Programme
11.00-11.15. UiO Rector Svein Stølen and CEES Chair Kjetill S. Jakobsen.
Opening remarks.
11.15-12.00. Professor Charles Swanton
Cancer evolution and immune evasion: Challenges and opportunities
Francis Crick Institute & UCL Cancer Institute, London, UK
Link to Swanton's profile page.
12.00-12.15. Professor Nils Chr. Stenseth
Announcing the winner of the Darwin Price.
12.15-12.45. Break
12.45-13.30. Professor Felicia Keesing
An evolutionary perspective on the ecology of infectious diseases
Bard College, New York, USA.
Link to Keesing's profile page.
13.30-14.15. Professor Bruce Levin
A Darwinian perspective on adaptive immunity, senescence, and why we get cancers
Emory University, USA.
Link to Levin's profile page.
14.15-14.20. Professor Kjetill S. Jakobsen.
Closing remarks.
BIO AND ABSTRACTS
Professor Charles Swanton
MDPhD, FRCP, FMedSci, FAACR, FRS. Francis Crick Institute & UCL Cancer Institute, London, UK. (Swanton's profile page.)
Lecture title
Cancer evolution and immune evasion: Challenges and Opportunities
Abstract
TRACERx is a longitudinal cancer evolution study that aims to understand the interaction of complex evolving heterogeneous tumours with the tumour microenvironment across hundreds of patients. We have found that Chromosomal instability, is a major driver of intratumour heterogeneity contributing to parallel evolution, subclone selection and poor clinical outcome. The diversity of such tumour subclonal events in late stage tumours combined with tumour plasticity will likely confound the ability of monotherapy drugs targeting single clonal driver events to achieve sustained clinical benefit. We have found that tumour clonal neoantigens that may be recognized by cytotoxic T cells are major determinants of clinical outcome in treatment naïve and immune checkpoint inhibitor therapy treated patients, providing a therapeutic vulnerability in cancers with a high mutational burden. However, TRACERx has revealed multiple tumour adaptive mechanisms to immune predation, highlighting cancer chromosomal instability driving immune evasion through HLA class I and clonal neo-antigen loss as major routes to immune escape. How cancer genetic diversity limits an effective immune response and the role of clonal neoantigens as therapeutic targets to mitigate resistance and treatment failure will be discussed.
Bio
Charles completed his MDPhD training in 1999 at the Imperial Cancer Research Fund Laboratories and Cancer Research UK clinician scientist/medical oncology training in 2008. Charles is a senior group leader of the Cancer Evolution and Genome Instability Laboratory at the Francis Crick Institute and combines his research with clinical duties at UCLH, as a thoracic oncologist, focussed on how tumours evolve over space and time. Charles researches branched evolutionary histories of solid tumours, processes that drive cancer cell-to-cell variation in the form of new cancer mutations or chromosomal instabilities, and the impact of such cancer diversity on effective immune surveillance and clinical outcome. Charles is chief investigator of TRACERx, a lung cancer evolutionary study and the national PEACE autopsy program. (Full length bio for Swanton (pdf)).
Professor Felicia Keesing
David & Rosalie Rose Distinguished Professor of the Sciences, Mathematics, & Computing.
Bard College, Annandale, New York, USA. (Keesing's profile page.)
Lecture title
An evolutionary perspective on the ecology of infectious diseases
Abstract
What do we know about the ecology of emerging infectious diseases that can help us prevent future pandemics like covid-19? Most emerging infectious diseases of humans are "zoonotic", meaning that they are caused by pathogens that are shared between humans and other vertebrate animals. Some have concluded that this means that areas rich in natural biodiversity are a threat to us because the animals that reside in them could be sources of new pathogens. The past decade of research in the ecology of infectious diseases teaches us something quite different, however. We now know that some kinds of animals are much more likely to share their pathogens with us, and those species tend to persist and even thrive as biodiversity declines. The ultimate causes of this phenomenon, and many others in disease ecology, are infused with evolutionary questions and explanations that would not have surprised Darwin were he transported to the 21st century. I will conclude with three important and unanswered evolutionary questions underlying our current understanding of the ecology of infectious diseases.
Bio
Felicia Keesing is a biologist at Bard College in New York, USA who studies the consequences of interactions among species, particularly as biodiversity declines. Much of her work focuses on how species diversity influences the probability that humans and other animals will be exposed to infectious diseases. In addition, she has worked in Kenya for over 20 years studying how the disappearance of elephants, giraffes, zebras, and other large mammals influences the way African savannas function. In 2000, she received a United States Presidential Early Career Award for Scientists and Engineers from President Bill Clinton.
Professor Bruce R. Levin
Samuel Candler Dobbs Professor of Biology at Emory University. (Levin's profile page.)
Lecture title
A Darwinian perspective on adaptive immunity, senescence, and why we get cancers
Abstract
This talk will be a synthesis of classical ideas about the evolution and role of the adaptive immune systems of higher vertebrates, surveillance, and that about the evolution of senescence, with computer simulations. I will argue (a verb weaker than demonstrate) that the incidence of cancers in humans increases by a factor of four or so with age can be attributed to the senescence of the adaptative immune system and thereby the efficacy of immune surveillance.
Bio
Levin obtained his Ph.D. at the University of Michigan, 1967. Our current research includes mathematical and computer simulation modeling and experimental studies of the population and evolutionary biology of bacteria and their viruses and plasmids. Besides addressing precious academic ecological and evolutionary questions, like the selective forces responsible for the evolution of lysogeny and CRISPR-Cas mediated adaptive immunity, our research applies population dynamic and evolutionary theory and experiments to address health-related issues. Included among the latter are studies of the pharmaco- and population- dynamics of antibiotic treatment; the evolution of antibiotic resistance; and the joint action of antibiotics, phage, and the innate immune system in the treatment of bacterial infection. (Also recommended is the profile of Levin in PNAS from 2014.)
