Plenary Lectures

Plenary 1

 

Balbir Singh

 

Faculty of Medicine and Health Sciences, UNIMAS, Sarawak Malaysia

PLASMODIUM KNOWLESI: PAST, PRESENT AND FUTURE

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.





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


Autophagy is a major degradation system in the cell. Intracellular components are sequestered by autophagosomes and then degraded upon fusion with lysosomes. Yeast genetic studies have identified more than 40 autophagy-related (ATG) genes. Many of these genes are conserved in higher eukaryotes, which brought about an exponential expansion of autophagy research in various organisms including mammals. The 2016 Nobel Prize in Physiology or Medicine was eventually awarded to the scientist who spearheaded the rapid development of the field, Dr. Yoshinori Ohsumi. However, there remain many fundamental questions in the autophagy field regarding its physiological roles and molecular mechanisms. For example, selective autophagy has become a hot topic but its precise mechanisms and physiological roles are still under investigation. We recently identified a novel receptor for autophagy of endoplasmic reticulum (ER-phagy). Also, it is now well appreciated that some ATG proteins have autophagy-independent functions or have made interesting evolution. We found that Plasmodium and Toxoplasma have a unique set of ATG proteins that contains a non-covalent type of the ATG12 system instead of the covalent type found in most eukaryotes. In this lecture, these novel findings made in vertebrates and parasites will be discussed.





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.





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


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 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


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 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


Autophagy is a major degradation system in the cell. Intracellular components are sequestered by autophagosomes and then degraded upon fusion with lysosomes. Yeast genetic studies have identified more than 40 autophagy-related (ATG) genes. Many of these genes are conserved in higher eukaryotes, which brought about an exponential expansion of autophagy research in various organisms including mammals. The 2016 Nobel Prize in Physiology or Medicine was eventually awarded to the scientist who spearheaded the rapid development of the field, Dr. Yoshinori Ohsumi. However, there remain many fundamental questions in the autophagy field regarding its physiological roles and molecular mechanisms. For example, selective autophagy has become a hot topic but its precise mechanisms and physiological roles are still under investigation. We recently identified a novel receptor for autophagy of endoplasmic reticulum (ER-phagy). Also, it is now well appreciated that some ATG proteins have autophagy-independent functions or have made interesting evolution. We found that Plasmodium and Toxoplasma have a unique set of ATG proteins that contains a non-covalent type of the ATG12 system instead of the covalent type found in most eukaryotes. In this lecture, these novel findings made in vertebrates and parasites will be discussed.





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.





Enquiries:

    

    Conference Secretariat 

    faobmbkl2019@gmail.com

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