HORIBA Medical and Siemens Healthineers have entered into a long-term agreement. The companies will collaborate in bringing new and innovative hematology solutions to the market globally. With HORIBA Medical as the original equipment manufacturer to complement the Siemens Healthineers portfolio, the companies will provide customers with expanded options to fulfill their hematology and multidisciplinary solution needs.
“With our commercial strength and global installed base of customers combined with HORIBA Medical’s innovative technologies, the relationship will expand the hematology solutions available to laboratories for diagnostics testing worldwide,” said Franz Walt, President, Laboratory Diagnostics, Siemens Healthineers.
“Our long-term vision and continuous investments coupled with our outstanding employees have resulted in innovative hematology technology solutions. I am extremely pleased that this long-term vision has resulted in an alliance with Siemens Healthineers” said Mr. Atsushi Horiba, Chairman, President & CEO of HORIBA, Ltd.
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For nearly 20 years, Tatyana Golovkina, PhD, a microbiologist, geneticist and immunologist at the University of Chicago, has been working on a particularly thorny problem: Why are some people and animals able to fend off persistent viral infections while others can’t? Mice from a strain called I/LnJ are especially good at this. They can control infection with retroviruses from very different families by producing specific antibodies that coat viruses and render them innocuous. Golovkina, a Professor of Microbiology, was interested in what makes these mice special, so she began searching for the genes responsible for their remarkable immune response. In a new study she and her colleagues identify this gene. They also began to uncover more clues how it might work to control anti-virus immune responses. Using a process called positional cloning, in which researchers progressively narrow down the location of a gene on the chromosome, they pinpointed it within the major histocompatibility complex (MHC) locus. The MHC locus is a well-known region of the genome involved with the immune system so it makes sense that the gene was located there, but this was a disconcerting discovery. “It was a bummer at first because there are tons of genes within the MHC locus all controlling immune response, not only against viruses, but also many other microbial pathogens and non-microbial disorders,” she said. “Most of the time when people map a gene to the MHC they give up and stop there, with an assumption that the gene encodes for one of the two major MHC molecules, MHC class I or and MHC class II.” But with the help of a biochemist, Lisa Denzin from Rutgers University, and a computational biologist, Aly Khan from the Toyota Technological Institute at Chicago, Golovkina and her team identified a gene called H2-Ob that enables this resistance. Together with another gene called H2-Oa, it makes a molecule called H2-O in mice and HLA-DO in humans. H2-O has been known for years as a negative regulator of the MHC class II immune response, meaning that it shuts down the immune response. Most researchers thought it was there to prevent autoimmune responses, which attack the body’s own tissues. But in this case, none of the I/LnJ mice showed signs of autoimmunity, so H2-O must have another purpose. Golovkina and her team discovered another interesting thing when they crossed I/LnJ mice that were resistant to infections with ones that were more susceptible. The resultant F1 mice were susceptible to infection. This indicated that the I/LnJ H2-Ob gene was recessive; both parents had to have a copy of the mutated gene to pass it on their offspring, and the product of the gene should be a non-functional protein. “That was really surprising,” Golovkina said. “Almost all pathogen-resistant mechanisms discovered so far are dominant, meaning that something needs to be gained to resist.” The immune system response to a virus in susceptible mice lasts three to four weeks, then the H2-O molecule tells it to stop. But the I/LnJ mice, which respond vigorously to infections, have a mutation on H2-Ob that makes it inactive. So, after they launch an immune response, it never shuts off. This keeps persistent retroviruses in check. Golovkina hypothesizes that while letting the immune response keep running may keep chronic infections in check, such as retroviruses or hepatitis B and C, other pathogens like tuberculosis can take advantage of a persistent immune response because they can get access to certain cells when they’re coated with antibodies (and I/LnJ mice happen to be susceptible to TB and produced anti-TB antibodies). At some point during the evolution of these genes, it was more advantageous to be able to switch off the immune response to some infections (such as intracellular bacterial pathogens), but it came at the cost of not being able to fight other long-term infections. Now that her team has identified the gene underlying anti-retrovirus and potentially anti-hepatitis B and C responses, Golovkina says that further research should be done to create genetic therapies to manipulate the function of this gene, or develop molecules that could interfere with the function of H2-O to allow the virus-specific response in chronically infected people.
University of Chicago Medicine sciencelife.uchospitals.edu/2017/08/15/scientists-identify-gene-that-controls-immune-response-to-chronic-viral-infections/
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When performed in tandem, two molecular biology laboratory tests distinguish, with near certainty, pancreatic lesions that mimic early signs of cancer but are completely benign. The lesions almost never progress to cancer, so patients may be spared unnecessary pancreatic cancer screenings or operations. The two-test combination is the only one to date that can accurately and specifically identify these benign pancreatic lesions. Its utility was described in one of the largest studies of patients with this form of pancreatic lesion by researchers from Indiana University, Indianapolis. Between 2 to 3 percent of all patients have some type of pancreatic lesions or cysts revealed on routine abdominal diagnostic radiology scans. Nearly all of these patients will later develop pancreatic cancer. The most common and deadliest form of pancreatic cancer—pancreatic adenocarcinoma—has a five-year survival rate of 12 to 14 percent for early-stage disease and 1 to 3 percent for advanced disease, according to the American Cancer Society. A small percentage of patients have serous cystic neoplasms (SCN) that do not harbour malignant potential or progress to cancer. Nevertheless, these patients undergo imaging or other surveillance every six months to spot changes indicative of cancer, or they undergo an operation to remove part of the gland as a precaution because SCN are difficult to find using standard diagnostic methods. More than 60 percent of SCN are not predicted preoperatively3 and 50 to 70 percent are missed or incorrectly diagnosed on radiology scans.4 However, the researchers determined that two proteins can play a significant role in ruling out pre-cancer and cancer. Vascular endothelial growth factor A (VEGF-A) is a protein associated with promotion of new blood vessel formation. VEGF-A is upregulated in many tumours, and its expression can be correlated with a tumour’s stage. Its utility in the diagnosis of pancreatic cysts was discovered by researchers at Indiana University. Carcinoembryonic antigen (CEA) is a protein associated with cell adhesion. It is present in low levels in healthy individuals, but it is increased with certain types of cancers. Tests for each of these proteins in pancreatic cyst fluid have accurately distinguished SCN from other types of pancreatic lesions. In the present study, VEGF-A, alone, singled out SCN with a sensitivity of 100 percent and specificity of 83.7 percent, and CEA had a 95.5 percent sensitivity and 81.5 percent specificity. Together, however, the tests approached the gold standard of pathologic testing: The combination had a sensitivity of 95.5 percent and specificity of 100 percent for SCN. Authors of the study concluded that results of the VEGF-A/CEA test could have prevented 26 patients from having unnecessary surgery.
American College of Surgeons www.facs.org/media/press-releases/2017/pancreatic062217
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Over the past decade, mutations in more than 60 different genes have been linked with autism spectrum disorder, including de novo mutations, which occur spontaneously and aren’t inherited. But much of autism still remains unexplained. A new study of nearly 6,000 families implicates a hard-to-find category of de novo mutations: those that occur after conception and therefore affect only a subset of cells. De novo mutations can occur in a parent’s sperm or egg. Alternately, they can occur after egg and sperm meet, arising in an embryonic cell. These are known as somatic mutations or post-zygotic mutations (PZMs). If a PZM happens very early, when the embryo has just a handful of cells, the mutation will show up in most of the mature organism’s cells. But the later PZMs occur during embryonic development, the fewer cells will carry them, making them harder to detect. “If the mutation is in a very small fraction of all cells, it will be missed by whole-exome sequencing,” said Elaine Lim, a postdoctoral fellow in the lab of Christopher A. Walsh, the Bullard Professor of Pediatrics and Neurology at Harvard Medical School and Boston Children’s Hospital. Lim is first author of the study; Walsh is the senior investigator. To identify PZMs, Lim, Walsh and colleagues obtained whole-exome sequencing data previously gathered from 5,947 families, usually through blood tests, courtesy of the Simons Foundation Autism Research Initiative Simplex Collection, the Autism Sequencing Consortium and Autism Speaks. They then re-sequenced some of the DNA from these children using three independent sequencing technologies in parallel. Based on their findings, they classified 7.5 percent of autism spectrum disorder subjects’ de novo mutations as PZMs. Of these, 83 percent had not been picked up in the original analysis of their genome sequence. Some PZMs affected genes already known to be linked to autism or other neurodevelopmental disorders (such as SCN2A, HNRNPU and SMARCA4) but sometimes affected these genes in different ways. Many other PZMs occurred in genes known to be active in brain development (such as KLF16 and MSANTD2) but not previously associated with autism spectrum disorder. The connection of these genes to autism may have been missed because the earlier studies focused on mutations that knocked down gene function, the authors said. “Some of the postzygotic mutations we found represented a gain of function, not a loss of function,” said Lim, who is also affiliated with the Wyss Institute for Biologically Inspired Engineering. Lim, Walsh and colleagues then brought in another huge data set: gene expression data from the BrainSpan project. These publicly available data came from autopsies of brain samples from deceased patients of different ages, from prenatal through adult. Comparing these with the genomic sequencing data, based mostly on blood DNA samples, allowed the researchers to estimate the timing of the PZMs and the brain regions they affected. “By overlapping the data, we can start to map where in the brain these genes are expressed and when the mutations occurred during development,” said Lim. These analyses showed that PZMs in the subjects with autism spectrum disorder occur disproportionately in genes expressed in the amygdala. “This was exciting to us, in that the amygdala has been proposed as an important region of the brain in autism,” said Lim. Overall, the work adds to the evidence that complex brain disorders, such as epilepsy, intellectual disability, schizophrenia and brain malformations, can arise from non-inherited mutations that occur at some point during prenatal development.
Harvard Medical Schoolhttp://tinyurl.com/yb2lpxd7
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Houston Methodist cancer researchers are now closer to creating a blood test that can identify breast cancer patients who are at increased risk for developing brain metastasis, and also monitor disease progression and response to therapy in real time. The discovery of identifying a distinct group of cells in the bloodstream of patients who have breast cancer brain metastases could lead to the creation of more sensitive screening tools. A proof-of-concept study led by Dario Marchetti, Ph.D., detected a distinct group of circulating tumour cells (CTCs) associated with brain metastasis. The finding brings cancer researchers closer to understanding how the “seeds” of metastatic disease can thrive in breast cancer patients and cause it to spread to the brain. “Our research confirmed that CTCs in breast cancer brain metastases are distinct from other circulating tumour cells. Moreover, unlocking the mystery of how these seeds of metastatic disease survive and thrive over a period of years, sometimes decades, is an enigma in cancer,” said Marchetti, senior author and director of the Biomarker Research Program at Houston Methodist Research Institute. “Now we can take this information and develop a more sensitive screening tool to detect metastatic cancer in the blood, possibly even before metastasis is radiologically detectable by MRI.” Magnetic resonance imaging is the accepted standard-of-care to diagnose breast cancer brain metastasis (BCBM) in patients. However, in most cases, by the time MRI detects the metastatic mass, the cancer has progressed to a stage where few curative treatment options are available, leading to poor overall survival. According to extensive clinical studies, approximately 20 percent of breast cancer patients will develop brain metastasis over their lifetime, and, in general, metastatic disease to the brain is estimated to become the number one cancer killer within the next decade. “Our lab is the first in this field to perform a comprehensive report of patient-derived circulating tumour cells at the gene expression level, so we now have a clearer picture of the signalling pathways that allows them to establish brain metastases. By comparing the whole genome expression patterns of CTCs isolated from patient blood samples diagnosed with or without BCBM, we uncovered a 126 gene-signature that is specific to these brain metastatic CTCs,” said Debasish Boral, Ph.D., the paper’s first author and a research associate with the Biomarker Research Program at Houston Methodist Research Institute. This research builds on a 2015 research paper where Marchetti’s lab isolated four distinct circulating tumour cell subsets that were implicated in breast cancer cell dormancy. Viable breast cancer cells can remain dormant in the patients’ bone marrow or other organs like the brain, lungs and liver, even decades after a primary tumour is surgically removed. These scattered cells are often undetectable by traditional clinical tools, making it nearly impossible to detect and treat metastatic disease while still amenable to therapy. The Houston Methodist researchers are now focused on broadening the study patient population, with the end goal of transforming this information into the development of two kinds of non-invasive liquid biopsies that could be used by treating physicians: a screening method to predict brain metastasis before the disease is detectable by current diagnostic standards (MRI); and another to monitor treatment efficacy in real-time in those patients diagnosed with brain metastasis.
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Tens of thousands of cancer patients each year may benefit from an immunotherapy regimen called PD-1 blockade, based on results from a new clinical study. The findings establish genetic markers that help physicians identify which patients might respond to the therapy, which had been approved previously for a select few classes of cancer. "What we describe in this paper applies to about 4% of patients with advanced cancer, regardless of the tumour type," said Bert Vogelstein of Johns Hopkins University, a senior author on the paper. In an 86-patient clinical trial encompassing 12 different kinds of cancers, Dung Le and colleagues at Johns Hopkins University demonstrated that the immunotherapy drug pembrolizumab (an anti-PD-1 antibody) was effective against multiple types of tumours. All of the patients had cancers with defects in a genome maintenance pathway called mismatch repair (MMR). "One patient, a young graduate student, was scheduled to go into hospice for terminal care two days prior to receiving the test result that showed he had an MMR-deficient tumour," said Vogelstein. "Shortly after beginning treatment, he went into remission. Since then he’s been able to finish his Ph.D., get married and live a happy and productive life." PD-1 blockade doesn’t directly destroy tumours, but instead aids the immune system in targeting cancer cells — which can suppress the body’s defences in order to thrive. Until recently, PD-1 blockade therapies were approved for only a select few classes of cancers, such as melanoma and lung cancer. Yet in a historic May 2017 decision , the United States Food and Drug Administration ruled that tumour genetics, rather than tissue of origin, could be used as a clinical indicator for pembrolizumab therapy. "This is the first approval for a treatment that is tissue agnostic, which means clinicians can use pembrolizumab for any tumour with mismatch repair deficiency," said Le. As many as 60,000 cancers every year might harbour MMR mutations that would render them susceptible to PD-1 blockade, according to Le and colleagues’ analysis of genome sequencing data from 12,019 cancers representing 32 distinct tumor types. PD-1 blockade takes advantage of the fact that MMR defects make cancer genomes inherently unstable, giving them a potential Achilles’ heel. "Tumours that have more chaotic genomes produce more proteins that are recognized by the immune system," said Geoff Lindeman, a breast cancer researcher at Walter and Eliza Hall Institute of Medical Research, who was not involved in the study. Different types of cancers experience various levels of genomic chaos. Most tumors harbor roughly 50 genetic alterations whereas skin and lung cancers tend to have mutation counts well in the hundreds, arising from exposure to environmental DNA-damaging agents like UV light or cigarette smoke. Problems with MMR can push tumors towards thousands of mutations per cell. Yet even with such high mutational loads, cancer can still escape from the immune system. "Tumors find ways to switch off the immune cells," said Vogelstein. "Checkpoint inhibitors like anti-PD-1 can re-awaken these immune cells for an extra weapon in the ongoing war between cancer and the immune system." Though the trial is still ongoing, 11 patients were able to stop taking the therapy; they have remained disease-free with no evidence of recurrence for an average of 8.3 months.
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New findings from the groundbreaking Trial Assigning Individualized Options for Treatment (Rx), or TAILORx trial, show no benefit from chemotherapy for 70 percent of women with the most common type of breast cancer. The study found that for women with hormone receptor (HR)-positive, HER2-negative, axillary lymph node-negative breast cancer, treatment with chemotherapy and hormone therapy after surgery is not more beneficial than treatment with hormone therapy alone. The new data will help inform treatment decisions for many women with early-stage breast cancer. The trial was supported by the National Cancer Institute (NCI), part of the National Institutes of Health, and designed and led by the ECOG-ACRIN Cancer Research Group. “The new results from TAILORx give clinicians high-quality data to inform personalized treatment recommendations for women,” said lead author Joseph A. Sparano, M.D., associate director for clinical research at the Albert Einstein Cancer Center and Montefiore Health System in New York City and vice chair of the ECOG-ACRIN Cancer Research Group. “These data confirm that using a 21-gene expression test to assess the risk of cancer recurrence can spare women unnecessary treatment if the test indicates that chemotherapy is not likely to provide benefit.” TAILORx, a phase 3 clinical trial, opened in 2006 and was designed to provide an evidence-based answer to the question of whether hormone therapy alone is not inferior to hormone therapy plus chemotherapy. The trial used a molecular test (Oncotype DX Breast Recurrence Score) that assesses the expression of 21 genes associated with breast cancer recurrence to assign women with early-stage, HR- positive, HER2-negative, axillary lymph node–negative breast cancer to the most appropriate and effective post-operative treatment. The trial enrolled 10,273 women with this type of breast cancer at 1,182 sites in the United States, Australia, Canada, Ireland, New Zealand, and Peru. When patients enrolled in the trial, their tumours were analysed using the 21-gene expression test and assigned a risk score (on a scale of 0–100) for cancer recurrence. Based on evidence from earlier trials, women in the trial who had a score in the low-risk range (0–10) received hormone therapy only, and those who had a score in the high-risk range (26 and above) were treated with hormone therapy and chemotherapy. Women in the trial who had a score in the intermediate range (11–25) were randomly assigned to receive hormone therapy alone or hormone therapy with adjuvant chemotherapy. The goal was to assess whether women who received hormone therapy alone had outcomes that were as good as those among women who received chemotherapy in addition to hormone therapy. “Until now, we’ve been able to recommend treatment for women with these cancers at high and low risk of recurrence, but women at intermediate risk have been uncertain about the appropriate strategy to take,” said Jeffrey Abrams, M.D., associate director of NCI’s Cancer Therapy Evaluation Program. “These findings, showing no benefit from receiving chemotherapy plus hormone therapy for most patients in this intermediate-risk group, will go a long way to support oncologists and patients in decisions about the best course of treatment.” The researchers found that the primary endpoint of the trial, invasive disease-free survival—the proportion of women who had not died or developed a recurrence or a second primary cancer—was very similar in both groups. Five years after treatment, the rate of invasive disease-free survival was 92.8 percent for those who had hormone therapy alone and 93.1 percent for those who also had chemotherapy. At nine years, the rate was 83.3 percent for those with hormone therapy alone and 84.3 percent for the group that had both therapies. None of these differences were considered statistically significant. The rates of overall survival were also very similar in the two groups. At five years, the overall survival rate was 98.0 percent for those who received hormone therapy alone and 98.1 percent for those who received both therapies, and at nine years the respective overall survival rates were 93.9 percent and 93.8 percent. The researchers also found that women with a score of 0–10 had very low recurrence rates with hormone therapy alone at nine years (3 percent). This confirms similar findings from earlier studies. In addition, they found that women with a score of 26–100 had a distant recurrence rate of 13 percent despite receiving both chemotherapy and hormone therapy. This finding indicates the need to develop more effective therapies for women at high risk of recurrence.
ECOG-ACRIN Cancer Research Group ecog-acrin.org/news-and-info/press-releases/tailorx-trial-finds-most-women-with-early-breast-cancer-do-not-benefit-from-chemotherapy
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Until very recently, Parkinson’s had been thought a disease that starts in the brain, destroying motion centres and resulting in the tremors and loss of movement. New research shows the most common Parkinson’s gene mutation may change how immune cells react to generic infections like colds, which in turn trigger the inflammatory reaction in the brain that causes Parkinson’s. The research offers a new understanding of Parkinson’s disease. “We know that brain cells called microglia cause the inflammation that ultimately destroys the area of the brain responsible for movement in Parkinson’s,” said Richard Smeyne, PhD, Director of the Jefferson Comprehensive Parkinson’s Disease and Movement Disorder Center at the Vickie and Jack Farber Institute for Neuroscience. “But it wasn’t clear how a common inherited mutation was involved in that process, and whether the mutation altered microglia.” Together with Dr. Smeyne, first author Elena Kozina, PhD, looked at the mutant version of the LRRK2 gene (pronounced ‘lark’). Mutations in the LRRK2 gene are the most common cause of inherited Parkinson’s disease and are found in 40 percent of people of North African Arab descent and 18 percent of people of Ashkenazi Jewish descent with Parkinson’s. However there’s been controversy around the exact function of the LRRK2 gene in the brain. “We know that gene mutation is not enough to cause the disease,” said Dr. Kozina, Post-Doctoral student at Jefferson.“We know that twins who both carry the mutation, won’t both necessarily develop Parkinson’s. A second ‘hit’ or initiating event is needed.” Based on his earlier work showing that the flu might increase risk of Parkinson’s disease, Dr. Smeyne decided to investigate whether that second hit came from an infection. Suspecting that the LRRK2 mutations might be acting outside of the brain, the researchers used an agent — the outer shell of bacteria, called lippopolysaccharide (LPS) – that causes an immune reaction. LPS itself does not pass into the brain, nor do the immune cells it activates, which made it ideal for testing whether this second hit was acting directly in the brain. When the researchers gave the bacterial fragments to the mice carrying the two most common LRRK2 gene mutations, the immune reaction became a “cytokine storm,” with inflammatory mediators rising to levels that 3-5 times higher than a normal reaction to LPS. These inflammatory mediators were produced by T and B immune cells expressing the LRRK2 mutation. Despite the fact that LPS did not cross the blood-brain barrier, the researchers showed that the elevated cytokines were able to enter the brain, creating an environment that caused the microglia to activate pathologically and destroy the brain region involved in movement. “Although more tests are needed to prove the link, as well as testing whether the same is true in humans, these findings give us a new way to think about how these mutations could cause Parkinson’s,” said Dr. Smeyne. “Although we can’t treat people with immunosuppressants their whole lives to prevent the disease, if this mechanism is confirmed, it’s possible that other interventions could be effective at reducing the chance of developing the disease.” Thomas Jefferson Universitywww.jefferson.edu/university/news/2018/03/21/Parkinsons_gene_triggers_the_disease_from_outside_brain.html
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A research team led by National University Health System (NUHS) and Duke-NUS Medical School has used genomic technologies to better understand intestinal metaplasia (IM), a known risk factor for gastric (stomach) cancer. Patients with IM are six times more likely to develop stomach cancer than those without. This study is an important part of an ambitious investigation to understand why some people develop stomach cancer, while others do not. The research could also help detect patients who are infected with the Helicobacter pylori bacteria, which is also linked to the disease. Stomach cancer is the third deadliest cancer in the world according to World Health Organization (WHO) statistics, and claims more than 300 lives yearly in Singapore. The disease is believed to be caused by infection with Helicobacter pylori but is potentially treatable if detected early. Unfortunately, more than two-thirds of stomach cancer patients are only diagnosed at an advanced stage. "Previous genetic studies on IM have mainly focused on patients who were already diagnosed with stomach cancer but these are limited in their ability to predict who are likely to develop the disease and how the disease will progress," said Professor Patrick Tan, co-lead investigator and Professor, Duke-NUS Medical School. Professor Tan is also Deputy Executive Director, Biomedical Research Council, Agency for Science, Technology, and Research, and a Senior Principal Investigator at the Cancer Science Institute of Singapore. "This new study is the first to comprehensively map out the genetic changes in IM in a cohort of stomach cancer-free subjects, which helps us better predict the possible occurrence and progression of the disease." Dr Yeoh Khay Guan, co-lead investigator and Deputy Chief Executive, NUHS as well as Dean, NUS Yong Loo Lin School of Medicine added, "Our study is the largest series of IM to be studied in detail by genetic analysis. These new findings help us understand why some people have a higher risk of progression to stomach cancer, and identify those who may benefit from closer follow-up to prevent cancer or to detect it early so that it can be cured." The researchers leveraged the near 3,000 participants-strong Gastric Cancer Epidemiology Programme (GCEP) cohort, recruited with the support of patients and doctors from four local public hospitals (National University Hospital, Tan Tock Seng Hospital, Singapore General Hospital, Changi General Hospital), to show that a comprehensive analysis of the genetic patterns of IM can predict its subsequent progression towards stomach cancer. The genetic analysis of IM helps to identify those with a higher risk of progression to stomach cancer, adding further information to what is available by microscopic examination alone. The research team is using this new information to identify biomarkers that can be applied in future in the clinic to identify people who have a high risk of progression to stomach cancer. EurekAlertwww.eurekalert.org/pub_releases/2018-01/nuos-lgs010518.php
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Genome-wide association studies (GWAS) have identified more than 150 genetic variations associated with increased risk for breast cancer. Most of these variants are not located in protein-coding gene regions but are assumed to regulate the expression of certain genes. One way to figure out what these variants are doing is to conduct a cis-eQTL analysis. That’s a way of detecting changes in the expression of genes presumably regulated by a nearby variant. Using four large-scale data sets from normal and cancerous breast tissue samples, Xingyi Guo, PhD, and colleagues identified 101 candidate breast cancer susceptibility genes with variant-associated gene expression changes. In breast cancer cells grown in culture, the researchers also demonstrated how three genes promoted tumour growth by disrupting normal cell behaviour. Their findings reveal potential target genes associated with an increased risk of breast cancer and provide additional insights into the underlying genetic and biological mechanisms that drive this common cancer.
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