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    Displaying items by tag: cells

    Researchers-revealed-the-way-for-success-in-gene-therapyScientists have found a new way to overcome one of the biggest obstacles to the use of viruses for therapeutic genes.
     
    Scientists from the Institute for research at national level have found a way to overcome one of the biggest obstacles to the use of viruses for administration of therapeutic genes, that is, how to prevent the immune system to neutralize the virus before it has delivered its genetic set.
     
    Gene therapy is one of the most promising possibilities for the treatment of genetic disorders such as muscular dystrophy, congenital blindness and hemophilia. Scientists explore gene therapy as a cure for certain types of cancer, neurodegenerative diseases, viral infections and other acquired diseases. In order to obtain a therapeutic gene into cells, scientists use viruses that deliver its genetic material in cells as part of their normal replication process.
     
    Again and again, these efforts were thwarted by the very immune system of the body that damages each viral vector. Thus the therapeutic gene can be delivered to diseased cells and disease raging in full force.
     
    A team led by Louis-Rodino Klapak, PhD, and Jerry Mendel, MD, principal investigator in the Center for Gene Therapy at Nationwide, show for the first time that using a process called plasmapheresis, just before delivery of the virus for gene therapy he is protected long enough to enter the cell and deliver their genetic material.
     
    In a study of gene therapy for the treatment of Duchenne muscular dystrophy (DMD), Dr. Rodino-Klapak using plasmapheresis in a large animal model, and then injected a virus carrying the gene micro-dystrophin. When studying the level of gene expression of the micro-dystrophin in animals, it was found that there is a 500% increase in the gene expression in the animals who received a plasmapheresis.
     
    Dr. Mendel believes that right now, gene therapy seems to work best in patients who have antibodies to the virus. It is this virus is used to supply the necessary gene. It is exactly this gene, which is a therapeutic, curative intent of the organism suffering from a disease. On the other hand, it limits the number of patients who can benefit from gene therapy. This is because in very few patients lacking antibodies against the virus.

    Using the method of plasmapheresis repeatedly increases the potential of gene therapy, as this eliminates the obstacle called immune response of the organism.
     
    As gene therapy becomes more widespread, it may be necessary, patients receiving more than one course of treatment.
     
    The main problem is that when you go home after the first treatment, their body develops antibodies to the virus used to deliver the therapeutic gene. The use of plasma in a patient who previously received gene therapy may allow him to be treated again.

    Published in News

    stem-cells-molecule-gentaurDiscovered a new molecule - the first of its kind that allows multiplication of stem cells from umbilical cord. This discovery is very important as these cells are used for transplantation for the treatment of blood diseases such as leukemia, lymphoma and myeloma.
     
    The blood from the umbilical cord of the infant is considered an excellent source of hematopoietic stem cells that could be used for transplants.
     
    These stem cells are less likely to cause an adverse reaction by the immunity in the recipient thereof to whom they are transplanted.
     
    Furthermore, unlike the adult stem cells from bone marrow, it is not necessary, and the donor recipient has to have immunological compatibility for successful transplantation.
     
    Such type of treatment, however, can not always lead to successful healing in adults, since the number of the collected stem cells from umbilical cord blood is small and insufficient. Scientists believe that by using the new molecule will be possible multiplication of stem cells to a sufficient quantity for the conduct of successful treatment.
     
    Molecule is called the UM171 and was discovered by researchers from the Institute of Cancer Research and immunological and the University of Montreal, Canada.
     
    Doctrine argue that UM171 has the potential to increase the number of blood units, ready for transplant to 10 times.

    Published in News
    Friday, 03 October 2014 16:09

    Stem cells can overcome the blindness

    gentaur stem cellsMacular degeneration is the leading cause of blindness worldwide. It affects one in five people 75 years of age.
     
    The loss of vision is closely related to the aging process. The infringement is not seen so much as an actual condition, but rather as an inevitable part of aging.
     
    New discovery by scientists from the UK, however, may soon change this data.
     
    Researchers from the University of Southampton, UK, identified a unique type of stem cells in the eye that can be converted into photovoltaic cells. What is more important is that have the potential to turn the processes associated with blindness due to macular degeneration.
     
    Affected by the condition suffer from blurred and "distorted" vision before it completely disappears. To a large extent the cause lies in the loss of photoreceptor cells - cells that require light. In this study, the team of researchers found a way to replace these lost cells and reverse the effects of the condition.
     
    Right on the front surface of the eye - between the cornea and sclera, is an area where stem cells have been shown to "behave" as photoreceptor when they are in a suitable environment.
     
    For the moment, this environment can be created only in the laboratory. Since stem cells exist in the eyes throughout life, it is believed that with more research in this area, they can be used in future therapies for the treatment of blindness caused by macular degeneration.

    Published in News

    Treatment of various diseases of the blood and immune system is about to be discovered by scientists that reveal the mystery of the origin of stem cells.
     
    gentau rrabbitelisatargattaccupowerelisakitsassaykitscellAvstraliyskoro study was conducted by the Institute for Regenerative Medicine at Monash University, Melbourne. It first establishes a mechanism that "unlocks" the body in the formation of hematopoietic stem cells (HSC).
     
    These cells are found in bone marrow and umbilical cord and are extremely important because they can "feed" the stock of blood cells in the body. Patients with leukemia have been successfully treated with HSC transplantation. Medical experts, however, believe that they can come into wider use.
     
    According to the lead researcher - Prof. Peter Curry, understanding the way the HSC is samopodnovyavat to fill blood cells is the "Holy Grail" of stem cell biology.
     
    Hematopoietic stem cells are the best therapeutic agent, since they can produce any cell in the body, said Curry, adding that they could be used for the treatment of severe blood diseases. But before that you need to understand how they emerge.
     
    During this study, researchers observed cells in the developing zebra fish - tropical freshwater fish known for its regenerative abilities and optically visible embryos.
     
    Using a microscope with high resolution scientists capture the manner in which the cells grow. The process of their formation is captured in dramatic detail.
     
    Observations found that HSC need a "friendly" type of cell that help their formation. Metaphorically, the researchers explain that these cells serve as a comfortable sofa where HSC accommodate. Researchers establish whether the genes that are required for the formation of these "friendly" cells.
     
    The most remarkable achievement of the experts is that they can identify the signals in these cells, helper, which are responsible for the formation of HSC, after which they could be used in vitro for the creation of various blood cells to "fix" all types of diseases related to the blood.

    Published in News

    Gentaur proteinProtein in the body can improve its ability to detect and treat viral infections such as influenza and hepatitis C. This conclusion leads a laboratory study by researchers from the University Institute of cancer in Pittsburgh, USA.
     
    To start playback in the body, the virus actually "invaded" cells and "takes" control over them.
     
    Experts explain that, despite progress in the field of vaccines and treatment diseases caused by viral infections remain among the leading causes of death in the world. According to them, there is a need for a new type of security and the new discovery appears to be promising for further studies.
     
    Scientists isolated protein of similar oligoadenylate synthetase-occurring in humans, suffering from liver cancer, prichinen of hepatitis C. When the Expert increase the levels of this protein in human cells, observed inhibition of virus replication.
     
    In later study found that murine organisms in which there is no presence of the protein are susceptible to a large extent of a viral infection, in comparison to those who have it.

    Viruses affect the ribonucleic acid (RNA), including hepatitis C, influenza and respiratory syncytial virus, using RNA as the genetic material, when played back.
     
    The types of treatment, based on the protein like oligoadenylate synthetase, can enhance the ability of cells to detect RNA, used by the virus, and thus to activate the immune system to stop its reproduction.

    Published in News
    Monday, 28 October 2013 09:53

    MRC-5 culture media

    Gentaur product and conditioning cells in laboratory culture
    - MRC5 - VERO-McCoy - HEP2

    - Possible packaging: frozen cells bulbs, ready cells
    in vials or tubes

    - Culture media Employment

     MRC-5 culture media1  MRC-5 culture media2  MRC-5 culture media3

    Designation Ref. Conditioning
    Cells
    MRC 5: human diploid cells - Lung
    (10 ampoules of 10 M
    fcetus
    84003c

    Frozen cells, 5 x 1 ml (5 bulbs 10 million cells min.)

    84003c10 Frozen cells. 10 x 1 ml
    (10 ampoules of 10 M cells min.)
    84002 Cells in suspension. 30 ml
    (30 ML cells min.)
    84003 Cells in suspension. 10 ml
    (10 ML cells min.)
    VERO: Cells African green monkey kidney 84005 Cells in suspension. 10 ml
    (10 ML cells min.)
    84009 Cells in suspension. 30 ml
    (30 ML cells min.)
    Mac COY: Fibroblasts from mice 84008 Cells in suspension. 10 ml
    (10 ML cells min.)
    84010 Cells in suspension. 30 ml
    (30 ML cells min.)
    Hep 2 human laryngeal carcinoma cells 84013 Cells in suspension. 10 ml
    (10 ML cells min.)
    84011 Cells in suspension. 30 ml
    (30 ML cells min.)
    Culture media Employment
    Growth medium for MRC·5(10%SVF) M0430c 10 x 125 ml
    Maintenance medium for M0431E 10 x 100 ml

     

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    Published in Promos
    Thursday, 29 August 2013 12:17

    DNA Damage: The Dark Side of Respiration

    Adventitious changes in cellular DNA can endanger the whole organism, as they may lead to life-threatening illnesses like cancer. Researchers at Ludwig-Maximilians-Universitaet (LMU) in Munich now report how byproducts of respiration cause mispairing of subunits in the double helix.

    The DNA in our cells controls the form and function of every cell type in our bodies. The instructions for this are encoded in the linear sequence of the four subunits found in DNA, the bases adenine (A), cytosine (C), guanine (G) and thymine (T). Random changes in the sequence can lead to cell dysfunction, and may result in unrestricted cell proliferation and malignancies. Mutations can be induced by a variety of agents. For example, cellular respiration, i.e. the reduction of inspired oxygen to water, which powers cell function, also generates highly reactive oxygen species that can damage DNA, with the purine bases G and A being particularly susceptible to this kind of attack.

    "Reactive oxygen species are responsible for two different sorts of DNA damage, as they induce formation of both 8-oxo-G and FaPy-G," says Professor Thomas Carell of the Department of Chemistry at LMU. In 2004, work done by Carell and his team defined how 8-oxo-G generates mutations. However, the basis for the mutagenic effect of FaPy-G has remained obscure -- until now. In their latest publication, Carell and his colleagues describe how FaPY-G leads to mispairing of bases in the double helix.

    Pernicious partner swapping One G in one strand of the double helix normally matches up with a C on the other, forming a G:C pair. But as a consequence of damage by reactive oxygen species, the guanine base may be transformed into FaPy-G, so that we get a FaPy-G:C base pair. "We have now shown that, in the course of DNA replication prior to cell division, FaPy-G interacts with adenine, leading to the formation of FaPy-G:A base pairs. This partner swap is unusual, since unmodified guanine normally does not team up with adenine," Carell notes.

    FaPy-G is subsequently recognized as abnormal and is removed by DNA repair enzymes. The missing base is replaced by a T -- which is the usual partner for A. The net result is that the original G:C base pair has been converted into an A:T pair, and the base sequence has undergone a potentially dangerous mutation.

    This outcome is made possible by the fact that the cell's damage-control systems find it surprisingly difficult to distinguish the normal guanine base from its aberrant derivative FaPy-G during DNA replication. "That this defect then leads to mispairing with adenine is one of the main reasons for the spontaneous development of tumors," says Carell. "So with every breath we take, our risk of getting cancer goes up by a teeny-weeny bit." Further insights into the reasons why FaPy-G often eludes the cell's detection and correction systems could help to improve the treatment of cancer, as the inhibition of DNA repair processes in tumor cells increases their sensitivity to chemotherapeutic drugs.

    The study was supported by DFG grants awarded to Collaborative Research Centers 646 and 749 and the Center for Integrated Protein Science Munich (CIPSM), an Excellence Cluster.

    Published in News

    A new report suggests that the concentration of one human cytokine, interleukin 7 (IL-7), in the semen of HIV-1-infected men may be a key determinant of the efficiency of HIV-1 transmission to an uninfected female partner. In their study published February 7 in the Open Access journal PLOS Pathogens, a research group from the Eunice Kennedy-Shriver National Institute of Child Health and Human Development (NICHD) led by Leonid Margolis report that the increased IL-7 concentration in semen facilitates HIV transmission to cervical tissue ex vivo.

    Semen is a complex biological fluid containing not only spermatozoa but also cytokines, a group of extracellular proteins that modulate immune responses. As a result of HIV infection, the concentrations of various cytokines in semen is profoundly modified, in particular the concentration of interleukin 7 (IL-7) is greatly increased. Despite this evidence of strikingly elevated IL-7 levels in seminal plasma, there was limited knowledge about any effects this cytokine might have on HIV-1 sexual transmission.

    To investigate the question about the effects of this increased IL-17 on HIV-1 sexual transmission, Andrea Introini and colleagues from the Margolis lab developed a system of explants of cervico-vaginal tissue that can be maintained outside of the body in culture for up to two weeks while preserving the cytoarchitecture of the tissue. In this system, HIV transmission can be simulated and studied under controlled laboratory conditions. When researchers added IL-7 in concentrations comparable to that found in the semen of HIV-1 infected men, HIV was transmitted more efficiently and replicated to a higher level than without IL-7. Normally, HIV-1-infected cells quickly die as the result of apoptosis, a programmed death triggered by HIV infection. IL-7 inhibits apoptosis of infected cells, allowing them to produce more virus and thus increasing the chances of the incoming virus to disseminate through the tissue. Also, IL-7 stimulates T cell proliferation, thereby also providing to HIV even more potential targets to infect.

    The authors speculate that IL-7, together with other cytokines, may determine sexual transmission rates of HIV-1 and that changes in the seminal cytokine load may explain differences in HIV transmission from different individuals. However, whether the effect of IL-7 that has been demonstrated ex vivo occurs also for sexual partners in vivo, is a subject for future research. If this increase does occur in vivo, then it should be investigated whether HIV-1 infected individuals that have been treated systemically with IL-7 in order to increase their T cell counts may have also resulted in the unintended increase of their seminal IL-7 levels. Finally, this study suggests that seminal cytokines may become new targets for HIV-preventive strategies.

    Published in News

    monoclonal antibodyResearchers have discovered a unique monoclonal antibody that can effectively reach inside a cancer cell, a key goal for these important anticancer agents, since most proteins that cause cancer or are associated with cancer are buried inside cancer cells. Scientists from Memorial Sloan-Kettering Cancer Center and Eureka Therapeutics have collaborated to create the new human monoclonal antibody, which targets a protein associated with many types of cancer and is of great interest to cancer researchers.

    Unlike other human therapeutic monoclonal antibodies, which can target only proteins that remain on the outside of cancer cells, the new monoclonal antibody, called ESK1, targets a protein that resides on the inside of the cell. ESK1 is directed at a protein called WT1, which is overexpressed in a range of leukemias and other cancers including myeloma and breast, ovarian, and colorectal cancers. WT1 is a high priority target for cancer drugs because it is an oncogenic protein, meaning that it supports the formation of cancer. In addition, it is found in few healthy cells, so there are less likely to be side effects from drugs that target it. "This is a new approach for attacking WT1, an important cancer target, with an antibody therapy. This is something that was previously not possible," said David A. Scheinberg, MD, PhD, Chair of the Sloan-Kettering Institute's Molecular Pharmacology and Chemistry Program and an inventor of the antibody. "There has not been a way to make small molecule drugs that can inhibit WT1 function. Our research shows that you can use a monoclonal antibody to recognize a cancer-associated protein inside a cell, and it will destroy the cell." 

    The first studies of the antibody are showing promise in preclinical research as a treatment for leukemia as reported March 13, 2013, in Science Translational Medicine. "ESK1 represents a paradigm change for the field of human monoclonal antibody therapeutics," said Cheng Liu, PhD, President and Chief Executive Officer of Eureka Therapeutics. "This research suggests that human antibody therapy is no longer limited to targeting proteins present outside cancer cells, but can now target proteins within the cancer cell itself."

    ESK1 was engineered to mimic the functions of a T cell receptor, a key component of the immune system. T cells have a receptor system that is designed to recognize proteins that are inside the cell. As proteins inside the cell get broken down as part of regular cellular processes, molecules known as HLA molecules carry fragments of those proteins -- known as peptides -- to the surface. When T cells recognize certain peptides as abnormal, the T cell kills the diseased cell. In the current study, the investigators showed that ESK1 alone was able to recognize WT1 peptides and kill cancer cells in the test tube and also in mouse models for two different types of human leukemia. "We were surprised that the antibody worked so well on its own," said Dr. Scheinberg, senior author of the paper. "We had originally expected that we might need to use the antibody as a carrier to deliver a drug or a radioactive therapy to kill the cancer cells, but this was not necessary."

    Additional studies must be done in the laboratory before ESK1 is ready to be tested in patients. But the monoclonal antibody was engineered to be fully human, which should speed the time it takes to move the drug into the clinic. Researchers expect that the first clinical trials, for leukemia, could begin in about a year.

    The antibody was developed under a collaborative effort between Memorial Sloan-Kettering and Eureka, which have jointly filed for patent protection. This work was supported by grants from the Leukemia and Lymphoma Society, the National Cancer Institute, the Sloan-Kettering Institute's Experimental Therapeutics Center and Technology Development Fund, the Commonwealth Foundation for Cancer Research, the Tudor and Glades Foundations, the Merker Fund, the Lymphoma Foundation, and the Mesothelioma Applied Research Foundation.

    http://www.sciencedaily.com

    Published in News
    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