Plenary Lectures

Plenary 1

 

Balbir Singh

 

Faculty of Medicine and Health Sciences, UNIMAS, Sarawak Malaysia

PLASMODIUM KNOWLESI: PAST, PRESENT AND FUTURE

Abstract


Tumor-infiltrating lymphocytes (TIL) are associated with survival in virtually every human cancer, but the mechanisms by which they confer protective immunity remain incompletely understood. Focusing on ovarian cancer, our group applies genomic and molecular pathology approaches to define the mechanisms by which the human immune system responds to the evolving tumor genome over space and time. We find that optimal anti-tumor immunity involves interactions between T cells and antibody-producing B cells in the tumor microenvironment. We have evidence that T cell clones track tumor clones over space and time and apply selective pressure that leads to reduced tumor clone diversity and progressive loss of immune recognition through several mechanisms. Our findings suggest new strategies to overcome these challenges through T cell engineering and other approaches. Toward this goal, I will discuss our cancer centre's new clinical trials program focused on T cell engineering strategies for gynecological and lymphoid cancers.





Plenary 2

 

Patrick Tan

Singhealth Duke-NUS Institute of Precision Medicine (PRISM) DUKE-NUS Medical School, Singapore

GENOMIC AND EPIGENOMIC PROFILES OF ASIAN ENDEMIC MALIGNANICES

Abstract


Many malignancies with high prevalence in Asia are caused by exposures to carcinogens, such as infectious agents and chemical toxins. Such cancers provide important “natural experiments” for understanding how environmental perturbations can disrupt normal cellular processes to ultimately drive tumour development, at both the genetic and epigenetic level. In this talk, I will describe how genomic approaches have led to important insights into the molecular processes driving various cancers with high-prevalence in Asia. Some of these insights may also prove relevant for treating such Asian cancers.





Abstract


Tumor-infiltrating lymphocytes (TIL) are associated with survival in virtually every human cancer, but the mechanisms by which they confer protective immunity remain incompletely understood. Focusing on ovarian cancer, our group applies genomic and molecular pathology approaches to define the mechanisms by which the human immune system responds to the evolving tumor genome over space and time. We find that optimal anti-tumor immunity involves interactions between T cells and antibody-producing B cells in the tumor microenvironment. We have evidence that T cell clones track tumor clones over space and time and apply selective pressure that leads to reduced tumor clone diversity and progressive loss of immune recognition through several mechanisms. Our findings suggest new strategies to overcome these challenges through T cell engineering and other approaches. Toward this goal, I will discuss our cancer centre's new clinical trials program focused on T cell engineering strategies for gynecological and lymphoid cancers.





Plenary 3

 

M Madan Babu

MRC Laboratory of Molecular Biology

Francis Crick Avenue, Cambridge Biomedical Campus

Cambridge CB2 0QH, UK

UNDERSTANDING VARIATION IN THE GPCR SIGNALLING SYSTEM

Abstract


G-protein-coupled receptors (GPCRs) participate in diverse physiological processes, ranging from sensory responses such as vision, taste and smell to those regulating behavior, the immune and the cardiac system among others. The ~800 human GPCRs sense diverse signaling molecules such as hormones and neurotransmitters to allosterically activate the associated G proteins, which in turn regulate intracellular signaling. In this manner, GPCRs regulate virtually every aspect of human physiology. Not surprisingly, GPCRs are the targets of over one-third of all prescribed human drugs. In this presentation, I will first discuss how one could leverage data on sequence changes across diverse species to infer selectivity determinants of GPCR-G-protein binding, which is critical to elicit the right intracellular response. I will then discuss how one could exploit data on completely sequenced genomes of over 60,000 individuals from the human population to gain insights into natural receptor variation, which can result in variable drug response. Finally, I will present ongoing work wherein by studying transcriptome data from over 30 different tissues in humans, one could begin to understand how alternative splicing can create diversity in GPCR signaling components, which may contribute to tissue-specific differences in receptor signaling. I will conclude by discussing how understanding variation at these different spatio-temporal dimensions, i.e. across different species, among different individuals of a species, and between tissues of a species, can provide a rich source of new hypotheses with implications for personalized medicine and understanding basic receptor biology.





Plenary 4

 

Leann Tilley

Department of Biochemistry and Molecular Biology, Bio21 Institute , The University of Melbourne,  Australia

NEW TECHNOLOGIES THAT PROVIDE INSIGHTS INTO MALARIA PARASITE VIRULENCE AND ANTIMALARIAL DRUG DESIGN

Abstract


Plasmodium falciparum is the most virulent of the human malaria parasites, causing ~440,000 deaths per year. Moreover, emergence of resistance to the first-line antimalarial drug, artemisinin, is looming as a major global health crisis. New therapeutic strategies are needed to prevent disease and to overcome drug resistance. My laboratory employs a suite of technologies to study P. falciparum – ranging from protein chemistry to drug development, from molecular genetics to cell biology, and from advanced imaging to structural biology techniques. The lecture will explore how pioneering imagining modalities such as Super-Resolution Optical Microscopy, Block-Face Scanning Electron Microscopy and single particle Cryo Electron Microscopy can provide insights into the workings of P. falciparum and in particular, the molecular basis of virulence. I will discuss the molecular mechanism of resistance to the front-line antimalarial drug family, the artemisinins, and describe our efforts to develop new antimalarial drugs that target protein homeostasis.





Plenary 5

 

Noboru Mizushima

Department of Biochemistry and Molecular Biology Graduate School of Medicine, The University of Tokyo, Tokyo , Japan

PHYSIOLOGICAL ROLES AND MOLECULAR MECHANISMS OF AUTOPHAGY

Abstract


Tumor-infiltrating lymphocytes (TIL) are associated with survival in virtually every human cancer, but the mechanisms by which they confer protective immunity remain incompletely understood. Focusing on ovarian cancer, our group applies genomic and molecular pathology approaches to define the mechanisms by which the human immune system responds to the evolving tumor genome over space and time. We find that optimal anti-tumor immunity involves interactions between T cells and antibody-producing B cells in the tumor microenvironment. We have evidence that T cell clones track tumor clones over space and time and apply selective pressure that leads to reduced tumor clone diversity and progressive loss of immune recognition through several mechanisms. Our findings suggest new strategies to overcome these challenges through T cell engineering and other approaches. Toward this goal, I will discuss our cancer centre's new clinical trials program focused on T cell engineering strategies for gynecological and lymphoid cancers.





Plenary 6

 

Brad Nelson

Co-Director, Immunotherapy Program

BC Cancer, Victoria BC, Canada

DECIPHERING AND RE-ENGINEERING THE IMMUNE RESPONSE TO CANCER

Abstract


Tumor-infiltrating lymphocytes (TIL) are associated with survival in virtually every human cancer, but the mechanisms by which they confer protective immunity remain incompletely understood. Focusing on ovarian cancer, our group applies genomic and molecular pathology approaches to define the mechanisms by which the human immune system responds to the evolving tumor genome over space and time. We find that optimal anti-tumor immunity involves interactions between T cells and antibody-producing B cells in the tumor microenvironment. We have evidence that T cell clones track tumor clones over space and time and apply selective pressure that leads to reduced tumor clone diversity and progressive loss of immune recognition through several mechanisms. Our findings suggest new strategies to overcome these challenges through T cell engineering and other approaches. Toward this goal, I will discuss our cancer centre's new clinical trials program focused on T cell engineering strategies for gynecological and lymphoid cancers.