Biography:

Shanmugasundaram Ganapathy Kanniappan obtained his PhD degree from the University of Madras, India and underwent Post-doctoral training at the National Institute of Immunology (NII, New Delhi), University of California at Los Angeles (UCLA) and Johns Hopkins University (USA). Currently, he is an Assistant Professor at the Johns Hopkins University School of Medicine. He has been a recipient of Research Fellowship/Lectureship, (CSIR-UGC, India), a Concept Award (Department of Defense (DoD), USA), and a Pilot Research Grant (SIR, USA). He has several publications, and serving as an active Editorial Board Member and reviewer for prestigious journals.

Abstract:

Our understanding of aerobic glycolysis or tumor glycolysis popularly known as the Warburg effect has significantly advanced in the past two decades. Besides facilitating tumor growth and survival under unfavorable conditions, aerobic glycolysis also plays a pivotal role in therapeutic resistance. For example, the extracellular accumulation of lactate, a product of glycolysis impacts the tumor microenvironment (TME) and contributes to its low-pH and acidity. Noteworthy, TME acts as a barrier that blocks the efficacy of anticancer agents including chemotherapeutics and immune therapeutics. Furthermore, aerobic glycolysis has also been ascribed to support the immune-evasion of cancer. Thus, tumor glycolysis which is an integral component of the metabolic reprogramming (hallmark of cancer) is linked with immune-evasion (another hallmark of cancer). Using preclinical models, we demonstrated that deregulation of tumor glycolysis and/or the induction of metabolic stress sensitizes cancer cells to natural killer (NK) cell-cytotoxicity. Mechanistically, metabolic perturbation up-regulated the stress-inducible ligands that are recognized by specific NK cell receptors for further elimination. Notably, our recent data also show that sub-lethal, metronomic treatment with current, clinically relevant chemotherapeutics may also up-regulate such stress-inducible ligands indicating their sensitivity to NK cell mediated cytotoxicity. Taken together, these findings reiterate that cancer metabolism remains a viable therapeutic target which could be exploited for both chemo- and immunotherapies.

Biography:

Qi-Fei Wang has completed his Master’s degree from Dalian Medical University and is a PhD candidate at Tianjin Medical University. He is the Supervisor of Postgraduate students at the Dalian Medical University. He is a member of Rehabilitation Medical Association of Liaoning province China. He has published more than 12 papers in reputed journals.

Abstract:

Biography:

Adnan Yousif Rojeab has done his Doctorate in Electrical Engineering; he is a University Lecturer and Researcher. He has also worked at the Queen Mary University of London, University of West London. He is currently working at the London College. His research interests include action of electromagnetic fields on human system.

Abstract:

Cancer is a phenomenon of special reaction mechanism, which is functioning against the threat of severely acted tissues in the body. It is only created to eliminate severe damages and dangers that occur in the cells of the body, when the immune system fails to cure the damages. The effect of the cancer could only be ended when a direct, right and simple treatment method should be applied to cure the previous diseases that have caused the cancer, but not to attempt to treat the cancer itself. For the telomere matter, cancer cells have similar lengthening characteristics to those of germ cells. While in somatic cells, the telomere is shortening in every DNA replication. By applying a suitable amount and direction of a magnetic action on opposing the cancer cells, the lengthening of the telomere of the cancer could be inhibited, towards the somatic cells characteristics, and this application could be accepted as a method to treat cancer.

Biography:

Abstract:

As the chance of surviving, or achieving long term control, after cancer is improving, the number of people living with the consequence of cancer treatments at any one time is dramatically increasing. In the UK alone, this number has increased from two-three million in just five years. As consequences, the case for developing effective, self-help initiatives has never been stronger. This talk summarizes the international evidence, which proves that physical activity, nutrition and other lifestyle strategies can substantially reduce the risk of developing cancer, improve outcomes and ameliorate many of the long toxicities of consequences of biological therapies, chemotherapy and hormones and radiotherapy. These include fatigue, hot flushes, weight gain, arthritis, osteoporosis and mood disorders. This talk also highlights the underlying biological processes that take place in the body after a healthy lifestyle, which can have direct and indirect anti-cancer effects. By looking only at the scientific evidence, it breaks down the myths behind which foods to avoid and which to eat more of including nutritional interventions. It highlights the results of the world’s largest double blind randomized study of the National Cancer Research Network (NCRN) evaluation of a polyphenol rich nutritional intervention (The Pomi-T study). It emphasizes the potential risks and benefits of mineral and vitamin supplements to boost a healthy diet.

Biography:

Sonia A Melo has completed her PhD from the Faculty of Medicine of University of Porto and Post-doctoral studies from Harvard Medical School and MD Anderson Cancer Center. She is a Principal Investigator at I3S - Institute of Research and Innovation of the University of Porto and Institute of Molecular Pathology and Immunology of Porto University. Her career is fully committed to cancer research and has published more than 20 papers in reputed journals.

Abstract:

Cancer treatment experienced significant advance over the last years. This has been mainly due to therapy targeting of key biological mechanisms such as cell survival, proliferation, apoptosis, angiogenesis and, more recently, tumor immune response. Cell communication, however, despite playing a fundamental role in all steps of tumor progression, up to metastasis and therapy resistance, is still off the cancer therapy landscape. Hence, the major challenge of our work is to bring cell communication into the realm of cancer therapy. Exosomes, extracellular vesicles secreted by all cells, are key mediators of cell to-cell communication in cancer. We have identified a network of communication mediated by cancer exosomes in vivo, through the identification of their recipient cells. Additionally we show that targeting the most frequent pancreatic cancer exosomes communication route can be an effective target for pancreatic cancer therapy. Our strategy includes unique genetically engineered mouse models (GEMMs), which allow for the first time to trace exosomes in vivo and model therapeutic targeting of exosomes biogenesis. Our work demonstrates the in vivo significance of pancreatic cancer exosomes and opens a new avenue for groundbreaking discoveries in the treatment of pancreatic cancer and, eventually, other cancers.

Biography:

Zofia F Bielecka is a Medical Biotechnologist, currently working on tyrosine kinase inhibitors resistance in renal cell carcinoma. She is a PhD student at Warsaw Medical University, Poland (International School of Molecular Medicine). She is also a Research Assistant at Military Institute of Medicine in Warsaw, Poland and works in Laboratory of Molecular Oncology. She has gained considerable experience at the University of York, England and at the Lund University, Sweden. She has published 7 papers in reputed journals and has been serving a Reviewer in Elsevier journals. She is also a co-author of one patent application.

Abstract:

Primary-like resistance phenomenon to sorafenib (TKI) was previously observed in hypoxic conditions in two 3D models as well as in one 2D model in HKCSCs (human kidney cancer stem-like cells) cell line (Celprogen, cat no. 36117-44). Herein, we investigated the molecular background behind this phenomenon in 12 hypoxic total protein samples (each in triplicate) of renal cancer cells: primary HKCSCs resistant to sorafenib in hypoxia and other cell lines sensitive to sorafenib treatment in the same conditions: parental HKCSCs cell line, primary and metastatic renal cell carcinoma (RCC) cells from Memorial Sloan Kettering Cancer Centre (SK-RC-44 and SK-RC-45), metastatic RCC cell line (pleural effusion) ACHN cell line and HEK-293 cell line as a control. Additional control condition was untreated adequate cell lines in hypoxia. The acquired MS/MS data were pre-processed with Mascot Distiller software (v. 2.5, Matrix Science), and a database search was performed using the Mascot Search Engine (Matrix Science, Mascot Server 2.4.1) against the Swiss-Prot database restricted to human proteins. The results revealed potential candidates as elements of molecular mechanisms of primary resistance to sorafenib in renal cell carcinoma; those results will be further confirmed using Western blot analysis, possible confirming that apart from impact of hypoxia, the addition of targeted therapies alter signaling pathways in renal cancer cells, which means that mechanisms other than those involving hypoxia-inducible factors (HIFs) may be responsible for TKI-resistance.

Biography:

Mahmood Faraz is a PhD student in Umea University, Sweden.

Abstract:

Biography:

Carolina F Ruivo has completed her Master’s in Biomedical Engineering from IST, Lisbon in collaboration with University of Twente, Netherlands. Currently, she is working on a pre-doctoral project about the role of exosomes in tumor heterogeneity at Professor Sonia Melo’s Lab, Genetic Dynamics of Cancer Cells Group at University of Porto, Portugal.

Abstract:

Tumors are known to be heterogeneous, containing different cell types with distinct genetic and phenotypic features. Pancreatic cancer is a well-known example of tumor heterogeneity, showing a hierarchical organization of subpopulations with different tumorigenic potential. Intercommunication between tumor subpopulations is the key to development, progression and metastasis processes. Recent evidence shows that exosomes are important mediators of intercellular communication both at local and distant sites. If and how exosomes play a role in subpopulation communication is still unknown. In our work we have identified five subpopulations of pancreatic cancer cells based on cell surface markers which discriminate cells with different tumorigenic and self-renewal capacity. Using stable clones of cancer cells that express exosomes markers fused with fluorescent reporter proteins and secrete color-coded exosomes, we have studied the flow of exosomes between distinct subpopulations of cancer cells. Here we show that subpopulations of cancer cells communicate with each other via exosomes through an organized dynamic communication network (ExoNet). The presence of multicolor positive cells showed that exosomes are exchanged between different cancer cell subpopulations forming distinct routes of communication. The ExoNet reshapes in the presence of therapy to allow the tumor to respond and overcome the challenge. We have demonstrated that subpopulations of cancer cells communicate between them in a non-random manner using exosomes, and form a dynamic network of communication, which conveys the tumor with plastic properties that allows it to adapt in response to therapy.

Biography:

Abstract:

Pancreatic cancer (PDAC) represents one of the most lethal cancers mainly due to a lack of reliable therapeutic options. Cell communication, in spite of playing a major role in tumor progression, is still off the cancer therapy landscape. Exosomes, extracellular vesicles derived from the endocytic pathway, are an important cell-to-cell communication system with neighbor/ distant cells. Our main aim is to study the role of exosomes biogenesis during PDAC progression and understand if cancer exosomes biogenesis could be a new therapeutic target in PDAC. Rab GTPases are crucial proteins in exosomes biogenesis and are involved in all stages of the endocytic pathway. We show that during PDAC progression Rab-5, -7, -27a and -27b are differently expressed. Increased expression of Rab-27a and -27b correlates with an increase in exosomes number, and these features are associated with a more aggressive phenotype. Additionally, when treated with, the standard care chemotherapeutic for PDAC, cancer cells change their exosomes biogenesis pattern, increasing exosomes release. Finally, we are using an inducible and conditional genetically engineered Rab27a knockout mouse model that spontaneously develops PDAC, to study the role of exosomes and its biogenesis in disease progression and therapy response, evaluating exosomes mediated communication as a new therapeutic option in PDAC.