo Clinic

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Common blood test could predict risk of 2nd stroke

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Researcher Stephen Williams said combining the CRP test with genetic factors can help doctors predict, and perhaps help prevent, a potentially deadly second ischemic stroke.

A new discovery about ischemic stroke may allow to doctors to predict patients’ risk of having a second stroke using a commonly performed blood test and their genetic profile.

Researchers have linked high levels of C-Reactive Protein, an enzyme found in the blood, with increased risk for recurrent ischemic stroke. C-Reactive Protein (CRP) is produced in the liver in response to inflammation, and it is already checked to measure people’s risk of developing coronary artery disease. The new research suggests it could be a useful tool for ischemic stroke patients as well.

“The biggest risk of death for someone who has already had a stroke is to have another one,” said University of Virginia School of Medicine researcher Stephen Williams, PhD. “So it’s really important to be able to try and target those individuals who are at the highest risk for the thing that very well may kill them.”

Ischemic Stroke Risk

Ischemic strokes result from blockages preventing blood flow to the brain; they are responsible for approximately 85 percent of all stroke cases. (Hemorrhagic strokes, on the other hand, occur when blood vessels burst and bleed into the brain.)

Stephen Williams, PhD

To better understand ischemic stroke, Williams and his colleagues set out to determine how our genes affect the levels of biomarkers such as CRP in our blood. Not only did they find that elevated CRP levels suggest increased stroke risk, they identified gene variations that drive those risks.

“So we have the genetics influencing [CRP] levels, which then increases the risk of having a recurrent stroke. Then we went back and said alright, can we predict the increased risk purely based on the genetics, which we were able to do,” Williams said. “There’s this shared genetic susceptibility not only for increased C-Reactive Protein but for increased risk for stroke. We could estimate what’s called a hazard ratio – basically the increased risk for having or not having a second stroke – based on the genetics.”

Williams, of the Department of Neurology and the Center for Public Health Genomics, envisions a day when doctors might focus on CRP levels and a patient’s genetic makeup to determine the patient’s overall risk for a second stroke. But even CRP levels alone could be a useful tool in assessing risk after the initial stroke. “Getting a CRP measure on someone is really simple. It’s just a blood draw. You don’t have to take something like a biopsy which patients might have an aversion to,” Williams said. “It’s not very expensive, and it’s part of routine workups that could be done for patients. However, combined with genetic information, we may have even more power to identify those at greatest risk.”

Findings Published

The findings have been published online by the scientific journal Neurology in an article written by Williams, Fang-Chi Hsu, Keith L. Keene, Wei-Min Chen, Sarah Nelson, Andrew M. Southerland, Ebony B. Madden, Bruce Coull, Stephanie M. Gogarten, Karen L. Furie, Godfrey Dzhivhuho, Joe L. Rowles, Prachi Mehndiratta, Rainer Malik, Josée Dupuis, Honghuang Lin, Sudha Seshadri, Stephen S. Rich, Michèle M. Sale and Bradford B. Worrall on behalf of METASTROKE, the Genomics and Randomized Trials Network Collaborative Research Group.

The National Institutes of Health funded research efforts critical to the study.

Source: University of Virginia

Alzheimer’s disease: Early biomarker defined

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Alzheimer’s disease results from the accumulation in the brain of protein deposits that are toxic to nerve cells. The deposits themselves are largely comprised of insoluble aggregates of so-called beta-amyloid peptides – short fragments cleaved from a protein found on nerve-cell membranes – and they begin to form decades before any overt symptoms of dementia emerge. Now research teams led by Christian Haass, who holds the Chair of Metabolic Biochemistry at LMU and is the speaker of the German Center for Neurodegenerative Diseases (DZNE) in Munich, and Professor Michael Ewers of the Institute for Stroke and Dementia Research (ISD) at Munich University Medical Center, now report that the concentration of a specific segment of the protein TREM2 in cerebrospinal fluid (CSF) is significantly elevated in early stages of Alzheimer’s disease. “Our findings indicate that TREM2 plays an important role in the progression of Alzheimer’s, and perhaps even other forms of dementia. It appears to be part of a defense mechanism that involves phagocytic cells that eliminate damaged nerve cells and toxic protein deposits, such as those made up of beta-amyloid peptides,” says Haass. The new study has now been published in the journal EMBO Molecular Medicine.

TREM2 is a cell-surface receptor that is essential for the function of specialized phagocytic cells called microglia, which are found only in the brain. Microglial cells serve as an arm of the innate immune system and act as the brain’s waste disposal squad, recognizing and destroying cell debris and other types of toxic particulate material. The detection by Haass, Ewers and colleagues of increased concentrations of a soluble fragment of TREM2 in the CSF of patients with mild symptoms of Alzheimer’s disease forges a further link between the protein and the neurodegenerative disorder. The same researchers had previously shown that mutations that affect TREM2 function also reduce the ability of microglia to clear amyloid aggregates and damaged cells.

An informative and versatile marker

In their latest work, the LMU team studied over 400 Alzheimer’s patients who showed cognitive defects of varying severity, and compared them with age-matched controls. Biochemical analyses of samples of CSF revealed that patients who exhibited mild cognitive deficits had the highest concentrations of a particular fragment of the TREM2 protein found in the study. The amounts detected in patients with advanced Alzheimer’s disease were significantly lower. “This correlates with the level of activity of the microglial cells, which falls off as the condition progresses. This in turn presumably means that less beta-amyloid and cell debris can be cleared away,” Haass points out. “We therefore believe that this biomarker provides us with a way to assess the capacity of innate immune cells in the brain to degrade and dispose toxic material.”

At the current stage it is still unclear whether the changes in the concentration of the TREM2 fragment in the CSF is a cause or a consequence of disease progression. However, the researchers favor the idea that the early increase in the level of TREM2 is attributable to the activation of microglia in response to initial signs of damage to the nerve cells in the brain. “Our results indicate that the alterations in TREM2 reflect physiological changes that occur at an early stage in the development of Alzheimer’s dementia. This makes TREM2 interesting from a therapeutic perspective,” says Michael Ewers.

The new biomarker could also make it possible to monitor the efficacy of novel anti-inflammatory approaches for treatment of Alzheimer’s disease. In addition, measurements of the levels of TREM2 in the CSF could help to define the most effective window for early interventions to combat or control the disorder. The LMU researchers propose a long-term longitudinal study, in which the concentration of TREM2 in CSF samples from individuals with mutations known to be linked to familial Alzheimer’s disease is determined at regular intervals under controlled conditions.

EMBO Molecular Medicine, doi: 10.15252/emmm.201506123

Source: www.en.uni-muenchen.de

‘Big data’ helps to discover key factors driving blood cell specification

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Cells with the ability to give rise to blood are normally specified in the early embryo over a number of developmental stages and eventually form blood stem cells that are maintained for life and generate trillions of blood cells every day.

By studying six consecutive stages of development and adopting a ‘big data’ approach using computational analyses, the consortium, funded by the Biotechnology and Biological Sciences Research Council, studied the behaviour of thousands of genes and the factors that regulate them.

Their findings, published in Developmental Cell, identified previous unknown regulators of blood cell development, significantly furthering our knowledge of this process. They also explained how regulatory elements in the DNA work together, driving gene expression and the switch of one developmental stage to another.

These data also revealed the minimum requirements for generating blood cells from an unrelated, cultured cell type, a method that is vital for the generation of patient-specific blood cells for regenerative medicine. To reach out to the scientific community and the interested public, group generated a website that allows unlimited data access.

The team believes that improved understanding of the key genes that drive the specification of blood cells and how they interact with each other will help to generate the stem cells that could be used to help patients suffering from blood disorders, such as myeloid leukaemia.

Professor Constanze Bonifer from the University of Birmingham explained, “We examined how develop towards by collecting “multi-omics” data from measuring gene activity, changes in chromosome structure and the interaction of regulatory factors with the genes themselves. Our research shows in unprecedented detail how a vast network of interacting genes control blood . It also shows how we can use such data to enhance our knowledge of this process”

Source: Phys.org

Free Webinar: Identification of Novel Psychoactive Substances Using Handheld Near-Infrared and Raman Spectroscopy

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Discover how novel psychoactive substances (NPS) are emerging onto the market and the toxicological problems they can cause. Gain insight into the identification of NPS and how spectroscopic techniques can be applied for their rapid identification.

March 17th, 2016. 08:00 PDT / 11:00 EDT / 15:00 GMT / 16:00 CET

Click here to check the time of the webinar in your country

Dr. Sulaf Assi, Lecturer in Forensic Science, Bournemouth University, will discuss:

  • The emergence of NPS on the drug market.
  • Toxicological problems associated with NPS.
  • How near-infrared and Raman spectroscopy can be applied for their rapid identification.

Click here to register for this online event and Q&A session. If you can’t make the live event, don’t worry – we will send all registrants a link to the on-demand version after the event.

More Information

Researchers find association between oral bacteria and esophageal cancer

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The findings, published recently in Infectious Agents and Cancer, only detected P. gingivalisin 12 percent of tissues adjacent to the cancerous cells, while this organism was undetected in normal esophageal tissue.

“These findings provide the first direct evidence that P. gingivalis infection could be a novel risk factor for ESCC, and may also serve as a prognostic biomarker for this type of cancer,” said Huizhi Wang, M.D., Ph.D., assistant professor of oral immunology and infectious diseases at the UofL School of Dentistry. “These data, if confirmed, indicate that eradication of a common oral pathogen may contribute to a reduction in the significant number of people suffering with ESCC.”

The esophagus, a muscular tube critical to the movement of food from the mouth to the stomach, is lined with two main kinds of cells, thus there are two main types of esophageal cancer: adenocarcinoma and squamous cell carcinoma. The latter is more common in developing countries.

In collaboration with the College of Clinical Medicine of Henan University of Science and Technology in Luoyang, China, Wang and his UofL colleagues Richard J. Lamont, Ph.D., Jan Potempa, Ph.D., D.Sc., and David A. Scott, Ph.D., tested tissue samples from 100 patients with ESCC and 30 normal controls.

The research team measured the expression of lysine-gingipain, an enzyme unique to P. gingivalis, as well as the presence of the bacterial cell DNA within the esophageal tissues. Both the bacteria-distinguishing enzyme and its DNA were significantly higher in the cancerous tissue of ESCC patients than in surrounding tissue or normal control sites. The researchers also found the presence of P. gingivalis correlated with other factors, including cancer cell differentiation, metastasis and overall survival rate.

According to Wang, there are two likely explanations: either ESCC cells are a preferred niche for P. gingivalis to thrive or the infection of P. gingivalis facilitates the development of esophageal cancer.

If the former is true, Wang says simple antibiotics may prove useful or researchers can develop other therapeutic approaches for esophageal cancer utilizing genetic technology to target the P. gingivalis and ultimately destroy the cancer cells.

“Should P. gingivalis prove to cause ESCC, the implications are enormous,” Wang said. “It would suggest that improving oral hygiene may reduce ESCC risk; screening for P. gingivalis in dental plaque may identify susceptible subjects; and using antibiotics or other anti-bacterial strategies may prevent ESCC progression.”

According to the Centers for Disease Control, about 15,000 people in the United States are diagnosed with esophageal cancer each year. As with most cancers, there are a number of risk factors including chemical exposure, diet, heredity and age. It is somewhat difficult to diagnosis this cancer early, and it is characterized by rapid progression and high mortality.

Source: Eurekalert.org

The way of prostate cancer diagnostics

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Prostate cancer diagnostics has been essentially changed within the last 5 years. While prostate-specific antigen (PSA) remains the basic parameter, the additional value of the two 2012 FDA-approved biomarkers prostate health index (PHI) in serum and prostate cancer gene 3 (PCA3) in urine has been confirmed numerous times [1]. The detection ofTMPRSS2-ERG gene fusions in the tissue of approximately 50% of all prostate cancer patients and the subsequently developed urinary assay [2] put hope on further diagnostic improvement that could unfortunately only be partially fulfilled [3–5].

The senior author of this article [6] in this issue of Clinical Chemistry and Laboratory Medicine played the key role in detecting PCA3 and developing urinary assays for PCA3 and TMPRSS2-ERG [7]. And this group is now the first that compared both markers in whole urine, urinary sediment and exosomes. With this new independent study, the authors completed and partly relativized previous data when they compared only the profile of these markers in urinary sediments and exosomes [8]. This comparative approach between various urine fractions can be considered as exemplary for testing other biomarkers not only for prostate cancer but also for renal cell carcinoma and bladder cancer. The positive effect of a digital rectal examination (DRE) of the prostate before urine sampling for diagnostic purpose was confirmed regarding the diagnostic validity of these markers in detecting prostate cancer. However, the main result was that whole urine results in a higher analytical sensitivity compared to sensitivity obtained using sediments and exosomes. In this respect, the advantage to use whole urine samples as applied in the tests for PCA3 and TMPRSS2-ERG instead sediments is not only justified from the practical point of view but also with regard to the improved analytical sensitivity. On the other hand, biomarker levels measured in the three tested urine fractions in this study and presented in table 4 proved that there was a distinct difference between the levels in the whole urine and the sum of the two other fractions [6]. Thus, it can be concluded that a great amount of these mRNAs in the urine obviously occurs in free forms without any association to particles (exosomes) and without cellular confinement (sediments). It is particularly worth mentioning that this comprehensively researched study by Hendriks et al. clears away the erroneous view that nucleic acids in urine as in this case of PCA3 mRNA and TMPRSS2-ERG mRNA are mostly detected in the released prostate cells. In consequence, the analytical focus on sediments as done in several studies does not let expect satisfying results. A similar phenomenon of differences between samples of whole urine, cell-depleted urine, and sediments was also observed in bladder cancer patients for various mRNAs [9]. In addition, the differences in that study were not uniform for all tested mRNAs but showed a particular behavior for specific mRNAs [9]. Thus, the focus on possible new urinary markers including non-coding nucleic acids like microRNAs, long non-coding RNAs, and piRNAs should draw attention to this aspect. These observations imply that whole urine analysis as starting point should be used before the markers are tested regarding their diagnostic usefulness in the different urine fractions. Even more, each new marker can be reliably assesed if measured in all urinary fractions.

Urine as a complex substrate with several fractions is not easy to handle and processing and mRNA or miRNA extraction depends on many factors including stability. Regarding sample stability and storage, whole urine further can be surely preferred since different commercially available procedures have been recommended. These technical devices, e.g. supplied by Norgen Biotek Corp., Thorold, Canada with its various kits for urine RNA concentration, preservation, and isolation facilitate the applicability of these nucleic acid-based markers in urine in practice despite reliable long-term storage data are missing so far.

However, from the analytical aspect it is easier to handle serum. (-2)proPSA and the formula (-2)proPSA/freePSA × √PSA, which is named prostate health index (PHI) shows a better correlation with tumor aggressiveness than PCA3 [1]. Despite a clear clinical usefulness of PCA3 [10] its limitations are the relative complicated measurement procedure and the low sensitivity at high values of >100 [11]. However, the combination of PCA3 and TMPRSS2-ERG scores within several PSA-based models improved the predicting of PCa and high-grade PCa [5]. But it should be noted that the PCA3and TMPRSS2-ERG-based Michigan-Prostate Score (MiPS) has costs of ~750 $. While this test improves prostate biopsy indication it cannot replace the biopsy itself. Here a multiparametric magnetic resonance imaging (MRI) and in cases of suspicious lesions by using the Prostate Imaging Reporting and Data System (PI-RADS) a subsequent MRI/ultrasound fusion biopsy is done [12]. A clinical aggressive and significant PCa will be almost always detected by MRI with a detection rate of up to 87% in summarized data of >1900 patients [12]. However, in case of a non-suspicious PI-RADS score ~27% of mostly Gleason 3+3=6 cancers are overlooked as they are exclusively detected in the additional systematic biopsies after MRI/ultrasound fusion biopsy [13]. However, despite this shift in PCa diagnostics towards PI-RADS score based MRI and MRI/ultrasound fusion biopsies in patients with or even without prior biopsy we propose a significant role for biomarkers in serum and urine. For example, a young man with a gray zone PSA of 2–10 μg/L and non-suspicious MRI may still suffer from a Gleason 3+3=6 PCa and the presence of high values of PHI, PCA3 or MiPS may help to force a subsequent systematic biopsy. Thus, the time of prostate biomarkers is not over but it should be used in combination with the MRI in an appropriate strategy. So far, there is only one study that compared MRI, PHI and PCA3 with an advantage for the MRI but no PIRADS score was used [14]. Further comparisons of the established and new biomarkers with the MRI are necessary to find the best possible PCa diagnostic pathway of the future.

Authors

Carsten Stephan (1, 2) / Klaus Jung (1, 2)

  1. Department of Urology, Charité – Universitätsmedizin Berlin, Berlin, Germany
  2. Berlin Institute for Urologic Research, Berlin, Germany

Corresponding author: Prof. Dr. Carsten Stephan, Department of Urology, Charité – Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany, Phone: +49-30-450 515052, Fax: +49-30-450 515904, E-mail: (email); and Berlin Institute for Urologic Research, Berlin, Germany

References:

  1. Stephan C, Jung K, Ralla B. Current biomarkers for diagnosing of prostate cancer. Future Oncol 2015;11:2743–55. [Web of Science] [CrossRef]
  2. Groskopf J, Siddiqui J, Aubin SM, Sefton-Miller L, Day J, Blase A, et al. Feasibility and clinical utility of a TMPRSS2:ERG gene fusion urine test [abstract]. Eur Urol Suppl 2009;8:195. [Web of Science] [CrossRef]
  3. Stephan C, Jung K, Semjonow A, Schulze-Forster K, Cammann H, Hu X, et al. Comparative assessment of urinary prostate cancer antigen 3 and TMPRSS2:ERG gene fusion with the serum [-2]prostate-specific antigen-based prostate health index for detection of prostate cancer. Clin Chem 2013;59:280–8. [CrossRef]
  4. Stephan C, Cammann H, Jung K. Re: Scott A. Tomlins, John R. Day, Robert J. Lonigro, et al. Urine TMPRSS2:ERG plus PCA3 for individualized prostate cancer risk assessment. Eur Urol 2015;68:e106–7.[CrossRef]
  5. Tomlins SA, Day JR, Lonigro RJ, Hovelson DH, Siddiqui J, Kunju LP, et al. Urine TMPRSS2:ERG plus PCA3 for individualized prostate cancer risk assessment. Eur Urol 2015;online available, doi:10.1016/j.eururo.2015.04.039.[CrossRef]
  6. Hendriks RJ, Dijkstra S, Jannink SA, Steffens MG, van Oort IM, Mulders PF, et al. Comparative analysis of prostate cancer specific biomarkers PCA3 and ERG in whole urine, urinary sediments and exosomes. Clin Chem Lab Med 2016;54:483–92.
  7. Hessels D, Schalken JA. Urinary biomarkers for prostate cancer: a review. Asian J Androl 2013;15:333–9.[CrossRef] [Web of Science]
  8. Dijkstra S, Birker IL, Smit FP, Leyten GH, de Reijke TM, van Oort IM, et al. Prostate cancer biomarker profiles in urinary sediments and exosomes. J Urol 2014;191:1132–8.
  9. Hanke M, Kausch I, Dahmen G, Jocham D, Warnecke JM. Detailed technical analysis of urine RNA-based tumor diagnostics reveals ETS2/urokinase plasminogen activator to be a novel marker for bladder cancer. Clin Chem 2007;53:2070–7. [CrossRef] [Web of Science]
  10. Filella X, Foj L, Mila M, Auge JM, Molina R, Jimenez W. PCA3 in the detection and management of early prostate cancer. Tumour Biol 2013;34:1337–47. [CrossRef]
  11. Roobol MJ, Schroder FH, van Leenders GL, Hessels D, van den Bergh RC, Wolters T, et al. Performance of prostate cancer antigen 3 (PCA3) and prostate-specific antigen in Prescreened men: reproducibility and detection characteristics for prostate cancer patients with high PCA3 scores (>/= 100). Eur Urol 2010;58:893–9.[CrossRef] [Web of Science
  12. Futterer JJ, Briganti A, De VP, Emberton M, Giannarini G, Kirkham A, et al. Can clinically significant prostate cancer be detected with multiparametric magnetic resonance maging? A systematic review of the literature. Eur Urol 2015;68:1045–53. [CrossRef]
  13. Cash H, Maxeiner A, Stephan C, Fischer T, Durmus T, Holzmann J, et al. The detection of significant prostate cancer is correlated with the Prostate Imaging Reporting and Data System (PI-RADS) in MRI/transrectal ultrasound fusion biopsy. World J Urol 2015;online available, doi:10.1007/s00345-015-1671-8. [CrossRef]
  14. Porpiglia F, Russo F, Manfredi M, Mele F, Fiori C, Bollito E, et al. The roles of multiparametric magnetic resonance imaging, PCA3 and prostate health index-which is the best predictor of prostate cancer after a negative biopsy? J Urol 2014;192:60–6.

Source: De Gruyter

A new issue of CCLM is available online! – March 2016

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CCLM is published on a monthly basis and is the most relevant Journal on Clinical Chemistry in Europe; it is a valuable and updated source of knowledge for the professionals in the field, well recognized all over the world.

Vol 54, Issue 3 -March 2016

Click here to see the future titles of Clin Chem Lab Med

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