News Article | December 9, 2016
An international team of researchers involving the University of Adelaide is tackling the controversy over what some scientists consider to be a "harmful" hormone, arguing that it could be a game changer in the fight against recurring breast cancers that are resistant to standard treatments. The controversy centers on the different effects in women of the naturally occurring sex steroid hormone progesterone compared with synthetic forms (i.e. progestins) designed to mimic its actions. Some, but not all, progestins have been linked with increased breast cancer risk when used in menopausal hormone therapy, leading to concerns in the scientific community about the use of these drugs. However, in a paper now published online ahead of print in the prestigious journal Nature Reviews Cancer, an international team - involving the University of Adelaide's Dame Roma Mitchell Cancer Research Laboratories (DRMCRL) and the Cancer Research UK (CRUK) Cambridge Institute - highlights that progesterone when used in menopausal hormone therapy does not increase breast cancer risk . Indeed, progesterone may have an important role to play in the safe and effective management of recurring breast cancer. "Breast cancer arises because of abnormal hormone activity, with about 75% of these cancers being driven by the estrogen receptor. Unfortunately, despite good initial responses in many women, drug resistance is common, usually leading to a recurrence and lethal spread of the disease," says Professor Wayne Tilley, Director of the Dame Roma Mitchell Cancer Research Laboratories at the University of Adelaide, and a lead author of the paper. "Moreover, current hormonal treatments that target the estrogen receptor in breast cancer, especially specific inhibitors that block estrogen production, can markedly impact quality of life, often leading women to stop taking the drugs or change their treatment." Professor Tilley says the team's recent studies, including landmark research already published in Nature, suggest that a safe way of improving treatment - without having a deleterious effect on quality of life - does exist, through the use of natural progesterone and certain other progestins. "There is a natural 'crosstalk' between estrogen and progesterone receptors that we strongly believe can be exploited," he says. "In particular, progesterone can reprogram estrogen action in the breast in a way that results in estrogen receptor action improving breast cancer outcomes. Because of this unique interaction of the two natural female sex hormones in the breast, we see great potential benefits in adding progesterone to existing drugs that target the estrogen receptor, thereby helping to switch off the growth of cancer cells. "This gives us a unique opportunity to develop a new hormonal treatment which, when used in conjunction with the current standard of care, would enhance and improve outcomes for many breast cancer patients. "Unfortunately, there are some serious misconceptions about the role of progesterone in cancer biology that have so far prevented it from being widely used in the management of breast cancer. We hope to change that thinking," Professor Tilley says. The team, which is highly regarded for its research into both breast and prostate cancer, believes this new paper will have a global impact on clinical, scientific and public opinion on the relative risks and benefits of using progesterone and certain progestins to treat women with breast cancer. "Ultimately, we hope this work will eventually result in saving women's lives," Professor Tilley says. The real proof will come from two new clinical trials being conducted by the international team, with patients being recruited for the studies in the UK early next year. One trial in collaboration with a UK group at the University of Liverpool will test the potential benefit of combining progesterone treatment with the breast cancer drug Tamoxifen in premenopausal women with breast cancer. A second trial involving postmenopausal women with breast cancer has been initiated by collaborators at the CRUK Cambridge Institute and will evaluate whether a particular progestin, Megace, provides added therapeutic benefit when combined with a current estrogen receptor target treatment, compared to the target treatment alone. Professor Tilley says the team's research has recently resulted in several substantial new sources of funding for Adelaide's Dame Roma Mitchell Cancer Research Laboratories to continue their ground-breaking research in breast cancer. These include: Professor Tilley was also awarded another NHMRC Project Grant of more than $946,000 to develop new and smarter therapies to inhibit the androgen receptor, which is the key driver of prostate cancer growth. "Resistance to current therapies that target the androgen receptor is the main cause of lethal prostate cancer. Researchers in the Dame Roma Mitchell Cancer Research Laboratories are developing and testing a new drug that is effective against the androgen receptor in preclinical models of treatment resistant prostate cancer. It is hoped that this new drug will inhibit the growth of tumors that currently kill approximately 3,300 men in Australia each year," he says. "Our recent funding success will ensure that South Australian research into breast and prostate cancer remains at the forefront of improving the health and quality of life for women and men afflicted by these diseases. "More importantly, this funding will make significant inroads into improving survival rates for patients who develop resistance to current hormonal treatments for these cancer types, which are major killers of Australian women and men," Professor Tilley says.
News Article | December 8, 2016
Research Triangle Park, NC and Cambridge, UK, Dec. 08, 2016 (GLOBE NEWSWIRE) -- Inivata, a global clinical cancer genomics company employing a revolutionary approach to circulating tumor DNA (ctDNA) analysis to improve personalized healthcare in oncology, presented data with collaborators from Gustave Roussy at the 17th World Conference on Lung Cancer in Vienna. The data generated in the joint project explores the clinical benefit for non-small cell lung cancer (NSCLC) patients treated with osimertinib who were EGFR T790M-positive based on a novel, blood-based liquid biopsy test, InVision(TM). The researchers looked at response rates specifically in advanced patients with resistance to at least one prior EGFR targeted therapy who were not able to have a tissue biopsy. They found that of the 48 patients tested, 24 patients (50%) were EGFR T790M-positive. Of the 24 positive patients, 9 patients had an allele fraction lower than 0.5%, at frequencies that may be missed using less sensitive assays. For the patients who were treated with osimertinib and evaluable for treatment response, the objective response rate was 62.5% with the remaining patients having stable disease as their best overall response. The study supports the use of liquid biopsies as a surrogate marker for T790M in tumor tissue, avoiding the need for invasive tumor biopsies for personalizing treatment in lung cancer patients. On December 7, Inivata presented analytical performance data for InVision comparing results from both their Cambridge, UK laboratory as well as their U.S. CLIA certified laboratory. The data showed high concordance across both laboratories including strong correlation of InVision ctDNA results compared to a digital PCR-based approach. "We are impressed with the performance of our InVision platform across a variety of clinical scenarios in terms of robustness, reproducibility, and actionability. The results are encouraging as we continue to generate further data to support clinical use of our InVision platform," said Clive Morris, Chief Medical Officer of Inivata. Details of the posters presented are provided below: Abstract ID: #6389 Title: Validation and Performance of a Standardized ctDNA NGS Assay across Two Laboratories, Abstract ID: #5472 Title: Osimertinib Benefit in ctDNA T790M Positive, EGFR-Mutant NSCLC Patients About Inivata Inivata, a clinical cancer genomics company, is employing the precision of ctDNA analysis to improve personalized healthcare in oncology. Using a simple blood test, ctDNA analysis is a new tool for oncologists to detect cancer, stratify patients, and assess individual response to treatment. Inivata's proprietary technology is based on pioneering research from the Rosenfeld Lab at the Cancer Research UK Cambridge Institute (CRUK-CI), University of Cambridge. Inivata's Invision ctDNA assay provides a highly sensitive analysis of a highly-select gene panel to identify actionable mutations for oncologists to treat their patients optimally. In 2016, Inivata opened a CLIA lab in Research Triangle Park, NC and launched a large-scale, prospective clinical validation study of the Company's ctDNA analysis in lung cancer. For more information and a full listing of investors, please go to www.inivata.com. Follow us on Twitter @Inivata.
News Article | December 20, 2016
Levels of circulating tumor DNA (ctDNA) detected in a blood test are correlated with the size of ovarian cancers and can predict a patient's response to treatment or time to disease progression, according to a retrospective study of cancer patients' blood samples published in PLOS Medicine by Nitzan Rosenfeld and James Brenton of Cancer Research UK Cambridge Institute and colleagues. Blood levels of a protein called CA-125 are currently used to gauge treatment response in women receiving chemotherapy for high grade serous ovarian cancer (HGSOC). However, CA-125 levels don't change rapidly enough to guide treatment changes after one or two cycles of chemotherapy. In the new study, researchers measured levels of ctDNA carrying mutations in the gene TP53, which are detected in 99% of patients with HGSOC. 318 blood samples from 40 HGSOC patients, taken before, during, and after standard-of-care treatment were analyzed. CT images of the patients' tumors were collected, as well as data on the progression of their cancers. The fraction of mutated TP53 in ctDNA (TP53MAF) was correlated with volume of disease as measured by CT scan (Pearson r=0.59, p "These findings have strong potential for clinical utility owing to the ease of assaying DNA in plasma and the low cost and speed of ctDNA testing," the authors say. "Having very early information on response would empower patients and physicians to test alternative treatment options and have high utility in trials that link biomarkers to targeted therapy." Funding: This work was supported by Cancer Research UK (http://www. ) Grant numbers: A15601-JDB; A11906-NR; A20240-NR; A18072-JDB. JDB was supported by the National Institute for Health Research Cambridge Biomedical Research Centre. CAP was supported in part by the Academy of Medical Sciences, the Wellcome Trust, British Heart Foundation and Arthritis Research UK. CAP, DG, AMP, HB, CH, HA, SF, PM, KH, IG, MJL, HME, WQ, NR and JDB are affiliated with Cancer Research UK but the funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing Interests: We have read the journal's policy and the authors of this manuscript have the following competing interests: DG, NR and JDB are co-founders, shareholders and officers/consultants of Inivata Ltd, a cancer genomics company that commercialises ctDNA analysis. Citation: Parkinson CA, Gale D, Piskorz AM, Biggs H, Hodgkin C, Addley H, et al. (2016) Exploratory Analysis of TP53 Mutations in Circulating Tumour DNA as Biomarkers of Treatment Response for Patients with Relapsed High-Grade Serous Ovarian Carcinoma: A Retrospective Study. PLoS Med 13(12): e1002198. doi:10.1371/journal.pmed.1002198 Author Affiliations: Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, United Kingdom Department of Oncology, Hutchison/MRC Research Centre, University of Cambridge, Cambridge, United Kingdom NIHR Cambridge Biomedical Research Centre, Cambridge, United Kingdom Cambridge University Hospitals NHS Foundation Trust, Cambridge, United Kingdom Cancer Research UK Major Centre--Cambridge, Cancer Research UK Cambridge Institute, Cambridge, United Kingdom IN YOUR COVERAGE PLEASE USE THIS URL TO PROVIDE ACCESS TO THE FREELY AVAILABLE PAPER: http://journals.
News Article | November 3, 2016
RESEARCH TRIANGLE PARK, N.C., CAMBRIDGE, England, and CONCORD, Mass., Nov. 03, 2016 (GLOBE NEWSWIRE) -- Inivata, a global clinical cancer genomics company employing a revolutionary approach to circulating tumor DNA (ctDNA) analysis to improve personalized healthcare in oncology, and N-of-One, Inc., a precision medicine oncology decision support company, are pleased to announce a new partnership to support analysis of patient cases for Inivata's InVision® liquid biopsy product line. This partnership will enable the delivery of clear, easy to interpret patient reports, providing physicians with a wealth of genomic information at their fingertips. Inivata's revolutionary approach to ctDNA analysis delivers industry leading sensitivity across a broad panel of clinically relevant genomic alterations. The Next-Generation Sequencing-based method utilizes eTAm-Seq(TM), a proprietary amplification process, prior to sequencing and advanced analytical methods that enables the separation of true cancer mutations from background noise. The collaboration with N-of-One will provide each physician with an individualized liquid biopsy report based on their cancer patient's unique genomic signature. N-of-One's oncologists and Ph.D. scientists will also provide the analysis needed to assess current treatments, analyze potential novel mutations and allow the oncologists to make more informed decisions for treatment strategies. Inivata has also recently announced the launch of a large-scale, prospective clinical validation study in non-small cell lung cancer and additional studies are currently underway. "N-of-One's experience in curating complex genomic information and translating this data into clinically relevant results on tens of thousands of patients has enabled them to develop a market-leading database and unparalleled expertise. We are excited to access their capabilities to ensure we provide physicians with the most actionable information in our easy to interpret report," said Michael Stocum, CEO of Inivata. N-of-One will support Inivata's liquid biopsy assay by providing oncologists and pathologists with the most relevant oncology treatment options through the analysis of each patient's unique molecular profile. The N-of-One solution will integrate the interpretation of multiple molecular tests on a patient to provide a comprehensive view of the cancer and, leveraging N-of-One's proprietary database, will identify individualized treatment options, including clinical trials for consideration by the oncologist. N-of-One's experience in oncology, and specifically liquid biopsies, makes them uniquely capable of interpreting the Inivata liquid biopsy test. "We are pleased to partner with Inivata in support of the launch of their revolutionary ctDNA platform capabilities," said Chris Cournoyer, CEO of N-of-One. "Pairing Inivata's highly sensitive analysis of actionable mutations with N-of-One's ability to analyze the data of novel mutations has the potential to help guide more personalized treatment decisions for patients prior to and throughout the cancer care continuum. About Inivata Inivata, a clinical cancer genomics company, is employing the precision of ctDNA analysis to improve personalized healthcare in oncology. Using a simple blood test, ctDNA analysis is a new tool for oncologists to detect cancer, stratify patients, and assess individual response to treatment. Inivata's proprietary technology is based on pioneering research from the Rosenfeld Lab at the Cancer Research UK Cambridge Institute (CRUK-CI), University of Cambridge. Inivata's Invision® ctDNA assay provides a highly sensitive analysis of a highly-select gene panel to identify actionable mutations for oncologists to treat their patients optimally. In 2016, Inivata opened a CLIA lab in Research Triangle Park, NC and launched a large-scale, prospective clinical validation study of the Company's ctDNA analysis in lung cancer. For more information and a full listing of investors, please go to www.inivata.com. Follow us on Twitter @Inivata. About N-of-One N-of-One is a leader in identifying patient-specific treatment options for precision medicine in oncology by leveraging its proprietary knowledgebase and its team of oncologists and Ph.D. scientists to integrate genomic data from multiple tests. Using N-of-One solutions can standardize and accelerate genomic clinical interpretation and molecular decision support while saving time and money. N-of-One's actionable solutions have provided treatment options, including clinical trials, to clinicians for tens of thousands of patient cases across hundreds of cancer types. N-of-One partners with leading hospital systems, cancer centers, and commercial labs around the world. For more information, please visit www.n-of-one.com or call 617-202-9808.
News Article | November 8, 2016
A weight loss condition that affects patients with cancer has provided clues as to why cancer immunotherapy - a new approach to treating cancer by boosting a patient's immune system -- may fail in a substantial number of patients. Cancer immunotherapies involve activating a patient's immune cells to recognise and destroy cancer cells. They have shown great promise in some cancers, but so far have only been effective in a minority of patients with cancer. The reasons behind these limitations are not clear. Now, researchers at the Cancer Research UK Cambridge Institute at the University of Cambridge have found evidence that the mechanism behind a weight loss condition that affects patients with cancer could also be making immunotherapies ineffective. The condition, known as cancer cachexia, causes loss of appetite, weight loss and wasting in most patients with cancer towards the end of their lives. However, cachexia often starts to affect patients with certain cancers, such as pancreatic cancer, much earlier in the course of their disease. In research published today in the journal Cell Metabolism, the scientists have shown in mice that even at the early stages of cancer development, before cachexia is apparent, a protein released by the cancer changes the way the body, in particular the liver, processes its own nutrient stores. "The consequences of this alteration are revealed at times of reduced food intake, where this messaging protein renders the liver incapable of generating sources of energy that the rest of the body can use," explains Thomas Flint, an MB/PhD student from the University of Cambridge School of Clinical Medicine and co-first author of the study. "This inability to generate energy sources triggers a second messaging process in the body - a hormonal response -- that suppresses the immune cell reaction to cancers, and causes failure of anti-cancer immunotherapies." "Cancer immunotherapy might completely transform how we treat cancer in the future -- if we can make it work for more patients," says Dr Tobias Janowitz, Medical Oncologist and Academic Lecturer at the Department of Oncology at the University of Cambridge and co-first author. "Our work suggests that a combination therapy that either involves correction of the metabolic abnormalities, or that targets the resulting hormonal response, may protect the patient's immune system and help make effective immunotherapy a reality for more patients." The next step for the team is to see how this discovery might be translated for the benefit of patients with cancer. "If the phenomenon that we've described helps us to divide patients into likely responders and non-responders to immunotherapy, then we can use those findings in early stage clinical trials to get better information on the use of new immunotherapies," says Professor Duncan Jodrell, director of the Early Phase Trials Team at the Cambridge Cancer Centre and co-author of the study. "We need to do much more work in order to transform these results into safe, effective therapies for patients, however," adds Professor Douglas Fearon, Emeritus Sheila Joan Smith Professor of Immunology at the University of Cambridge and the senior author, who is now also working at Cold Spring Harbor Laboratory and Weill Cornell Medical College. "Even so, the results raise the distinct possibility of future cancer therapies that are designed to target how the patient's own body responds to cancer, with simultaneous benefit for reducing weight loss and boosting immunotherapy." The research was largely funded by Cancer Research UK, the Lustgarten Foundation, the Wellcome Trust and the Rosetrees Trust.
News Article | March 24, 2016
Genetic 'signatures' of early-stage embryos confirm that our development begins to take shape as early as the second day after conception, when we are a mere four cells in size, according to new research led by the University of Cambridge and EMBL-EBI. Although they seem to be identical, the cells of the two day-old embryo are already beginning to display subtle differences. Once an egg has been fertilised by a sperm, it divides several times, becoming a large free-floating ball of stem cells. At first, these stem cells are 'totipotent', the state at which a stem cell can divide and grow and produce everything—every single cell of the whole body and the placenta, to attach the embryo to the mother's womb. The stem cells then change to a 'pluripotent' state, in which their development is restricted to generating the cells of the whole body, but not the placenta. However, the point during development at which cells begin to show a preference for becoming a specific cell type is unclear. Now, in a study published in the journal Cell, scientists at the University of Cambridge and the European Bioinformatics Institute (EMBL-EBI) suggests that as early as the four-cell embryo stage, the cells are indeed different. The researchers used the latest sequencing technologies to model embryo development in mice, looking at the activity of individual genes at a single cell level. They showed that some genes in each of the four cells behaved differently. The activity of one gene in particular, Sox21, differed the most between cells; this gene forms part of the 'pluripotency network'. The team found when this gene's activity was reduced, the activity of a master regulator that directs cells to develop into the placenta increased. "We know that life starts when a sperm fertilises an egg, but we're interested in when the important decisions that determine our future development occur," says Professor Magdalena Zernicka-Goetz from the Department of Physiology, Development and Neuroscience at the University of Cambridge. "We now know that even as early as the four-stage embryo - just two days after fertilisation - the embryo is being guided in a particular direction and its cells are no longer identical." Dr John Marioni of EMBL-EBI, the Wellcome Trust Sanger Institute and the Cancer Research UK Cambridge Institute, adds: "We can make use of powerful sequencing tools to deepen our understanding of the molecular mechanisms that drive development in individual cells. Because of these high-resolution techniques, we are now able to see the genetic and epigenetic signatures that indicate the direction in which early embryonic cells will tend to travel." More information: Heterogeneity in Oct4 and Sox2 Targets Biases Cell Fate in Four-Cell Mouse Embryos. Cell; 24 March 2016. DOI: 10.1016/j.cell.2016.01.047
News Article | December 7, 2016
Experts have warned of a $100bn (£79bn) "protection gap" in the global insurance sector as a result of the rising impact of climate risks. ClimateWise, based at the University of Cambridge, warned that the gap of uninsured or under-insured assets had quadrupled over the past three decades. The insurance sector's role as society's risk manager was under threat, warned one senior figure. The network outlined its findings in two reports published on Wednesday. "What we have seen is that over the past 30 years, as societal exposure to climate change has increased, is that the traditional response of insurance - which is to reassess, re-underwrite, and reprice - is almost becoming the sector's Achilles heel if you like because it is repricing itself out of risk but it is not addressing the root cause of the problem, which is that society is increasingly vulnerable to climate risks and it is in need of enhancing its resilience," explained ClimateWIse programme manager Tom Herbstein. He said the protection gap was the difference between total economic loss and the value of assets that were covered by insurance policies. "We have seen this gap open up from about US $23bn about 30 years ago to over US $100bn today," Dr Herbstein told BBC News. He said that the burden of covering the cost of the protection gap fell on other parts of society, such as governments and asset owners. "In some cases, no-one covers it at all," he added. The details of the widening protection gap in the global insurance market was published in ClimateWise's annual review of its 29 members' activities. ClimateWise, a network of leading insurance companies, was established in 2008 by the Cambridge Institute for Sustainability. The network's chairman, Maurice Tulloch, who is also chairman of global general insurance at Aviva, warned: "The insurance industry's role as society's risk manager is under threat. "Our sector will struggle to reduce this protection gap is our response is limited to avoiding, rather than managing, society's exposure to climate risk." In another ClimateWise report, Investing in Resilience, the network highlighted ways that the industry could help support its clients to build a more robust infrastructure. Dr Herbstein said the report published by ClimateWise's Societal Resilience Programme, identified a number of approaches that would allow the global insurance industry to use its expertise and data in risk management to support its clients and the wider financial world to deliver climate resilience. "One is how insurers can start to invest in resilience internally, within its existing investment portfolio - such as increased investment in green bonds," he said. "Interestingly, it also looks at what insurance can do, given all of its data and expertise, to help the wider financial system to better understand its risk exposure. "There potential for the insurance industry to support banks to better understand the risk exposure that their mortgage portfolio is facing from climate change, on the basis that if banks are more aware of the risks the properties they are lending to might face, such as the knock-on effect of a loss in property values. "Insurance companies have a vested interest in banks making a more strategic decisions because that would have a knock-on impact on the decisions that developers, local governments and property owner will make in terms of where they plan to locate new properties or protect existing ones." "Our argument is that the really powerful role the insurance sector can play is to support external stakeholders to start investing in climate resilience. "If the industry can start working outide its traditional risk-carrying role, it is going to have huge knock-on benefits. There is a real case for change," Dr Herbstein observed.
News Article | November 8, 2016
Cold Spring Harbor, NY - One of the worst cruelties of lethal cancer is the phenomenon called wasting, or in medical terms, cachexia (pronounced ka-CHEX-ia), in which a patient seems literally to diminish in bodily terms as the cancer ravages one or more internal organs. Today, a team at Cancer Research UK Cambridge Institute, led by Professor Douglas Fearon, M.D., of Cold Spring Harbor Laboratory in New York and a Distinguished Scholar of the Lustgarten Foundation, publishes in Cell Metabolism results of experiments showing that tumors interfere with the patient's ability to cope with wasting and may even impair their ability to respond to immunotherapy. In mouse models of human pancreatic and colon cancer, the team traces cachexia to a molecular reprogramming of the liver induced by the tumor, the effect of which is to alter the liver's normal response to caloric deficiency. As the caloric deficiency worsens and weight continues to decline, the body responds by releasing stress hormones. The team found that these hormones, in turn, prevent the immune system from responding to the tumor. Thus the new research helps explain two ways in which pancreatic and colon tumors have long vexed doctors attempting to treat them: these tumors themselves set in motion the process that results in wasting; and wasting, in turn, accounts for why immune therapy for such cancers has typically failed. Providing massive caloric supplementation - what doctors call hyperalimentation - does not vanquish wasting; and immune therapy does not impair the tumor's ability to thrive. The researchers in Cambridge, led by M.D.-Ph.D. student Thomas R. Flint and oncologist Tobias Janowitz, M.D., Ph.D., performed experiments demonstrating that in mouse models of pancreas and colon cancer, liver reprogramming begins during pre-cachexia, when wasting has just begun but is not yet manifest. Signals broadcast by tumor cells induce the release of interleukin 6 (IL-6), a molecular beacon of the immune system called a cytokine, that normally helps induce an immune response. IL-6, in turn, impairs the capacity of the liver to respond to caloric deprivation, which is already under way in pre-cachectic mice. The team proposes this liver reprogramming is the result of IL-6 suppressing a gene-regulating protein, or transcription factor, called PPAR-alpha, which in turn suppresses a vital process in the liver called ketogenesis. "Translated into human terms, this means that when a cancer patient loses his or her appetite and decides not to eat, the liver is not going to generate sufficient energy to compensate for the caloric loss," explains Dr. Fearon. Often, cancer patients don't eat, Dr. Fearon clarifies, not because they are nauseous due to chemotherapy; rather, they feel full and simply lose their appetite. Importantly, he adds, his team's discovery that the tumor is programming the liver not to make calories, which are essential for continued brain function, assures two things. One is that wasting will continue; the other is that the body, massively releasing glucocorticoids, or stress hormones, will thereby short-circuit the immune system's ability to respond to the tumor. It's a vicious circle that sadly ends in death. The team's discovery not only sheds light on why conventional caloric supplementation fails to curtail cachexia in cancer patients. It also helps to account for the failure of T-cell checkpoint targeted immunotherapies in pancreatic and colon cancers. The tumor, in effect, is fooling the immune system into thinking the tumor is not a threat but rather just normal regenerating tissue. The team tested several ways of addressing liver reprogramming in pre-cachectic mice. Using a mouse model that recapitulates human pancreatic cancer, they administered an antibody that targets and inactivates IL-6; the same mice received massive caloric supplements via infusion. According to Dr. Flint, "Our data suggest that successful reversal of cachexia in people may well depend on co-administration of anti-IL-6 with nutritional support." The team also noted that their findings may have relevance in a wide range of IL-6-associated illnesses in which weight loss in observed. These include sepsis, HIV, tuberculosis, chronic obstructive pulmonary disease, cardiac failure and rheumatoid arthritis. The research described here was supported by: The Lustgarten Foundation for Pancreatic Cancer Research; Cancer Research UK; The Ludwig Institute for Cancer Research; the NIHR Biomedical Research Centre and the Cambridge ECMC. "Tumor-induced IL-6 reprograms host metabolism to suppress anti-tumor immunity" appears November 8, 2016 in Cell Metabolism. The authors are: Thomas R. Flint, Tobias Janowitz, Claire M. Connell, Edward W. Roberts, Alice E. Denton, Anthony P. Coll, Duncan I. Jodrell and Douglas T. Fearon. The paper can be viewed at: http://www. Founded in 1890, Cold Spring Harbor Laboratory has shaped contemporary biomedical research and education with programs in cancer, neuroscience, plant biology and quantitative biology. Home to eight Nobel Prize winners, the private, not-for-profit Laboratory employs 1,100 people including 600 scientists, students and technicians. The Meetings & Courses Program hosts more than 12,000 scientists from around the world each year on its campuses in Long Island and in Suzhou, China. The Laboratory's education arm also includes an academic publishing house, a graduate school and programs for middle and high school students and teachers. For more information, visit http://www. The Lustgarten Foundation is the largest private foundation dedicated to funding pancreatic cancer research. The Foundation supports research to find a cure for pancreatic cancer, facilitates dialogue within the medical and scientific community, and educates the public about the disease through awareness campaigns and fundraising events. Since its inception, the Foundation has directed more than $125 million to research and assembled the best scientific minds with the hope that one day, a cure can be found. Thanks to private funding, 100 percent of every dollar donated to the Foundation goes directly to pancreatic cancer research. For additional information, please visit http://www. .
News Article | November 14, 2016
A NEW personalised breast cancer programme which will map patients' DNA and RNA to tailor treatment for individuals launches at the Cancer Research UK Cambridge Institute. The project, which was launched with £1.1 million funding from Addenbrooke's Charitable Trust (ACT), will analyse the genome and all expressed genes of tumour cells from 250 breast cancer patients to improve diagnosis and tailor treatment. Finding out what genes have become faulty in breast cancer cells will help researchers understand more about how cancer develops and spreads. It will also help doctors choose the best treatment for their patient. Breast cancer patients are treated based on the broad types of cancer, for example, those that are likely to respond to hormone therapies, but it can be difficult to predict how individual patients will respond to treatment. The researchers hope to find out how this personalised diagnosis and treatment programme could be implemented in the National Health Service's (NHS) breast cancer unit in Cambridge and hope that one day this will extend around the UK. Professor Richard Gilbertson, director of the CRUK Major Cancer Centre at Cambridge University, said: "The Personalised Breast Cancer Project is truly ground-breaking. By sequencing the entire tumour genome of women with breast cancer in our clinic and integrating this extensive data with other biological and clinical observations, we will assign patients to optimal therapy, changing the way we treat breast cancer forever." Professor Carlos Caldas, project lead at the Cancer Research UK Cambridge Institute, said: "We already know that there are around 10 different types of breast cancer, as we reported in 2012, and these respond differently to the available treatments. We're looking at ways to predict this response ensuring individual patients get the best treatment for them. We hope that this project will accelerate progress in developing personalised treatment for breast cancer patients." Dr Jenny Longmore, Director of Research at Addenbrooke's Charitable Trust (ACT), said: "ACT is pleased to have been able to support the initiation of this clinical research project with more than £1.1 million of funding from many generous supporters. The project will involve patients from the Cambridge Breast Unit at Addenbrooke's Hospital, and we expect that the outcomes of the research will be valuable to patients both nationally and internationally in years to come." Sir Harpal Kumar, Cancer Research UK's chief executive officer, said: "Today eight in 10 women with breast cancer survive their disease for at least 10 years. The ability to tailor treatment to individual patients will help ensure this number continues to rise and should help reduce side effects. This project will bring us closer to making personalised medicine a reality in the NHS and beyond."
News Article | February 24, 2017
New Review of ctDNA Liquid Biopsies in Nature Reviews Cancer Co-Authored by Inivata CSO Nitzan Rosenfeld Research Triangle Park, NC and Cambridge, UK 24 February 2017 -- Inivata, a global clinical cancer genomics company employing a revolutionary approach to circulating tumor DNA (ctDNA) analysis to improve personalized healthcare in oncology, today announces the publication of a new review of the use of ctDNA as a liquid biopsy for cancer treatment in the journal Nature Reviews Cancer co-authored by Inivata's Chief Scientific Officer and Founder Nitzan Rosenfeld and Co-Founder and Clinical Advisor James Brenton. In "Liquid biopsies come of age: towards the implementation of circulating tumour DNA" (available online at www.nature.com/nrc/journal/vaop/ncurrent/full/nrc.2017.7.html) the authors* review the potential of ctDNA in cancer diagnosis, treatment selection and monitoring disease burden. They also highlight the importance of assay sensitivity, as sampling often yields low concentrations of ctDNA, and review currently available approaches for sensitive detection. The authors conclude that liquid biopsies have demonstrated broad potential clinical utility across a range of applications and they are beginning to be used for patient benefit. 1Cancer Research UK Cambridge Institute, 2Cancer Research UK Cambridge Centre, 3Clinical Trials Unit, Clinic Institute of Haematalogical and Oncological Diseases, Hospital Clinic de Barcelona, 4Department of Oncology, University of Cambridge Hutchison-MRC Research Centre. About Nitzan Rosenfeld Nitzan Rosenfeld is a senior group leader at the Cancer Research UK Cambridge Institute, University of Cambridge, and Inivata's co-founder and CSO. Nitzan trained in Physics, and specialized in quantitative molecular biology, obtaining a Ph.D. in the field of Systems Biology from the Weizmann Institute of Science. In 2005 he joined Rosetta Genomics Ltd, where he was head of Computational Biology and led development of molecular diagnostic tests. In 2009 Nitzan joined Cancer Research UK's Cambridge Institute. His research group combines molecular technologies with genomic approaches to develop new diagnostic strategies. The focus of current research, the application of circulating tumour DNA for personalised cancer diagnostics, formed the basis of Inivata. In 2013 Nitzan was awarded the CRUK Future Leaders in Cancer Research prize, the British Association for Cancer Research Translational Research Award, and a prestigious ERC Starting Grant. At the end of 2015, Nitzan received the Foulkes Medal which is awarded biennially to an outstanding bioscience researcher within ten years of completing their PhD. About Inivata Inivata, a clinical cancer genomics company, is employing the precision of ctDNA analysis to improve personalized healthcare in oncology. Using a simple blood test, ctDNA analysis is a new tool for oncologists to detect cancer, stratify patients, and assess individual response to treatment. Inivata's proprietary technology is based on pioneering research from the Rosenfeld Lab at the Cancer Research UK Cambridge Institute (CRUK-CI), University of Cambridge. Inivata's Invision ctDNA assay provides a highly sensitive analysis of a highly-select gene panel to identify actionable mutations for oncologists to treat their patients optimally. In 2016, Inivata opened a CLIA lab in Research Triangle Park, NC and launched a large-scale, prospective clinical validation study of the Company's ctDNA analysis in lung cancer. For more information and a full listing of investors, please go to www.inivata.com. Follow us on Twitter @Inivata.