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GENTAUR Europe

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    Thursday, 14 February 2013 10:22

    JX-594 Anti-Cancer Virus Found in Canada

    antibodies-jx-594 cancer-cellsRecent news suggests that Canadian Cancer Specialists have found what researchers have labelled a medical first, in that an engineered virus which is injected into the cancer patients blood stream targets cancer cells throughout the body killing them, or at least not letting them get any bigger. Out of 23 patients, who have highly metabolized cancer, which means that the cancer has spread throughout their body and doesn’t show signs of being decreased, have been injected with a cancer fighting virus which hopes to kill the cancer cells. This is not the first time that a cancer virus has been suggested to the public. However, normally with cancer viruses, the virus itself had to be administered and injected directly into the tumor. This is extremely difficult as, tumors are not always stationary within the human body. The anti-cancer virus JX-594 was injected into the blood of 23 patients. 8 out of the 23 patients had the JX-594 replicating itself inside the cancer tumors, and not spreading into other healthy non-cancer cells.

    "We are very excited because this is the first time in medical history that a viral therapy has been shown to consistently and selectively replicate in cancer tissue after intravenous infusion in humans.” Said, Professor John Bell, who is the lead research from the University of Ottawa. Professor Nick Lemoine, director of Barts Cancer Institute said, “Viruses that multiply in just tumor cells - avoiding healthy cells - are showing real promise as a new biological approach to target hard-to-treat cancers. This new study is important because it shows that a virus previously used safely to vaccinate against smallpox in millions of people can now be modified to reach cancers through the bloodstream - even after cancer has spread widely through the patient's body. "It is particularly encouraging that responses were seen even in tumors like mesothelioma, a cancer which can be particularly hard to treat."

    What happened to the other 15 patients who did not show sign of progress? Well...it’s not said. However, 6 of the patients did have infection which prevented the growth of any tumor progress. JX-594 was only given to the 23 patients at a small does, and only one does, because it is so early in the stages.
     

    Dose-Finding Results

    Oncolytic immunotherapies are designed to selectively replicate within cancer cells and, subsequently, to lyse them, Dr. Reid and colleagues explain. JX-594 is designed to induce virus-replication-dependent oncolysis and tumor-specific immunity, and to disrupt the "viral thymidine kinase gene for cancer selectivity and insertion of human granulocyte-macrophage colony-stimulating factor (hGM-CSF) and beta-galactosidase transgenes for immune stimulation and replication assessment, respectively," they note.

    The complete response of bulky tumors and systemic efficacy was seen in phase 1 trials of JX-594.

    In this phase 2 trial, 30 patients with advanced HCC received 1 of 2 injections into liver tumors on days 1, 15, and 29: low-dose JX-594 (108 pfu) or high-dose JX-594 (109 pfu).

    Kaplan–Meier survival estimates were significantly longer in the high-dose group than in the low-dose group at 1 year (66% vs 23%) and at 18 months (35% vs 11%). Survival did not correlate with the origin of the tumor.

    In the 19 patients with multiple tumors at baseline (10 in the high-dose group and 9 in the low-dose group), median overall survival was longer in the high-dose group (13.6 vs 4.3 months; HR, 0.19; P = .018).

    Median survival in patients with multiple tumors was half that of patients with single tumors (8.8 vs 16.6 months). The authors note that there was no correlation between survival duration and the presence of detectable neutralizing antibodies to the vaccinia virus at baseline, compared with the absence of such antibodies (HR, 0.68)

    Both doses of JX-594 were generally well tolerated, Dr. Reid and colleagues report, and there were no treatment-related deaths. One patient in the high-dose group experienced a treatment-related serious adverse event (nausea and vomiting requiring prolonged hospitalization), and 8 patients (4 in each group) experienced nontreatment-related serious adverse events.

    Antiangiogenesis Results

    In the phase 2 antiangiogenesis trial, Dr. Breitbach and colleagues tested the hypothesis that a vaccinia virus engineered to target cells that activate the ras/MAPK signaling pathway would specifically infect and express transgenes (hGM-CSF, beta-galactosidase) in tumor-associated vascular endothelial cells in humans.

    Preclinical research in mice demonstrated that an intravenous infusion of JX-594 resulted in virus replication in tumor-associated endothelial cells, disruption of tumor blood flow, and hypoxia within 48 hours, and massive tumor necrosis within 5 days. In a phase 1 clinical trial, an intravenous infusion of JX-594 showed dose-dependent endothelial cell infection in tumors.

     

    Dr. Breitbach and colleagues found that JX-594 disrupted perfusion to the tumor as soon as 5 days after treatment in both VEGF-receptor inhibitor-naïve and -refractory patients with advanced HCC.

    This "technology opens up the possibility of multifunctional engineered vaccinia products that selectively target and infect tumor-associated endothelial cells, as well as cancer cells, resulting in transgene expression, vasculature disruption, and tumor destruction in humans systemically," they note.

    Funding for the dose-finding study was provided by Jennerex, Transgene SA, and the Green Cross Corporation. Several coauthors report receiving individual grants, as detailed in the paper.

    Published in News
    Sunday, 10 February 2013 17:44

    Two Antibodies Are Better Than One

    A new approach mimicking the body’s natural defenses could help treat a therapy-resistant breast cancer

    Cancer drugs of the new, molecular generation destroy malignant breast tumors in a targeted manner:  They block characteristic molecules on tumor cells – receptors for the hormones estrogen or progesterone, or a co-receptor, called HER2, that binds to many growth factors. But about one in every six breast tumors has none of these receptors. Such cancers, called triple-negative, are particularly aggressive and notoriously difficult to treat.

    Some of these therapy-resistant cancers have a potential molecular target for cancer drugs, a growth-factor receptor called EGFR, but an EGFR-blocking drug has proved ineffective in treating them. In a study published recently in the Proceedings of the National Academy of Sciences, Weizmann Institute researchers propose a potential solution: to simultaneously treat triple-negative breast cancer with two EGFR-blocking antibodies instead of one. In a study in mice, the scientists showed that a certain combination of two antibodies indeed prevented the growth and spread of triple-negative tumors. The research team, led by Prof. Yosef Yarden of the Biological Regulation Department and Prof. Michael Sela of the Immunology Department, included Drs. Daniela Ferraro, Nadège Gaborit, Ruth Maron,  Hadas Cohen-Dvashi,  Ziv Porat and Fresia Pareja, and Sara Lavi, Dr. Moshit Lindzen and Nir Ben-Chetrit.

    Of the different combinations they tried, the scientists found that the approach worked when the two antibodies bound to different parts of the EGFR molecule. The combined action of the antibodies was stronger than would have been expected by simply adding up the separate effects of each.  Apparently, the use of the two antibodies created an entirely new anti-cancer mechanism: In addition to blocking the EGFR and recruiting the help of immune cells, the antibodies probably overwhelmed the EGFR by their sheer weight, causing it to collapse inward from the membrane into the tumor cell.
     
    Deprived of EGFR on its surface, the cells were no longer receiving the growth signals, preventing the growth of the tumor. This approach resembles the natural functioning of the immune system, which tends to block essential antigens at several sites by targeting them with multiple antibodies.

    If supported by further studies, the two-antibody approach, in combination with chemotherapy, might in the future be developed into an effective treatment for triple-negative breast cancer.
    Prof. Michael Sela is the incumbent of the W. Garfield Weston Professorial Chair of Immunology.
    Prof. Yosef Yarden’s research is supported by the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation; the M.D. Moross Institute for Cancer Research; the Steven and Beverly Rubenstein Charitable Foundation , Inc.; Julie Charbonneau, Canada; the European Research Council; and the Marvin Tanner Laboratory for Research on Cancer. Prof. Yarden is the incumbent of the Harold and Zelda Goldenberg Professorial Chair in Molecular Cell Biology.
     
     
    Published in News
    Friday, 08 February 2013 12:32

    Kronos Dio

    A luminometer for real-time reporter assay with 8 dish incubator and multicolor measurement system

    Kronos dio AB-2550-kronosDioA luminescence monitoring tool to observe gene expressions with bioluminescent markers under long-term culture. Can be used in studies of internal biological clock, circadian rhythms in organisms, gene silencing, drug stimulation, etc. Kronos Dio is equiped with cell culture system within its housing to provide real-time periodical luminescence measurement with multi-color luciferase assay, enabling users to analyse the effects of complex factors influencing gene expression in the cell or the tissue. Internal temperature control (range: 20 to 45 °C) and carbon dioxide circulation allows for convenient cell culture over a long period of time.

     

    Price: 29 500 Euro / 36 000 USD / 27 600 GBP

     

    kronos-dio-gentaur-colours 

    Installation and training

    For the price GENTAUR provides notebook, installation and training (demonstration of basic software and hardware functionality). 6 hours of installation and training is inclusive in the price at no extra cost for USA and Europe. The necessary materials and tools for connecting the device to the Carbone dioxide source at the expense of the customer.

    20141105 033403

    kronos dio installation

    kronos dio installationkronos dio installation kronos dio installation

     

     

     

     

    Download Catalogue

     

    See also: Cellgraph AB-3000B

    Literature

    Customer references:

    Aaron Rowland, Ph.D.
    Assistant Professor of Toxicology
    Department of Chemistry & Biochemistry
    New Mexico State University
    1175 North Horseshoe Drive
    P.O. Box 30001
    Las Cruces, NM 88003-8001


    We are wanting to explore the ability of human breast cell lines to exhibit circadian rhythm.  We are also interested in influence of environmental toxicants on circadian rhythm as well as general gene regulation.  I felt that the Kronos dio would be the proper equipment to perform this task as it has a CO2 hook up and can monitor 3 colors at once.  Therefore, I could transfect the BASIC luciferase construct using one color and the gene of interest using a different luciferase and monitor reporter activity in real time.  
    Observation that Irritant of Environmental toxin on Human’s breast cell lines reaction and changes.

     

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    Published in Promos

    The quest for longer and healthier life, if not immortality, has been part of the human experience since we evolved the ability to recognize the total annihilation of individual death. Our understanding of the biology of aging at the molecular level is advancing so rapidly that it appears inevitable that another decade or two of life will be enabled before long. A new step in what may be the right direction has just been published by researchers at the University of California, Berkeley.

    The ravages of aging appear to be related to oxidative stress combined with telomere exhaustion, along with many other known and unknown factors. The subject of the new Berkeley study is a class of proteins called sirtuins that are known to play a central role in regulating aging and longevity in many non-human models (such as mice).

    There is good evidence that these proteins also play a similar role in humans. For example, research has shown that, of two variants of the SIRT3 sirtuin protein (known to have strong anti-oxidant properties), humans who live past 90 years of age only have one of the variants in their bodies, the variant that enhances production of SIRT3. The difference between the two variants results from a change of one gene by one mutation, and appears to be sufficient to significantly affect an organism's longevity. This suggests a strong link between SIRT3 and longevity.

    The genetics of longevity are quite interesting, but still more interesting would be finding an approach to offset the hand you were dealt at birth, or better yet, to stack the deck. The authors of the Berkeley study decided to see if SIRT3 could rejuvenate blood stem cells extracted from old mice.

    Their first step was to see what happened as mice, which did not possess the SIRT3 gene, aged. When young, these "knockout" mice followed the same course of aging as did a set of normal control mice. However, when the mice were two years old (about an average lifespan for a lab mouse), the knockout mice had far fewer blood stem cells than did the control group.

    What causes the difference in the course of aging? Young cells have low levels of oxidative stress (the generation of reactive oxygen species during metabolism), low enough that the body's normal anti-oxidants can keep up with the resulting damage. When they get older, they can't keep up, and need a boost of SIRT3 to help them. When there is no SIRT3, the progress of old age occurs sooner and more rapidly.

    “When we get older, our system doesn’t work as well, and we either generate more oxidative stress or we can’t remove it as well, so levels build up,” said Chen. “Under this condition, our normal anti-oxidative system can’t take care of us, so that’s when we need SIRT3 to kick in to boost the anti-oxidant system. However, SIRT3 levels also drop with age, so over time, the system is overwhelmed.”

    So it appears that age-related degeneration speeds up in the absence of SIRT3 in the system – at least among mice. The Berkeley team decided to see if increasing SIRT3 levels could rehabilitate the blood stem cells. This was done by infusing the blood stem cells with the SIRT3 protein, following which their ability to make new blood cells did indeed return.

    Further studies will address if SIRT3-induced rejuvenation will apply to whole organisms, so that they might live longer when so treated, even after experiencing normal aging events.

    Published in News

    Researchers from the Institute of Bioengineering and Nanotechnology (IBN) and IBM Research today unveiled the first-ever antimicrobial hydrogel that can break apart biofilms and destroy multidrug-resistant superbugs upon contact. Tests have demonstrated the effectiveness of this novel synthetic material in eliminating various types of bacteria and fungi that are leading causes of microbial infections, and preventing them from developing antibiotic resistance. This discovery may be used in wound healing, medical device and contact lens coating, skin infection treatment and dental fillings.

    IBN Executive Director Professor Jackie Y. Ying said, “As a multidisciplinary research institute, IBN believes that effective solutions for complex healthcare problems can only emerge when different fields of expertise come together. Our longstanding partnership with IBM reflects the collaborative creativity across multiple platforms that we aim to foster with leading institutions and organizations. By combining IBN's biomaterials expertise and IBM’s experience in polymer chemistry, we were able to pioneer the development of a new nanomaterial that can improve medical treatment and help to save lives.”

    Dr Yi-Yan Yang, Group Leader at IBN said, “The mutations of bacteria and fungi, and misuse of antibiotics have complicated the treatment of microbial infections in recent years. Our lab is focused on developing effective antimicrobial therapy using inexpensive, biodegradable and biocompatible polymer material. With this new advance, we are able to target the most common and challenging bacterial and fungal diseases, and adapt our polymers for a broad range of applications to combat microbial infections.”

    More than 80% of all human microbial infections are related to biofilm. This is particularly challenging for infections associated with the use of medical equipment and devices. Biofilms are microbial cells that can easily colonize on almost any tissue or surface. They contribute significantly to hospital-acquired infections, which are among the top five leading causes of death in the United States and account for US$11 billion in healthcare spending each year.

    Published in News
    Friday, 01 February 2013 16:15

    Rapid Canine Brucella Ab Test Kit

    Canine Brucella Ab rapid test

    Catalog number : RB21-03
    Quantity: 1T x 10/Kit
    Availability: Yes
    Details: Rapid Canine Brucella Ab Test Kit is a solid phase chromatographic immunoassay for the qualitative detection of Brucella canins antibody in canine blood.

    Special features

    - Earlier detection of C. Brucella Ab than blood culture and 2-ME RSAT
    - World's first & sole C.brucella Ab Rapid Test Kit
    - One step testing procedure: Easy to use, Saving time and labor
    - No additional equipment is required

    Specifications
    - Principle: lmmunochromatographic assay
    - (LPS capture)-(blood)-(Monoclonal anti-canine lgG detector) = LPS (Lipopolysaccharide) antigen originated from Brucella canis
    - Purpose: Detection of Brucella canins antibody
    - Specimen: Canine whole blood, plasma, or serum.
    - Reading time: 20 minutes
    - Sensitivity: 93% vs. blood culture
    - Specificity: 100% vs. blood culture
    - Shelf life: 24 months
    - Storage temperature: 2-30ºC

    Price: 96 EUR

    PDF-IconDownload datasheet

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    Published in Top Products

    Bullous pemphigoid is a subepidermal blistering disorder associated with tissue-bound and circulating autoantibodies directed mainly to the hemidesmosomal component collagen XVII. While recapitulating the main immunopathological features of the human disease, frank skin blistering does not develop in the absence of skin rubbing in experimental pemphigoid models that have been established in neonatal mice.

    Moreover, due to their experimental design they only allow for short-term disease observation. In the present study we aimed to establish a model that reproduces the frank skin blistering seen in patients and allows for longer observation times.

    Methods: Rabbit and sheep antibodies specific to several fragments of collagen XVII were generated and the purified antibodies were passively transferred into adult mice.

    Results: Collagen XVII-specific IgG bound to the basal membrane of the skin and mucous membranes activating murine complement in vivo.

    Mice injected with collagen XVII-specific antibodies, in contrast to mice receiving control antibodies, developed frank skin blistering disease, reproducing human bullous pemphigoid at the clinical, histological and immunopathological levels. Titres of circulating IgG in the serum of mice correlated with the extent of the clinical disease.

    Mice receiving sheep antibodies specific to murine collagen XVII showed an early onset and a more active disease when compared to litter mates receiving specific rabbit antibodies.

    Conclusion: This novel animal model for bullous pemphigoid should facilitate further investigations of the pathogenesis of bullous pemphigoid and the development of innovative therapies for this disease.

    Published in News

    In an approach with the potential to aid therapeutic vaccine development, Whitehead Institute scientists have shown that enzymatically modified antibodies can be used to generate highly targeted, potent responses from cells of the immune system.

     

    The approach, referred to as "sortagging," relies on the bacterial enzyme sortase A to modify antibodies to carry various payloads, such as peptides, fluorophores, lipids, fluorophores, and proteins. In this case, the scientists, whose findings are reported online this week in theProceedings of the National Academy of Sciences, attached a variety of small antigens to an antibody directed at the surface of key immune cells. Through sortagging, the scientists were quickly able to prepare various antibody-antigen fusions and to deliver the antigens to their intended targets and track them as the immune cells mounted their intricate responses.

    "Sortagging is remarkably specific and efficient," says Lee Kim Swee, a researcher in the lab of Whitehead Member Hidde Ploegh. "We were able to create 50 different constructs (antibody-protein attachments), which wouldn't have been feasible if we had relied on the more traditional approach of genetic fusion."

    Swee and colleagues tested the approach in a mouse model of herpes virus, sortagging 19 known viral epitopes to a cell-specific antibody. They created a vaccine cocktail and immunized a group of mice. Upon subsequent re-exposure to the virus, vaccinated mice showed a 10-fold reduction in the amount of circulating virus.

    "This is proof of principle that one could in fact use sortagging on antibodies to easily attach a tailored set of antigens, toward which the immune system can be educated," Swee says. "This technique also helps us understand how to design better antibody-based vaccines."

    For paper co-author Carla Guimaraes, sortagging's value is bolstered by its flexibility. She likens it to "playing with Legos," because it allows "you to mix and match" proteins of diverse shapes, sizes, and functions. The process can be used, for example, to attach the relatively large green fluorescent protein (GFP) to antibodies without hindering GFP's desirable fluorescing activity or the binding of the conveying antibody to its intended target.

    "Imagination is really your only limitation," says Guimaraes, who is also a postdoctoral researcher in the Ploegh lab. "You could for example, use sortase to attach a toxin to an antibody and use that antibody to deliver the toxin to specific cells." Such an approach, she notes, would be an appealing strategy for developing better-tolerated cancer therapies.

    Hidde Ploegh's primary affiliation is with Whitehead Institute for Biomedical Research, where his laboratory is located and all his research is conducted. He is also a professor of biology at Massachusetts Institute of Technology.

     

    Published in News

    Immunomedics, Inc. is a biopharmaceutical company primarily focused on the development of monoclonal antibody-based products for the targeted treatment of cancer, autoimmune and other serious diseases. On 21 of December they announced that it has received notice that their patent application for "Anti-CD19 antibodies," will issue as US patent No. 8,337,840 really soon. The claims, allowed under the patent cover the use of specific humanized anti-CD19 monoclonal antibodies and fragments thereof for the treatment of autoimmune diseases. The fragments and antibodies thereof can be used alone, conjugated to at least one therapeutic agent or in combination with other humanized, chimeric, human or murine monoclonal antibodies, such as antibodies reactive with CD20, CD22, CD74 or HLA-DR. The patent, which provides coverage until 2024, also protects (19)-3s, a novel T-cell redirecting agent made as a DOCK-AND-LOCK™ (DNL™) complex using the Company's patented platform technology. The DNL™ complex recognizes CD19 on B cells and binds to CD3 on T cells. At last year's Annual Meeting of the American Society of Hematology (ASH), (19)-3s was reported to bind to T cells and non-Hodgkin lymphoma (NHL) cells simultaneously, and induce T-cell-mediated killing of NHL cells at less than 1 picomolar (pM) concentrations in an ex vivo setting, with maximal activity at 10 pM.

    Published in News
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