Atlas Genetics raises £16.9m for market entry of Chlamydia-diagnostics
Bristol – Atlas Genetics has raised £16.9m from a syndicate of new and existing investors led by Novartis Venture Funds, and Consort Medical plc. The series B round will be drawn down over three years to help to commercialize infectious disease tests, especially the global launch of the Velox diagnostic-kit for Chlamydia and gonorrhea. Commercial launch of the system is planned for 2012. The money will also be used for the development of other infectious disease tests and to expand the immunoassay capability of the Velox system. Velox is a point of care-diagnostic system for a broad range of infectious diseases using either nucleic acid or immuno-assays. Atals’s CEO John Clarkson commented: “We are delighted to welcome the new investors at this time when the company’s first productn is being transferred to manufacture and the core capabilities of the sensor chemistry are being expanded.“ The new investors in this series B financing are Novartis Venture Funds, LSP (Life Sciences Partners), BB Biotech Ventures and Johnson & Johnson Development Corporation. The newly announced financing follows a £1.5 million round in February 2011 supported by Consort Medical plc and other investors. The Company has been funded previously, and continues to be supported, by YFM Equity Partners, Braveheart Investment Group, Wyvern Asset Management, the Crescent Seedcorn Fund and private investors.
Cambridge – Restoring absent p53 to lung tumour cells in mice can induce mregression in aggressive tumours, but does not have the same effect on early-stage tumours or less malignant cells residing in more advanced tumours. The...
Cambridge – Restoring absent p53 to lung tumour cells in mice can induce mregression in aggressive tumours, but does not have the same effect on early-stage tumours or less malignant cells residing in more advanced tumours. The finding, reported by researchers from the UK and the US in Nature, highlights a practical limitation of p53-directed cancer therapeutics. Mutations in the p53 tumour suppressor pathway are very common in human cancers and many drug development efforts to target this pathway are in progress. Tyler Jacks and colleagues from Massachusetts Institute of Technology (Cambridge, US) show that reactivating absent p53 only leads to regression in malignant adenocarcinomas and not in low-grade adenomas, in a lung cancer mouse model. They suggest that p53's tumour destroying effect is only induced when increased signalling of MAP kinase (a driver of malignant tumour progression) activates the ARF tumour suppressor pathway. Additional Evidence is being reported from Gerard Evan (University of Cambridge, UK). According to results from his group, only the most aggressive cells within each tumour respond to the restoration of p53. It is only late in tumour progression when the oncogenic signal reaches a threshold sufficient to activate the ARF pathway, they suggest. Early stage mtumours, meanwhile, might not alert the body's tumour surveillance mmechanisms. As established tumours typically contain sections at all stages of oncogenic evolution, p53 restoration might, at best, help to contain the tumour's growth rather than eradicating it completely.
Bristol – British biochemists have unravelled why metastatic prostate cancer cells do not stop migration on contact with non-cancer cells (Nature Cell Biol, DOI: 10.1038/ncb2122). Their findings may lay the foundations for...
Bristol – British biochemists have unravelled why metastatic prostate cancer cells do not stop migration on contact with non-cancer cells (Nature Cell Biol, DOI: 10.1038/ncb2122). Their findings may lay the foundations for finding inhibitors of that particular dysregulation. According to the team headed by Catherine Nobes from Bristol University, the binding of so-called Eph receptors by Ephrin ligands expressed by neighbouring cells determines whether cell migration will be contact-inhibited or not. When they blocked expression of the receptors EphB3 and EphB4, which are normally overexpressed on the surface of prostate cancer cells by their ligand ephrin‑B2, the cancer cells were unable to migrate into a layer of fibroblasts that they had co-cultivated with PC-3 cancer cells. This restoration of contact inhibition was dependent on inactivation of Cdc42. Conversely, collisions between two cancer cells resulted in contact inhibition of locomotion, mediated by EphA-Rho-Rho kinase signalling. The researchers conclude that migration of cancer cells can switch from restrained to invasive, depending on the Eph-receptor profile of the cancer cell and the ephrin ligands expressed by neighbouring cells.
Swansea – Probiotic bacteria can reduce the length of diarrhoea and significantly cut the risk of episodes lasting for more than four days. These are the findings of a new systematic review of data from 63 trials involving 8,014...
Swansea – Probiotic bacteria can reduce the length of diarrhoea and significantly cut the risk of episodes lasting for more than four days. These are the findings of a new systematic review of data from 63 trials involving 8,014 patients by Welsh Cochrane researchers. Giving probiotics in conjunction with rehydration fluids reduced the duration of diarrhoea by around a day and reduced the risk of diarrhoea lasting four or more days by 59%, reported the team headed by Stephen Allen from Swansea School of Medicine. No serious adverse effects were reported in the trials and although vomiting was quite common, it also occurred with placebos. "The beneficial effect was consistent and significant across many different types of trials," said Allen. "However, more research needs to be carried out on the specific strains of bacteria that are effective in treating diarrhoea and on preventing the progression from short-term to persistent diarrhoea." Currently, diarrheal diseases kill nearly 2 million people in developing countries annually, mostly children. Therapies such as rehydration fluids do not reduce the length of illness.
London – Broker and middle-market investment bank Piper Jaffray has announced it will stop selling securities for European issuers, which means biotech companies will have less access to full-service banks that offer a range of...
London – Broker and middle-market investment bank Piper Jaffray has announced it will stop selling securities for European issuers, which means biotech companies will have less access to full-service banks that offer a range of capabilities across capital markets, M&A and research. The bank said its European business is unprofitable. With the decision to exit Europe, the region’s lead biotech underwriter is leaving the stage. Since 2008, Piper has served as an underwriter for at least eight offerings for European biotech companies, including Movetis N.V., and most recently French firm Stentys S.A. It remains unclear how the exit will influence the fundraising environment for European biotechs, but analysts presume the consequences of Piper’s European withdrawal are likely to be felt in the UK. The brokerage also announced it will significantly cut the headcount at its London office.
British drug delivery company Hospira (Leamington) has named Svend Andersen a Corporate VP and President for Europe, the Middle East and Africa. Under Andersen’s leadership, Hospira is aiming to increase its current market share...
British drug delivery company Hospira (Leamington) has named Svend Andersen a Corporate VP and President for Europe, the Middle East and Africa. Under Andersen’s leadership, Hospira is aiming to increase its current market share in biosimilar and generic injectable drugs as well as in infusion devices and consumables. Andersen served at Actavis as the company’s Executive Vice President (Western Europe). He was also a vice president and general manager at Alpharma, and was the VP for Commercial Operations at Ferrosan.
London – In its spending review, the British government has said it will maintain its science research budget in cash terms over the next four years, with resource spending of £ 4.6bn (EUR5.2bn) per year. The Department of...
London – In its spending review, the British government has said it will maintain its science research budget in cash terms over the next four years, with resource spending of £ 4.6bn (EUR5.2bn) per year. The Department of Business, which oversees science spending in Britain, said it is protecting the science budget to “ensure continuity of investment in science and research.” Other government departments saw spending drop by a whopping 19 % on average.
Novel tech transfer centres
Hard on the heels of that good news for the country’s life sciences sector came even more: the UK Technology Strategy Board has set up a £ 50m (EUR 57.1m) programme in personalised medicine. The Stratified Medicines Innovation platform will be aimed at catalysing the development of new diagnostics and medicines targeted at smaller subgroups of patients. British Prime Minister David Cameron also gave the go-ahead for a £ 200m (EUR 228.4m) programme to develop technology innovation centres modelled on Germany’s Fraunhofer Institutes to help business and academia work closely on translating research into products and services. The new PM also pledged that more of the government’s procurement budget would be spent with small and medium size enterprises to help them “bridge the gap between innovation and commercial success.” Moreover, the government announced another effort – the Therapeutic Capability Clusters programme – to boost collaboration between academics, clinicians and the life sciences industry in drug development. Inflammatory diseases are among the first issues to be addressed in specific therapy area clusters.
London-based drug developer PepTcell Ltd. (London) has appointed Manfred Scheske as its CEO of Consumer Health. Scheske joins the firm from GlaxoSmithKline, where he worked for 25 years, most recently as President of Consumer...
London-based drug developer PepTcell Ltd. (London) has appointed Manfred Scheske as its CEO of Consumer Health. Scheske joins the firm from GlaxoSmithKline, where he worked for 25 years, most recently as President of Consumer Healthcare Europe.
London - The UK's Technology Strategy Board launched the Stratified Medicines Innovation Platform to provide over L50 million for personalized medicines research over the next five years. The platform will bring together...
London - The UK's Technology Strategy Board launched the Stratified Medicines Innovation Platform to provide over L50 million for personalized medicines research over the next five years. The platform will bring together researchers, policymakers and the private sector in an initiative for research and development in areas such as tumour profiling to improve cancer care and biomarker development to enhance drug effectiveness. The first three funding competitions will provide up to L5.6 million ($8.9 million) for tumor profiling and for IT to collect and store tumor data; up to L4 million ($6.4 million) for identifying inflammation biomarkers; and up to L1.5 ($2.4) million for business models to enable drug and diagnostics companies to work together to develop drugs and companion diagnostics. Applications open in January 2011. The Platform is a five-year partnership programme that will develop a series of activities at national level to address the challenges of stratification for the benefit of business, healthcare providers and the wider economy. The BioIndustry Association also welcomed the initiative, pointing out that establishing a stratified disease strategy was one of the recommendations in the Review and Refresh of Bioscience 2015, an independent report published in January 2009 by the Bioscience Innovation and Growth Team.
Atlanta - The world's first clinical trial of a therapy derived from human embryonic stem cells has started, US-researchers announced on October 11th. A first patient with spinal cord injury was treated at Shepherd Center, a...
Atlanta - The world's first clinical trial of a therapy derived from human embryonic stem cells has started, US-researchers announced on October 11th. A first patient with spinal cord injury was treated at Shepherd Center, a spinal cord and brain injury center in Atlanta. The study, run by Geron Corp. of Menlo Park, California, will enrol up to 10 patients who have suffered spinal cord injuries between the third and 10th thoracic vertebrae, injecting the cells within 14 days of the injury. If the treatment is shown to be safe and well tolerated, researchers will move on to test its effectiveness. Geron is licensing a method invented by Hans Keirstead, a neurobiologist at the Reeve-Irvine Research Center at UC Irvine. Keirstead's team managed first to turn human embryonic stem cells into oligodendrocytes, the cells that insulate nerve fibers with coatings of fatty myelin. Growing the "tubing" that protects nerve cells could in many cases be enough to allow signals to travel up and down the spine again, the researchers hope. In the animal trials, rats with spinal cord damage which had lost control of their hind limbs regained at least a partial ability to walk and run after treatments with the stem cells. Geron's European competitors are cautious. Great Britain could see the start of a clinical trial with embryonic stem-cells derived retinal pigmented epithelium for patients with wet age-related macular degeneration. Pfizer's UK-based regenerative medicine unit hopes to start clinical trials in 2012. ReNeuron of Guildford in Surrey is another UK-based entity which develops stem cell therapies. Patient recruitment for a ground-breaking, first-in-man clinical trial has recently commenced in the UK. The lead programme ReN001 is targeting patients who have been left disabled by an ischaemic stroke. ReN001 is based around a neural stem cell line, originally extracted from the brain tissue of an aborted fetus. Patient recruitment for the trial recently commenced in the UK.
At the 10-year anniversary of the Human Genome Project, we stand poised to sequence entire cancer genomes from large numbers of clinical samples and gain an unprecedented insight into the genomic landscape of a wide range of...
Our success in translating these catalogues of somatic mutations into clinically relevant therapeutic targets will depend on our ability to use reliable preclinical models to assess the therapeutic efficacy of candidate agents, and to match the right drug with the right genetic context. Such a model should be capable of screening the large number of targeted therapeutic agents currently available against a wide range of genetic backgrounds, and to identify statistically significant correlations between a specific genetic event and sensitivity to a given drug. Targeted molecular therapies that disrupt specific intracellular signaling pathways are increasingly used for the treatment of cancer
Towards a registry of cancer drug sensitivity
Established human cancer cell lines have been used for many years as in vitro models of how cancer cells will behave when exposed to drugs. The earliest screen of this type involved 60 cancer cell lines encompassing a range of tissue types (the NCI-60 cell line panel) which were screened against thousands of compounds. The limitations of using only 60 cell lines have become increasingly apparent in recent years as evidence has accumulated that there is enormous genetic heterogeneity within cancers arising from the same tissue type. For example, in non-small cell lung cancer, only 10% of tumours harbor a mutation in the gene EGFR that makes them sensitive to an EGFR kinase inhibitor. Therefore any screen of cancer cell lines should include sufficient numbers to capture these genetic subsets of cell lines that may show dramatic sensitivity to specific drugs. Towards this aim, we have begun to screen a range of anticancer therapeutics against a large number (>1,000) of genetically characterised human cancer cell lines, and to correlate drug sensitivity with existing genomic data in order to identify biomarkers of sensitivity. To our knowledge, this is the largest collection of cell lines worldwide to be screened against cancer drugs. This information can be used to inform physicians about the optimal clinical application of cancer drugs, as well as for the design of clinical trials of investigational compounds being developed for the clinic. Furthermore, all data generated will be released at three-month intervals, and can be accessed through one of the resource links at the Cancer Genome Project (www.sanger.ac.uk/genetics/CGP/translation).
Linking cell genomics to
drug sensitivity testing
The Genomics of Drug Sensitivity in Cancer Project is part of a five-year collaboration between The Cancer Genome Project at the Wellcome Trust Sanger Institute (UK) and the Center for Molecular Therapeutics at Massachusetts General Hospital Cancer Center (US). The Center for Molecular Therapeutics has pioneered the use of high-throughput platforms for examining the relationship between tumour cell genomics and sensitivity to anti-cancer agents. The Cancer Genome Project has led the way in the systematic analysis of cancer genomes to identify genes critical in the development of human cancers. This collaboration will develop and integrate the expertise at both sites toward the goal of identifying cancer biomarkers that can be used to identify genetically defined subsets of patients most likely to respond to targeted therapies. As part of this collaboration, we plan to screen more than 1,000 genetically characterised human cancer cell lines with approximately 400 anti-cancer therapeutics. This large collection of cell lines enables us to capture much of the genomic heterogeneity that underlies human cancer, and which appears to play a critical role in determining the variable response of patients to treatment with specific agents. These compounds include classical chemotherapeutics as well as targeted therapeutics from commercial sources, academic collaborators, and from the biotech and pharmaceutical industries. The sensitivity patterns of the cell lines will be correlated with extensive genomic data to identify genetic features that are predictive of sensitivity. The correlations between mutations and drug sensitivity are graphically represented as plots that encapsulate the statistical significance of the interaction, the number of cell lines involved and the magnitude of the effect of that gene on either sensitivity or resistance to that drug (Fig. 2).
Expanding the database
At present we’re correlating drug response with mutation data or copy number data for 51 known cancer genes, but we plan to incorporate gene expression data into these analyses in the future. In addition, over the next five years we plan to carry out exome sequencing on the entire cell line collection to provide sequence data on 22,000 genes, as well as RNA-sequencing and gene fusion screens in specific groups of cell lines. This data will also be used to correlate with drug sensitivity, and will be available through the project’s website. In summary, advances in sequencing technology coupled with the ability to screen large numbers of cancer cell lines in a high-throughput manner should enable us not only to generate lists of somatic mutations in clinical samples from cancer patients, but also to attach a biological function to these mutations and thereby identify those that are therapeutic targets. This is a step closer to the goal of ‘personalised cancer medicine’, and that maximises the likelihood of obtaining a response to treatment in cancer patients.D
7th Berlin Conference on IP in Life Sciences: Big Data, Big Drugs
The health care industry faces significant transformation, driven by a boom in knowledge within biomedical sciences and breakthrough technologies such as gene sequencing. The management of "big data“ will change the understanding of diseases, development of drugs and treatment of patients. more