We have scheduled our Programs dividing them into Day 1, Day 2, Day 3 in order to make it convenient for you to attend in absolute comfort.
Dr. Dillman is Chief Medical Officer, AIVITA Biomedical Inc., Irvine, CA., and Clinical Professor of Medicine, University of California Irvine. His research focus is personal, patient-specific therapeutic cancer vaccines. He previously directed a bench-to-bedside translational cell biology laboratory specializing in patient-specific cell-based therapies. He was Chairman of the Cancer Biotherapy Research Group and a founding member and past-president of the Society for Immunotherapy of Cancer (SITC). He has authored over 300 publications. He earned degrees from Stanford and Baylor College of Medicine, then trained in internal medicine at Baylor, and hematology and oncology at the University of California San Diego.
Tumor initiating cells are an attractive target for cancer therapy. We have utilized short-term cultures of self-renewing tumors cells as a source of autologous tumor antigens (ATA). Such cells share phenotypic markers with stem cells, produce tumors in animals, and contain numerous non-synonymous mutations that may encode neoantigens. An irradiated tumor cell vaccine (TCV) was associated with a 29% 5-year overall survival (OS) in patients with metastatic melanoma. Autologous dendritic cells (DC) loaded with ATA from irradiated tumor cells (DC-ATA) was associated with a 33% 5-year OS in patients with metastatic renal cell cancer and 50% OS in metastatic melanoma patients. The superiority DC-ATA over TCV in metastatic melanoma was confirmed in a randomized trial: median survival more than doubled (20 to 43 months) and the risk of death was reduced by 70%. Toxicity was minimal. DCs were reliably derived from peripheral blood mononuclear cells, but only about 50% of tumor samples resulted in cell lines within four months. We are now using media that facilitates tumor-spheres with satisfactory cultures in less than four weeks. This approach has been associated with greater than 95% success in glioblastoma, ovarian cancer, melanoma, and hepatocellular cancer. At the time of treatment, DC-ATA are suspended in granulocyte-macrophage colony stimulating factor for subcutaneous injection at weeks, 1, 2, 3, 8, 12, 16, 20, and 24. Multi-institutional trials are in progress including: a double-blind randomized phase II trial in patients with a primary diagnosis of stage 3 or 4 ovarian cancer, and a single-arm phase II trial in patients with newly diagnosed glioblastoma that can be at least partly resected surgically. A trial is in development for patients with locally advanced hepatocellular cancer, and another trial has been approved for DC-ATA in combination with anti-PD-1 agents in metastatic melanoma.
Prof. Leong joined the California Pacific Medical Center in November 2009 as Chief of Cutaneous Oncology, Associate Director of the Center for Melanoma Research and Treatment and Member of the California Pacific Medical Center Research Institute from his previous position as Professor of Surgery and Director of the Sentinel Lymph Node Program, University of California San Francisco School of Medicine. His current research interest is in the molecular mechanism of cancer metastasis based on the clinical outcome of patients following resection of their primary tumor and sentinel lymph nodes.
Prof. Leong has been sitting on many positions since 1974 and has won numerous Honors & Awards since 1981, such as he is the Chair of Outcomes Research Committee of the Society of Surgical Oncology and Member of NCI Challenge Grant Review Committee in 2009.
Primary cancer grows within the cancer microenvironment (CM) consisting of fibroblasts, lipocytes, immune cells, lymphatic and vascular vessels and other parenchymal cells. Cancer growth is genetically dependent. Using multiplexed microscopy, genomic profiling and microRNA analysis, cancer growth in the CM and its routes of spread via the lymphatic and vascular vessels may be further defined on a molecular basis. Mutation gives rise to the unique characteristics of cancer heterogeneity with various clones competing to survive within the CM. By evading the host immune surveillance and by its intrinsic proliferative advantages using unique signaling pathways, cancer clones grow by expansion locally and tend to spread first through the sentinel lymph node (SLN) as a gateway in over 90% of the time. Patients with negative SLNs and yet develop systemic metastasis later represent those whose cancer cells would spread through the vascular system bypassing the SLNs. Recent mouse studies have found that VEGF-C induces lymphangiogenesis in the SLNs and facilitates systemic metastasis. The cancer-immune interaction varies among different patients and it is further complicated by continuous dynamic changes. The cancer cells may evolve into an aggressive form and the immune system may become tolerant to the newly evolved cancer clones when they develop PD-L1 or other molecules resulting in their growth. Alternatively, CTLA-4 on T Cells inhibits immune response against cancer. To date, blockade of the immune checkpoint pathways such as ipilimumab (anti-CTLA-4), pembrolizumab and nivolumab (both anti-PD-1) have resulted in significant anti-tumor responses with subsequent FDA approval of these drugs. The immune system and cancer growth are so complex that perhaps artificial intelligence needs to be developed to elucidate the proliferation of cancer cells in relationship to the structure and physiology of the lymphatic system in a new field, which may be coined as Oncolymphology. Cancer clonal dominance is akin to Darwin’s survival of the fittest developing under the influence of natural selection, in this case the CM acts like natural selection to allow the emergence of the fittest cancer clone(s). Understanding the molecular relationship between cancer growth and CM in the primary and metastatic sites as well as the host influence such as the immune system on cancer progression may allow the development of new therapy to block these elements either against the cancer cells directly or stromal cells indirectly.
Barbara Azzimonti is an assistant Professor of Microbiology and clinical Microbiology at the University of Piemonte orientale (UPO), in Novara, Italy.She received a master’s Degree in Biology at the University of Milan and a Specialization in clinical Pathology at the UPO.She is currently Head of the Laboratory of applied Microbiology at the Center for Translational Research on Autoimmune and Allergic Diseases (CAAD) in Novara.Her main research interests include the role of high-risk HPVs and bacteria in squamous epithelial malignancies, such as those of the skin, cervix,head & neck, and autoimmune disorders.
As highlighted in the last cancer report of the human Papillomavirs (HPV) Information Centre, the main viral etiological factor, responsible for anogenital and head & neck squamous epithelial (HNSCC) tumors, is represented by persistent high-risk HPVs (HR-HPVs) infection, which causes globally about half a million new cases/year. Several evidences are now strongly suggesting how also the microbiota has a role on the inflammatory, epithelial mesenchymal transition and transformation processes, although with mechanisms not yet clarified.In this review the state of the art on this theme and on the most promising in vitro models useful for the comprehension of host-pathogen interplay which occurs during anogenital and HNSCC carcinogenesis has been described.A deep MEDLINE search of the most pertinent scientific literature published in PubMed Central® was made. The investigation was limited to the indexed international articles and reviews published in the last 10 years.Overall, despite futher research is needed to obtain the same complexity of the in vivo environment, this analysis reported how in vitro 3D epithelial modeling is useful in the reproduction of the pathophysiological features of the epithelial tumors and therefore in the elucidation of the microbiota's role in HPV-related carcinogenesis
Professor Margaret Ng is currently Clinical Professor and Director of Blood Cancer Cytogenetics and Genomics Laboratory, Department of Anatomical & Cellular Pathology, the Chinese University of Hong Kong and also Honorary Chief of Service, Department of Anatomical & Cellular Pathology, Hospital Authority, Hong Kong SAR, China.
Professor Ng is a haematopathology specialist. She obtained MRCPath (UK) in 1993 and became FRCPath (UK) in 2002. FHKCPath and FHKAM (Path) were awarded in 1994 and 1995 respectively. Professor Ng also holds a MBA (Warrick, UK) awarded in 1996. She obtained her MD, CUHK in 2003 based on the theme-based research on cytogenetics and epigenetics of Chinese myeloma that led to the publication of a series of papers in British Journal of Haematology, Clinical Cancer Research, American Journal of Pathology, Human Pathology, Apoptosis, Leukemia & Lymphoma and Oncology Reports.
Her research interests mainly center on cytogenetics and genomics studies on blood cancers particularly myeloma and acute myeloid leukaemia. She published widely on Blood Cancer Research, Epigenetics and HLA studies in high impact factor journals like Blood, Haematologica, Clinical Cancer Research and Molecular Cancer.
Europe : +44 2039665767
Asia : +91 email@example.com
Subscribe To Newsletter