just at first sight, I see at least two of these 6 "Cancer Core Europe" have ties to Peregrine/PS Targeting and I'm sure there is more but back to work
Guido Kroemer, Shigekazu Nagata and others..... all coming full circle..and every single one of these individuals are top in the world in understanding cell death and naturally, would understand completely 100% if Dr. Rolf Brekken explained to them the MOA of PS Targeting/Bavituximab. For now, as in the past... will just highlight Nagata because of his connect the dot pieces that lead back to Peregrine Pharmaceuticals. Notice how they don't really mention "Phosphatidylserine" in Nagata's bio below ?? but we all know that the Nagata Lab is 100% about targeting Phosphatidylserine and all based on my previous exposed links/posts all related to Nagata. I've had many Nagata posts and will just toss one out below and if you want to verify others you can follow back/forward the chain of posts.
In the previous post, Nagata went to Canada in 2013 and Brazil in 2014 (Keystone Symposia events..), talking exposure of Phosphatidylserine. Now, this Japanese based lab, is "ALL" about targeting phosphatidylserine. Shigekazu is the expert of "Interferon", just as Peregrine KOL Dmitry Gabrilovich is the expert of MDSC's.
More interesting is "Robert Peter Gale" that was presenting this week as well, who studied in the lab of the late "John Fahey" and its dot connecting time since we have a "James T. Fahey" on this class action law suit so how much information ( was it legal? ) to be trading/investing so much into Peregrine in the summer of 2012 as James had done, unless James just based his gut feeling on the rise of PPHM on IHUB posts saying the stock was going to $100 pps. There may have been other links why he invested ...
09:30—11:45 Inflammation and the Dynamics of the Tumor Microenvironment
Registered attendees can view abstracts starting on 01/08/2015
Van Horne Ballroom A/B
Robert Peter Gale, Hammersmith and Celgene, USA The Diversity of Myeloid Cell Populations Driving Carcinogenesis
Amy-Jo Casbon, University of California, San Francisco, USA Short Talk: Tumors Reprogram Early Myeloid Differentiation in the Bone Marrow to Generate Immunosuppressive Neutrophils
Guido Kroemer, Institut Gustave Roussy, France How Chemotherapeutics Start an Intratumoral Anticancer Immune Response
Again, just posting this May 2015 Belgium Conference because it has all, 100% to do with the cascade of events that take place during PS Targeting and these are more key, global players that can't contradict the MOA of bavituximab (if walked thru it). Math is the only universal language, as PS Targeting will prove to be universal in the chain reaction of events that take place-> Notch Signaling.
Welcome to the 15th International TNF Conference, 20-23 May 2015, Ghent, Belgium
Peter Vandenabeele and Henning Walczak, organisers of the 15th International TNF meeting
Shigekazu Nagata
Dr. Nagata obtained a Ph.D. in 1977 from University of Tokyo for the thesis "Purification and characterization of polypeptide chain elongation factor from pig liver". From 1977 to 1981, he did post-doctoral research in laboratory of Prof. Charles Weissmann (Institute of Molecular Biology, University of Zürich), where human interferon-a cDNA was identified. In 1982, Dr. Nagata returned to Institute of Medical Science, University of Tokyo as an assistant professor, and identified cDNA for granulocyte colony-stimulating factor (G-CSF). In 1987, Dr. Nagata was appointed as a Head of Molecular Biology Department of Osaka Bioscience Institute, where he characterized G-CSF receptor, and started to work on apoptosis. From 1995-2007, he was a professor in Department of Genetics, Osaka University Medical School. In 2007, he moved to Kyoto University as a professor in Department of Medical Chemistry, Graduate School of Medicine.
Dr. Nagata was the president of Japanese Biochemical Society (2005-2006), and Japanese Society of Molecular Biology (2007-2008). He was a councilor for Human Frontier Science Program in Strasbourg from 2006 to 2009, and a member of Science Council of Japan since 2008. Dr. Nagata serves or served as an editorial member of various journals including Science, Immunity, and Cancer Cell. The awards include Emil von Behring Prize (Germany), Robert Koch Award (Germany), Prix Lacassagne (France), and Japan Academy Prize and Imperial Prize from the Japan Academy. Dr. Nagata is recognized as a Person of Cultural Merit from the Japanese Government in 2001 and nominated to an associate of The Japan Academy in 2010. He obtained a Honorary Doctorate from University of Zürich in 2012, and received Tomizo Yoshida Award (Japanese Cancer Association) and Debrecen Award for Moleculare Medicine from Debrecen University (Hungary) in 2012. He received Keio Medical Science Prize from Keio University in 2013. www.tnf2015.org/content/Shigekazu-Nagata
David Baltimore
The Baltimore lab is involved in two major research thrusts. One is basic investigation of the development and functioning of the mammalian immune system. The other is Engineering Immunity: translational studies using viral vectors to carry new genes into immune cells to increase the range of pathogens effectively fought by the immune system and to make the immune system resist cancer growth more effectively.
The basic studies have two directions: to understand the remarkable range of activity of the NF-kB transcription factor and to understand the normal and pathologic functions of microRNAS. NF-kB activates perhaps 1000 genes in response to a wide range of stimuli. It has different physiologic roles in different cells. How one factor can be so varied in its activity is the puzzle that has interested us for many years and that we study at many different levels.
MicroRNAs are small (~22 nucleotide) RNAs that regulate the amount of protein made by a particular messenger RNA and that therefore provide a level of fine control over gene expression. We have been interested in their role in hematopoietic cell development and function. We have recently concentrated on microRNAs that modulate myeloid cell development. Most interesting is miR-146a, which is a feedback regulator of NF-kB activation. A mouse knockout of the gene encoding miR-146a is normal at birth but slowly develops myeloid hyperproliferation and, ultimately, cancer. We have traced the earliest events to dysregulation of hematopoietic stem cells suggesting that a normal function of miR-146a is to be a guardian of hematopoietic stem cell health and longevity.
Our translational work centers on using gene transfer methods to reprogram the immune system. We first showed that we could design a retrovirus vector able to express cDNAs encoding both chains of the T cell receptor (TCR) protein. When mouse hematopoietic stem cells are transduced with the vector and then inoculated into irradiated mice, many of the resulting T cells express the TCR encoded by the vector. When the TCR is able to recognize specific peptides from a tumor antigen, the animal can reject tumors carrying the antigen. We are extending these studies to TCRs that react with human tumor antigens with the goal of developing a human therapy. We have also developed therapies based on transfer of lentiviral vectors that encode small, interfering RNAs and vectors that carry antigen genes into dendritic cells. Because we found it difficult to make lentiviral vectors that would reprogram B cells to make specific antibodies, we switched to adeno-associated virus (AAV) vectors carrying genes that encode antibodies and have used them to reprogram muscle cells in mice to make anti-HIV and anti-influenza virus antibodies. There are 4 programs presently moving into clinical development. Selected Awards: Nobel Prize in Physiology or Medicine (1975) National Medal of Science (1999) Warren Alpert Foundation Prize (2000) http://www.tnf2015.org/content/david-baltimore
Vishva M. Dixit
Vishva M. Dixit has made many contributions to biomedicine and his early work on apoptosis is prominent in introductory textbooks of biology and medicine [for a historical perspective see Nature (2008, 453:271-273), Nature Cell Biology (2010, 12:415)] and The Journal of Immunology (2013, 190:3-4)
His laboratory was among the first to: i) show that caspases are components of the death receptor-induced apoptotic pathway; ii) demonstrate that death receptors signal by an entirely novel mechanism of recruiting and activating a death protease (FLICE/caspase-8) by an induced proximity mechanism; iii) identify the mammalian death protease equivalent to the CED3 protein in worms (YAMA/caspase-3) as well as other pro-apoptotic caspases including caspase-6,-7 and -9. iv) show that the death domain-containing molecule MyD88 is a key signaling adaptor; vi) discover paracaspases and metacaspases: two ancient families of caspase-related proteins, one of which plays a key role in MALT lymphoma; vii) discover the non-canonical inflammasome pathway.
He is a Foreign Member of the European Molecular Biology Organization, a member of the Institute of Medicine, the American Academy of Arts and Sciences and the National Academy of Sciences. http://www.tnf2015.org/content/vishva-dixit
Peter Krammer
Prof. Dr.med. Peter H. Krammer was born in Rheydt, Rhineland, Germany. He received his medical training in Freiburg, Germany, St. Louis, USA, and Lausanne, Switzerland. He did his thesis on extracellular streptococcus antigens at the Institute for Microbiology and Hygiene at the University of Freiburg, and investigated the role of small nuclear RNAs at the Institute of Pathology, also in Freiburg.
In 1973, at the age of 27, he became a member of the Basel Institute for Immunology and spent almost three fruitful years at the Institute studying T cells and their specificity. From Basel, he moved via the Max-Planck-Institute for Immunobiology in Freiburg, where he stayed one year to continue T cells studies, to Heidelberg to the German Cancer Research Center, where in 1976 he started his work in the Division of Immunogenetics. There, again, his main work was on T cells and T cell clones, their receptor specificities and their activities. Later, in the early 1980s, he focused on T cell-derived cytokines. He investigated the activation of macrophages by macrophage activating factors and in a fruitful, longstanding collaboration with E. Vitetta and her associates from Dallas, discovered IL-4 as a B cell immunoglobulin switch factor. With fondness he remembers his days as a visiting professor in Dallas and the friendliness of the Texans who hosted his stay. In 1984/85, he felt that molecular biology would leave a significant mark on immunology and he spent one and a half years in A. Sippelës laboratory at the Center for Molecular Biology in Heidelberg to learn the thinking and the techniques in this field. In the mid-to-late 1980s, his interest shifted very much towards negative regulation of tumor cell growth and apoptosis. In this context he and his associates discovered the CD95(APO-1/Fas) system, highlighted by the first publication in Science in 1989. CD95, its signalling machinery and its role in physiology and diseases remained at the center of his interest.
Peter Krammer has received numerous prizes for his work and is a reviewer for and serves on the editorial board of many journals. Presently, he is the Director of the Tumor Immunology Program of the German Cancer Research Center. He runs a large group of scientists and his main interest is sensitivity and resistance in apoptosis and the role of apoptosis in the immune system and in diseases. http://www.tnf2015.org/content/peter-krammer
Tania Watts
Tania Watts was educated at the University of Alberta, Canada, obtaining a B.Sc. and Ph.D. in Biochemistry. Watts conducted post-doctoral studies in Chemistry at Stanford University under the mentorship of Harden McConnell, where she pioneered the use of supported planar membranes to study the interaction of T cells with MHC II/peptide complexes. Watts joined the University of Toronto as a faculty member in the department of Immunology in 1986, where she is now Professor of Immunology and holds the Sanofi Pasteur Chair in Human Immunology. Watts is also director of the Toronto Human Immunology Network, a Federation of Clinical Immunological Societies (FOCIS) center of excellence and director of the Faculty of Medicine Flow cytometry facility at the University of Toronto. Research in the Watts laboratory is funded by the Canadian Institutes of Health Research and the Canadian Cancer Society Research Institute.
Watts’ team currently studies the role of tumor necrosis factor family receptors in T lymphocyte survival and control of viral infections and cancer. Work from the Watts lab has shown that TNFR family members are highly regulated with severity of infection. Sustained expression of 4-1BB during severe as compared to mild influenza infection allows a prolonged CD8 T cell response and improves viral control and mouse survival. In contrast, the 4-1BB signaling pathway becomes desensitized during chronic LCMV or HIV infection through loss of a key signaling adaptor, TRAF1. On the other hand, our recent work shows that the TNFR family GITR remains functional throughout a chronic infection LCMV clone 13, but the pathway is turned off through persistent down-regulation of its ligand. Our laboratory also studies the role of TRAF1 in human disease, particularly in HIV, lymphoma and inflammatory diseases. http://www.tnf2015.org/content/Tania-Watts
Hilde Cheroutre
Dr. Cheroutre joined LIAI in 1998 and is currently Division Head and Professor in the Division of Developmental Immunology. Dr. Cheroutre's research focuses on the selection, regulation and activation of different classes of T cells, such as regulatory and memory T cells.
Dr. Cheroutre received her Licentiate in Sciences from the State University of Ghent in Belgium in 1978. She received her Ph.D. from the same university in 1984, earning highest honors. That same year, Dr. Cheroutre began her postdoctoral work at the California Institute of Technology in Pasadena. In 1988, Dr. Cheroutre began a three-year stint working in the lab of Mitchell Kronenberg, Ph.D., current President and Chief Scientific Officer of LIAI, in the Department of Microbiology and Immunology at the University of California, Los Angeles. From 1991 to 1997, Dr. Cheroutre was co-director of UCLA's Transgenic Mouse Facility.
Dr. Cheroutre has been awarded the NATO postdoctoral fellowship twice, as well as the Markey Foundation Postdoctoral Fellowship and the Cancer Research Coordinating Committee Fellowship from the State of California. Research focus
Hilde Cheroutre and her team are studying the development, function, and regulation of white blood cells, a type of T lymphocytes. The laboratory is investigating how the immune system provides protection at "interfaces," or places where the outside world comes in contact with the inside of the body, such as skin, lungs, mouth, and the largest surface of all, the intestine.
Studying how the immune system works in the intestine is of particular interest because the immune system has to be able to distinguish pathogenic antigens from harmless food peptides and bacteria. The laboratory is investigating how the immune system succeeds in differentiating between the two and what causes the system to fail, allowing the antigens to invade the body.
The lab's research has been expanded to studying immune memory cells that resist re-entering pathogens or cancer cells. Tumor cells produce tumor antigens, which are cell surface proteins that differ from the proteins expressed by the surrounding normal cells. White blood cells recognize and destroy these transformed cells. Some of these tumor-fighting white blood cells go on to become immune memory cells. These are long-lived cells that activate immediately when they re-encounter tumor antigens, in the case of metastasis or re-occurrence of the tumor.
Understanding the function of immune memory T cells will help in the development and improvement of effective vaccines. At the same time, the ability to specifically eliminate these cells is a key requirement in the therapeutic intervention against autoimmune diseases and the rejection and/or destruction of host tissue following transplantation. http://www.tnf2015.org/content/hilde-cheroutre
Marcos Vidal, PhD
Marcos Vidal is a group leader at the Beatson Institute for Cancer Research in Glasgow, UK (www.beatson.gla.ac.uk). His research activities focus on understanding the roles of inflammation in cancer using Drosophila melanogaster as the model system. Drosophila counts with a potent innate immune system and can recognize and tumours and trigger cell death via the involvement of the haemocytes, the macrophage like immunosurveillance cells which express the TNF homologue Eiger.
He obtained his PhD degree at the University of Rosario, Argentina, were he studied Vitamin D metabolism in macrophages. He performed his postdoctoral studies in Drosophila cancer models in the laboratory of Ross Cagan in Mount Sinai School of medicine, New York. He became a group leader in March 2009, and elected a member of the Young Academy from the Royal Society of Edinburgh 2013. http://www.tnf2015.org/content/marcos-vidal
Jiahuai Han
Dr. Jiahuai Han is known for the discovery of the p38 signaling pathway, one of the most important pathways in intracellular signaling transduction. This pathway plays important roles in many biological processes including cell cycle regulation, cell proliferation, cell differentiation and senescence, as well as immune reactions, development and tumorigenesis. Another current focus of Han`s lab is molecular mechanisms of RIP3 dependent necrosis, which is based on a recent finding in this laboratory revealing that RIP3 is a major player in controlling programmed necrosis.
The research in Han’s Lab will lead to a better understanding of the molecular mechanisms of inflammation, cardiovascular disease and tumorigenesis, and thus provides new ideas for the development of therapeutic intervention for these diseases.
Research and Professional Experience
1987 – 1992 Research Fellow, Department of Internal Medicine and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas, USA 1992 – 1993 Research Associate, Department of Immunology, The Scripps Research Institute, La Jolla, California, USA 1993 – 1996 Assistant Member (Assistant Professor), Department of Immunology, The Scripps Research Institute, La Jolla, California, USA 1996 – 2004 Associate Professor, Department of Immunology, The Scripps Research Institute, La Jolla, California, USA 2004 – 2007 Professor, Department of Immunology, The Scripps Research Institute, La Jolla, California, USA 2007 – Present Adjunct Professor (Professor of Immunology), Department of Immunology, The Scripps Research Institute, La Jolla, California, USA 2007 – Present Professor, School of Life Sciences, Xiamen University, China
Awards
Jean Stas Award (Belgium), 1991 Established Investigatorship Award (American Heart Association), 1995 Distinguished Young Scholar (B class, National Science Foundation of China), 2001 Lu Jiaxi Excellent Mentor (Lu Jiaxi Science and Education Foundation), 2009 YaoMingKangDe Life Science and Chemistry Award (1st Prize, Wuxi Pharma), 2009 Chang Jiang Scholar Achievement Award (The Ministry of Education of China), 2009 First Prize in Natural Science Research (The Ministry of Education of China), 2011 http://www.tnf2015.org/content/jiahuai-han
Francis Chan
Francis Ka-Ming Chan is a molecular immunologist with a strong interest in cell death and inflammation. He obtained his Ph.D. degree at the University of California, Berkeley. As a graduate student in Dr. Astar Winoto’s laboratory at UC Berkeley, he cloned one of the first cell cycle inhibitors, INK4d-p19. He went to the National Institutes of Health, USA to pursue his postdoctoral training with Dr. Michael Lenardo, where he first developed an interest in TNF biology. During his postdoctoral work, he discovered a new paradigm of TNF receptor signaling: that TNF receptors exist and functions as pre-assembled trimers that undergo conformational change in response to ligand binding.
As an independent investigator at the University of Massachusetts Medical School, his research has focused on how TNF induces a non-apoptotic form of cell death termed programmed necrosis or necroptosis. His group was among the first to describe an obligate role for the Receptor Interacting Protein kinases RIPK1 and RIPK3 in TNF-induced necroptosis and in anti-viral immunity. http://www.tnf2015.org/content/francis-chan
Harald Wajant
Harald Wajant is Professor at the Department of Internal Medicine II of the University Hospital Würzburg and head the Division of Molecular Internal Medicine. He graduated in the Institute of Botany of the University of Stuttgart, Germany in 1993 and was then a postdoctoral research fellow and group leader at the Institute of Cell Biology and Immunology. Since 2003 he is Professor at the University Hospital Würzburg.
In the 1990s during his time in Stuttgart, Professor Wajant worked on the cloning, expression and biotechnological application of plant hydroxynitrile lyases but also started to work in the completely different field of TNF receptor signaling. Since then the scientific interests of Professor Wajant fully shifted to the TNF field and are now focused on the mechanisms of TNF receptor activation, apoptotic and non-apoptotic death receptor signaling and the development of antibodies and TNF ligand fusion proteins targeting TNF receptors. http://www.tnf2015.org/content/harald-wajant
David Wallach
David Wallach did his M.Sc. and doctoral studies at the Department of Biological Chemistry, The Hebrew University of Jerusalem, Israel, and his postdoctoral training at the National Cancer Institute, Bethesda, Maryland, USA. He is currently a professor at the Weizmann Institute of Science, Rehovot, Israel.
His studies were the first to provide conclusive evidence that the ‘type I’ (anti-viral) and ‘type II’ (immune) interferons act through distinct mechanisms and have distinct patterns of effects.
Over the past 30 years, Prof. Wallach and his colleagues have been engaged in elucidating the mode of action of cytokines of the TNF family. They contributed to the isolating TNF, to the isolating and cloning the soluble and cells surface forms of the two TNF receptors and to the study of the shedding mechanisms of these receptors. His research group was of the first to decipher the extrinsic apoptotic cell-death pathway, to clone its major components (FADD/MORT1, caspase-8/MACH, and cFLIP/CASH) and to define their structural motifs (death domain, death-effector domain). They were also of the first to clone several of the signaling proteins that mediate effects of the TNF family on the NF-?B transcription factors. They continuously explore further the mechanisms of action of these signaling proteins and their physiological functions. http://www.tnf2015.org/content/david-wallach
Michael Croft
Professor Michael Croft is Head of the Division of Immune Regulation at the La Jolla Institute for Allergy and Immunology. He received a Ph.D. in the U.K, and after doing postdoctoral work at the University of California, San Diego, became an Assistant Professor at the La Jolla Institute for Allergy and Immunology in 1996. He became Professor in 2005, and was appointed Head of the Division of Immune Regulation in 2010.
Professor Croft’s research has centered on several proteins in the tumor necrosis factor receptor (TNFR) family, including OX40, 4-1BB, CD27, HVEM and LTBR, with a primary goal of understanding how these molecules control T cell immunity and contribute to the balance between effector T cells and regulatory T cells that are important for tolerance. Over the years, he has pursued the role of these molecules in several autoimmune and inflammatory diseases, with a particular focus on asthma and lung inflammation. More recently, he has also studied the activity of the TNF family protein LIGHT in non-hematopoietic cells relevant to chronic tissue damage. Another line of research has been to investigate how agonists that can signal T cells and other immune cells through TNFR family proteins can be used to increase natural immune responses to combat the growth of viruses or growth of tumor cells. http://www.tnf2015.org/content/michael-croft
Jaewhan Song
Professor Jaewhan Song studied the mechanism of molecular chaperones during his Ph.D. years at Northwestern University, USA. Following a postdoctoral fellowship at the same university with Prof. Richard I. Morimoto, he moved to the Department of Bioengineering at Sungkyunkwan University, Korea, as an assistant professor in 2002. Since 2010 he held the position of professor in Biochemistry Department, Yonsei University. The main theme of Prof. Song’s laboratory is to understand tumorigenesis through studies of cellular senescence and death. During past years his lab worked on the function of tumor suppressors and oncogenes that directly or indirectly involved with intrinsic or extrinsic apoptosis. In particular, the mechanisms of how they are regulated in the post-translational status have been the major questions. Some of the recent findings are as follows. Using animal and cellular models, his laboratory identified for the first time the E3 ligases of FADD, a major adaptor protein prompting extrinsic apoptosis, and how their interactions could be manipulated to suppress breast cancer development. Working on p14ARF, a major tumor suppressor inducing senescence, his research showed that its regulator E3 ligase MKRN1 could induce gastric tumor cancer by suppressing p14ARF function. Currently, members of his laboratory are also concentrating on the mechanisms of alternative death pathway, called necroptosis, and how they are regulated by post-translational modifications in cancer and immune pathophysiology. http://www.tnf2015.org/content/jaewhan-song
Holbrook Kohrt
Dr. Kohrt currently investigates novel therapeutic strategies to enhance anti-tumor immunity, including the discovery of checkpoint inhibitors and cancer vaccine strategies. Dr. Kohrt is a member of the Cancer Immunotherapy Trials Network. As a faculty member at Stanford, Dr. Kohrt is developing novel vaccine strategies which induce tumor antigen-specific immunity and improve graft-versus-tumor reactions without exacerbation of graft-versus-host disease. His studies also include efforts to identify and develop immunomodulatory antibodies targeting immune effector cells subsets, such as natural killer cells, which enhance the anti-tumor activity of tumor-targeting antibodies. Dr. Kohrt is a leader in the clinical development of agents including IL-15, IL-7, anti-CTLA-4, anti-CD137, anti-PD-1, anti-PD-L1, BTK inhibitors, and HPV-targeted and WT1-targeted vaccines. Dr. Kohrt attended Stanford University Medical School, where he trained in Internal Medicine through the Clinical Investigator Pathway and completed a fellowship in Hematology and Oncology at Stanford with a research focus on preclinical models for novel immunomodulatory antibodies. During this time, he developed, validated, and nationally implemented a nomogram for risk prediction in early stage breast cancer. Dr. Kohrt received his Ph.D. in clinical trial design, biostatistics, and tumor immunology from Stanford under mentor Ron Levy with a thesis including the first report of an agonistic monoclonal antibody capable of enhancing the efficacy of tumor-targeting therapeutics. This antibody is now in three Phase 1/2 clinical trials. http://www.tnf2015.org/content/holbrook-kohrt
John Silke
John completed a law degree in King's College London, before seeing the error of his ways and completing a second degree in Biochemistry at Churchill College, Cambridge (1992). He completed a PhD in Zurich (1997), Switzerland under Prof. Walter Schaffner, looking at the role of DNA methylation in the regulation of transcription. A Swiss fellowship allowed John to go to Australia to work on cell death mechanisms as a post-doc for Dr. David Vaux in the WEHI (1997-2005). After a five year stint running a lab in La Trobe University, he returned to the WEHI (2011) where his lab focuses on the programmed cell death pathways; apoptosis and necroptosis. He has collaborated with several pharmaceutical companies and is a strong advocate and proponent of using small drug like molecules to complement genetic analyses to investigate cell death pathways involved in regulating inflammation. In particular he is interested in the regulation of TNF signalling by TRAFs and Inhibitor of APoptosis proteins and their ability to regulate signalling cascades involving RIP Kinases. http://www.tnf2015.org/content/john-silke
Domagoj Vucic
Domagoj Vucic, PhD, is a Principal Scientist at Genentech, Inc. in South San Francisco, USA. He obtained his B.S. from the University of Zagreb, Croatia, and his Ph.D. from the University of Georgia, USA. He completed his postdoctoral training in the laboratory of Dr. Vishva Dixit. He discovered the TNF dependence of IAP antagonist stimulated cancer cell death, which allowed the initiation of clinical trials for testing IAP antagonists as anti-tumor agents in people.
Dr. Vucic’s laboratory investigates the biological role of modulators of signaling pathways (e.g. ubiquitination-mediated regulation of NF-kB pathways), and their involvement in cellular processes triggered by TNF family ligands and other pro-inflammatory stimuli. At Genentech, his group is developing compounds that block uncontrolled inflammatory responses and/or enhance the survival of damaged cells and tissues. His laboratory also studies the physiological role of RIP family of kinases and inhibitors of apoptosis (IAP) proteins in modulation of immune responses. http://www.tnf2015.org/content/Domagoj-Vucic
Bill Dougall
In his role as Scientific Director of Research, Cancer Biology, Dr. Dougall led Amgen’s oncology research efforts to develop inhibitors of RANKL for the treatment of skeletal complications of malignancies. Dr. Dougall led internal research program at Amgen for development of denosumab, currently approved in US for a number of indications including the prevention of skeletal-related events in patients with bone metastases from solid tumors. Dr. Dougall was part of the research group that originally identified RANK and RANKL and subsequently demonstrated the obligate role for RANK in osteoclastogenesis using genetic models. His research interests have included the function of the RANK/RANKL/OPG axis in cancer-induced bone diseases and, more recently, in the mechanisms of breast tumor initiation. Within the Therapeutic Innovation Unit, his current research interests include the use of systematic genetic functional screens for target identification and drug mechanism of action, osteotropism of breast and prostate cancer, development of the mammary gland and basic mechanisms of breast cancer initiation and progression.
Dr. Dougall received his Ph.D. in Biochemistry and Molecular Biology at the University of Florida and completed a post-doctoral fellowship at the University of Pennsylvania Department of Pathology, Division of Immunology. http://www.tnf2015.org/content/Bill-Dougall
Carl Ware
Carl F. Ware, Ph.D. is recognized for his scientific discoveries and advances in the study of the immune system. His research program is focused on the structure-function relationships and clinical utility of the TNF Superfamily of cytokines, and immune evasion mechanisms by persistent viruses. Dr. Ware is currently Director of the Infectious and Inflammatory Diseases Center at the Sanford|Burnham Medical Research Institute in La Jolla, and Professor at University of California, San Diego. Dr. Ware received his doctorate in Molecular Biology and Biochemistry from the University of California, Irvine in 1979 with GA Granger. Dr. Ware is noted for discovering several cytokines in the TNF Superfamily, including Lymphotoxin b and LIGHT (TNFSF14). He is a recipeint of National Merit Award from the US National Insitutes of Health, and past President of the International Cytokine Society and Scientific advisor for the International TNF Superfamily Conference. http://www.tnf2015.org/content/Carl-Ware
Rivka Dikstein
Dr. Dikstein’s lab is at the Department of Biological Chemistry at The Weizmann Institute of Science in Rehovot, Israel. The broad research interests of the Dikstein lab are to elucidate the means by which regulatory information encoded within the genes is decoded during transcription and translation, and to reveal the connections between the two processes. To this end their goals are: (i) to investigate the mechanisms underlying transcription, basal and regulated, of coding and non-coding RNAs (ii) to study the molecular basis of a unique form of translation initiation that is linked to transcription. They have a long-term interest in the mechanisms underlying transcription activation by the pro-inflammatory transcription factor NF-?B. A major research area is the structure, function and significance of the core promoter, a central regulatory element that serves as a docking site for the transcription machinery. Another objective is to find important transcriptional features of microRNA genes. Lastly, with their discovery of TISU, a unique dual regulatory element of transcription and translation, their research interest expanded to the translation field, aiming to decipher TISU-directed translation initiation. http://www.tnf2015.org/content/Rivka-Dikstein
Alexander Hoffmann
Alexander Hoffmann is the Thomas M Asher Professor of Microbiology and Immunology at UCLA, and the founding director of the Institute for Quantitative and Computational Biosciences (QCBio). The Hoffmann lab focuses on developing a predictive understanding of the cellular responses to pathogens and TNF family members. Quantitative experimentation is iteratively coupled with computational modeling to derive insights and develop hypotheses. The Hoffmann lab models of the regulatory modules within the immune response and inflammatory networks are being used by an increasing number of researchers. http://www.tnf2015.org/content/Alexander-Hoffmann
Liming Sun, PhD
Linda Burkly
Linda Burkly was educated at the Tufts University Sackler School of Biomedical Science in Boston, MA where she earned a Ph.D in Immunology. She conducted a postdoctoral fellowship in the laboratory of Dr. Richard Flavell in Cambridge, MA, where she dissected the role of MHC Class II in specific immune cell types using transgenic mouse technology and demonstrated a non-deletional mechanism for peripheral T cell tolerance in mice with MHC Class II expression restricted to pancreatic islet b cells.
Burkly joined Biogen, Inc., as a scientist in 1989, and is currently a Sr. Distinguished Investigator, Vice President, in the Dept. of Immunology, Biogen Idec, Cambridge, MA. Burkly has deep experience in both discovery research and drug development in the biopharmaceutical industry, where she has contributed to drug target identification, mechanistic and translational studies, and advanced promising therapeutic candidates into clinical development for the treatment of autoimmune and inflammatory diseases.
Burkly’s main research interests include the TNF/ TNFR superfamily, particularly the CD40L/CD40 and TWEAK/Fn14 pathways, where she has contributed significantly to elucidate understanding of their roles in health and disease. She has developed antibody-based approaches to targeting these pathways and contributed to advancing these novel therapeutic antibodies in clinical trials for the treatment of systemic lupus erythematosus. Dr. Burkly has published over 100 peer-reviewed original papers, as well as numerous reviews and book chapters, and is an inventor on over 20 issued patents and patent applications.
Burkly’s team is currently working on the role of the TWEAK/Fn14 pathway in tissue fibrosis, and more broadly on pathways and mechanisms underlying the pathogenesis of human fibrotic diseases. http://www.tnf2015.org/content/Linda-Burkly
Lionel Ivashkiv
Lionel B. Ivashkiv, M.D. is Associate Chief Scientific Officer of Hospital for Special Surgery and Professor of Medicine and Immunology at Weill Cornell Medical College and Graduate School of Medical Sciences. He received his undergraduate degree from Columbia College and medical degree from Harvard Medical School. His laboratory studies cytokine-mediated pathogenic mechanisms in autoimmune and inflammatory diseases. He focuses on regulation of cytokine signaling, cytokine production, and inflammatory phenotype of myeloid cells and synovial fibroblasts that are important in disease pathogenesis, especially in rheumatoid arthritis, inflammatory osteolysis and systemic lupus erythematosus. His laboratory has worked extensively on signal transduction crosstalk and downstream transcriptional regulation and in recent years has established a research program connecting signaling pathways to chromatin and epigenetic regulation of inflammatory cell phenotypes. TNF-related projects in his laboratory include identifying novel signaling pathways and epigenetic mechanisms that regulate late phases of the TNF response. http://www.tnf2015.org/content/Lionel-Ivashkiv
David Komander
David Komander trained as a structural biologist at the MRC Protein Phosphorylation Unit in Dundee, working on the structure of PDK1, a master kinase in insulin signalling. During his postdoc in David Barford’s laboratory at the Institute of Cancer Research in London, he became interested in deubiquitinases regulating NF?B signalling, and determined structures of A20 and CYLD. His laboratory at MRC Laboratory of Molecular Biology aims to understand the cellular roles of unstudied ‘atypical’ ubiquitin chain types, and uses a wide range of techniques, from mouse models to single molecule approaches. http://www.tnf2015.org/content/David-Komander
Marja Mikkola
Marja Mikkola (née Rikkonen) received her PhD in 1994 in Department of Genetics, University of Helsinki, Finland in the field of molecular virology. In 1997 she changed her research focus and joined the laboratory of Professor Irma Thesleff as a post-doctoral fellow at the Institute of Biotechnology of the University of Helsinki. There she studied the function of the TNF-ligand ectodysplasin (Eda), which had been identified in 1996 as the causative gene behind the X-linked hypohidrotic ectodermal dysplasia syndrome.
Marja Mikkola is currently a team leader at the Developmental Biology Program of the Institute of Biotechnology. The research focus of her team is epithelial morphogenesis – how simple epithelial sheets are rearranged into more complex 3D structures. They use mainly hair follicle and mammary gland as model organs, and a combination of mouse models and organ and cell culture methods to elucidate the molecular and cellular basis of epithelial morphogenesis. Another field of interest is cell fate specification in these organs. They study the gene regulatory networks that operate during hair and mammary gland development, with focus on the Tnf/ectodysplasin/NF-?B and its downstream targets. Dr. Mikkola’s research team is particularly interested in how the numbers, patterns, and shapes of epithelial organs are determined. http://www.tnf2015.org/content/Marja-Mikkola
Martin Glennie
Professor Glennie received his PhD from The University of Southampton and continued his scientific career at the Department of Immunology, Babraham, Cambridge, UK, before returning to University of Southampton to become an academic lecturer in immunology specialising in antibody effector systems.
Throughout his career Professor Glennie has focused on translational research and understanding and improving how monoclonal antibodies (mAb) can be used in controlling cancer. He was one of the first to demonstrate effective treatment of cancer with antibody and to show that structural changes to an antibody, such as changing its valency, could have surprising benefits to therapeutic efficacy. More recently, he has turned his attention to an exciting new class of mAbs, which do not target the tumor directly, but which stimulate the body’s own immune system to promote long-last cancer protection. http://www.tnf2015.org/content/Martin-Glennie
"Bavituximab is a first-in-class phosphatidylserine (PS)-targeting monoclonal antibody that is the cornerstone of a broad clinical pipeline." -- Big Pharmas nightmare... unless they are fortunate enough to have The Bavi Edge!
