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Fourth Philosophy of Cancer Biology Workshop

6 December | 10 h 45 min - 8 December | 16 h 20 min

The Fourth Philosophy of Cancer Biology Workshop will be held in Bordeaux, France.

Campus Victoire Amphi Sigalas (Building C – 2nd Floor)

3ter Place de la Victoire, 33000 Bordeaux, France

Programme

Registration

Context

Cancer is one of the main causes of death globally according to the World Health Organization. The biological complexity and heterogeneity of this disease (or group of diseases) make it very difficult to apprehend, control, and cure. For a long time, cancer has been little studied by philosophers of science. Most of the work in the humanities and the social sciences has focused on the social, anthropological, psychological, and ethical dimensions of cancer. Yet cancer is now becoming increasingly an object of study for philosophers of biology and philosophers of medicine. In particular, the scientific explanation, definition, classification and prediction of cancer as a biological and medical phenomenon face many epistemological challenges. Cancer research raises a host of experimental, theoretical, and conceptual issues that connect with most, if not all, the domains of today’s biology and medicine.

The main goal of this workshop is to provide a forum where philosophers of biology/medicine, scientists, and medical doctors meet to discuss the biological and medical science of cancer.

 

This workshop will be available through Zoom (ID: 818 4513 7866).

Registration is required.

This workshop will be recorded and available on our Youtube channel.

 

Plenary speakers

Maria Blasco (Centro Nacional de Investigaciones Oncológicas, Madrid, Spain)

Telomeres, Cancer and Aging

Telomeres are nucleoprotein complexes which protect the ends of linear chromosomes and which play a pivotal role in cellular and organismal ageing. Over the past two decades short telomeres have been associated with a large disease spectrum including degenerative diseases and cancer. In addition, a number of diseases known as telomeropathies or telomere sydromes, including some cases of aplastic anemia and pulmonary fibrosis, are linked to mutations in telomere maintenance genes. Our laboratory has made significant contributions to dissect the role of telomerase and telomere length as one of the key molecular pathways underlying cancer and aging. We previously demonstrated that telomerase activation by means of transgenesis as well as vector-based gene therapy delays a variety of age-related pathologies and increases survival in wild-type mice. Here, I will discuss our more recent work validating the effectivity of telomerase gene therapy for the treatment of diseases related to the presence of short telomeres including models for myocardial infarction, aplastic anaemia and pulmonary fibrosis.

Andrew J. Ewald (Professor and Director of Cell Biology, Johns Hopkins Medical School; Professor of Oncology and Co-Leader of the Cancer Invasion and Metastasis Program, Sidney Kimmel Comprehensive Cancer Center)

Unraveling the logic of cancer through analysis of cellular and molecular dynamics

From a patient perspective, the key distinction among tumors is whether the cancer cells remain confined with the tissue barriers of the original organ (localized disease, 99% 5 year survival) or whether they have spread through the body and formed new tumors in distant organs (metastatic disease, 27% 5 year survival). These facts led us to focus on understanding how breast cancer cells acquire the ability to metastasize. Metastasis is difficult to study directly because it occurs deep inside the body, takes place over months to decades, and involves many changes in the cancer cell and its microenvironment. To overcome these barriers, we have developed a series of ‘3D culture’ assays in which we explant tissue from normal organs or breast tumors into 3D gels composed of the structural proteins that surround cells in the body (extracellular matrix; ECM). These assays enable us to study how tumors grow, invade, enter blood vessels, evade the immune system, and establish new metastatic tumors. We use techniques from genetics and bioinformatics to identify the molecular programs driving metastatic cell behaviors and determine ways to stop those behaviors. We use techniques from tissue engineering and immunology to understand how the ‘tumor microenvironment’ conspires with cancer cells to drive metastasis and how we can leverage those insight to identify patients at the greatest risk of metastatic recurrence. I will present select examples from these research programs to provide context for a broader discussion of what we can glean of the underlying logic of cancer progression. Our starting framework is: (1) that developing epithelia exhibit most of the features we might think of as characteristic of cancer progression, including proliferation, ECM-degradation, and cell migration, (2) that these cell behaviors can be induced with simple molecular signals but that key decisions typically involve many molecular exchanges, and (3) that a key barrier that must be overcome during metastatic progression is the cell-death wiring that enforces tissue compartmentalization and multicellularity. I look forward to a robust trans-disciplinary discussion.

***

Carlo Maley (Arizona State University, USA)

What is cancer? A view across the tree of life

Cancer has usually been defined clinically by how it appears in humans, for understandable reasons. It is typically defined as a neoplasm that invades through a basement membrane or metastasizes to a distant tissue. However, cancer is a problem for any multicellular organism, and many of those organisms do not have basement membranes. The fundamental nature of cancer can be better understood by investigating the commonalities across the different branches on the tree of life that have independently evolved multicellularity, and how those foundations of multicellularity break down. I will also touch on our investigations across species to try to understand patterns of cancer susceptibility and resistance in animals.

***

Nicholas McGranahan (London, UK)

Exploring Cancer Evolution and Immune Escape

Cancer development within an individual is an evolutionary process. This has important clinical implications for cancer prevention and therapy, as well as our understanding of cancer progression and metastatic spread. Historically, applications of evolutionary biology to understand and control cancer progression have received relatively little attention.

Evolution by natural selection requires heritable variation within a population, and for this variation to influence survival. To understanding cancer evolution, then, we must: determine what generates diversity within tumours, evaluate how extensive this diversity is; distinguish between functional and non-functional diversity; and consider these factors in the context of the environment in which cancer evolution occurs.

In this talk, I will outline how we can exploit sequencing data to decipher cancer evolutionary histories. I will explore the importance of large-scale genomic events, including whole genome doubling, in shaping cancer evolution. I will consider how we can use bioinformatics tools to shed light on the interface between the cancer cell and the immune microenvironment, and mechanisms of immune escape.

***

Anya Plutynski (Washington University, USA, via Zoom)

Whither Philosophy of Cancer? Four Open Questions 

Philosophical work on cancer is relatively new. In this talk, I raise and provide preliminary answers to four open questions that should be of broad interest to any scholars with interests in this area: First, what tools are relevant to philosophy of cancer, or required to do philosophical work on cancer well? What needs to be invented? What can be adapted from other domains? Second, how can philosophical work on cancer contribute to philosophy more generally, or philosophy of science, in particular? Third, what is the larger agenda of philosophical work on cancer (i.e., beyond philosophy)? I.e., How can or should work on philosophy of cancer contribute to domains outside of philosophy? What role can or should philosophers play in engaging cancer researchers, whether in clinical oncology, epidemiology, or public health? How can or should philosophers contribute to the conversation with cancer patients, families and communities affected by cancer? Fourth and last, what are the major challenges facing current research? Where does philosophical work on cancer need to go next?

***

Eric Solary (INSERM U1287, Institut Gustave Roussy / Université Paris-Saclay, Villejuif, France)

What is the roadmap of early tumor development?

Cancer is commonly seen as a consequence of somatic evolution in which driver mutations accumulate in a cell, typically a stem or a progenitor cell. Most of these mutations (1-10 per cell division) are neutral passenger events, with only rare variants being potentially advantageous driver mutations in oncogenes and tumor suppressors. Contrary to germ cells, most somatic cells tolerate these potentially toxic alterations with a near complete absence of negative selection. The forces that subsequently promote tumor growth, progression and relapse are typically fuel by genetic and epigenetic diversification.

The recent demonstration that evolution of positively selected, genetically modified clones harboring common cancer driver gene mutations in a given tissue does not necessarily imply the presence of cancer in this tissue has blurred our understanding of cancer emergence mechanisms.  The frequency of some driver mutations is much higher in normal tissue than in cancer, suggesting that corresponding clones may not necessarily be destined for evolution to cancer and could even negatively select for carcinogenesis.  The accumulation of these clones in healthy tissues throughout life and their emergence promoted by chronic inflammation and lifestyle-related toxic insults negatively affect tissue function. The reasons why one of these clones becomes an overt malignant tumor while the others do not in a given tissue remain challenging, which limits our ability to accurately prevent cancer development and detect early-stage cancers.

We need a new roadmap of early tumor development, from a mutated but phenotypically normal cell to an invasive malignancy through localized tumor promoting events that may not always involve mutagenic processes. The increased number of mutated clones in ageing and chronically inflamed tissues interrogates the way we could stop cancer before it starts and interrogates the impact of rejuvenating or interception strategies eradicating non-malignant clones in healthy tissues to preserve the tumor suppressive properties of healthy tissues and decrease the risk of cancer development. The computational analysis of single-cell multi-omics and images collected longitudinally from a number of patients and patient-derived experimental models during the progression from health to disease may allow establishing an atlas of pre-neoplastic lesions and cells to guide an interceptive medicine applied to the eradication of early-stage cancers with otherwise lethal potential. We may also decipher the negative impact of specific ecosystems, including individual (genetic, epigenetic) and collective (chemicals, pathogens, radiations) ecosystems, on cancer emergence to generate innovative strategies that improve disease prevention.

 

Invited speakers

Bertrand Daignan-Fornier (Institute for Genetics and Cell Bilogy, IBGC, CNRS & Univ. Bordeaux, France) (Genetics, multicellularity and cancer)

Cancer and multicellularity: general ideas and an experimental approach

Multicellularity is a precondition to cancer, but, is cancer a breakdown of multicellularity? Current answers to this question schematically vary from cancer being a partial loss of cooperation, to cancer being a full way back to unicellularity. Those diverse answers lead to very different hypotheses on the origin of the disease and its overall raison d’être. Primarily, this debate questions the nature of multicellularity, the conditions of its emergence and maintenance, and how cancer interferes with these processes. To move along further in this debate, it would be helpful to be able to tackle experimentally the relationship between multicellularity and cancer. One way to do it would consist in asking: do cancer promoting conditions disfavor multicellularity? And if yes how? This could be done by comparing the effects of cancer promoting conditions on uni- and multicellular organisms otherwise as genetically similar as possible. However, multicellularity, as we know it, emerged a long time ago and there are no direct ways to conclusively compare unicellular and multicellular organisms that have evolved independently of each other for millions of years. To circumvent these issues, we are setting up an experimental approach based on synthetic biology on a yeast model that will allow us to compare ‘isogenic’ uni- and multicellular derivatives confronted to conditions that are known to promote cancer. Advantages and limits of the model will be discussed.

***

Mathieu Giraudeau (LIENSs, CNRS & Univ. La Rochelle, France) (Cancer and evolution)

Wildlife species as a source of inspiration in our fight against cancer?

Although the aetiology of cancer in humans and laboratory model organisms has received ample attention, many aspects of cancer remain poorly understood or seriously understudied. For instance, it is now widely recognized that cancer not only affects humans, but it occurs in most species of the animal kingdom, from hydra to whales. Despite increasing interests, our knowledge on cancer in wildlife is extremely limited, even regarding its prevalence in major vertebrate clades, its causes, consequences, life-history, genetic or physiological predictors or how environmental changes contribute to emerging cancer cases. Accurate estimates on cancer in wildlife promise extremely valuable information on oncogenic processes, as the limited research conducted on non-standard model organisms already provided tremendous insights on the natural mechanisms of cancer resistance. Very low cancer rates are ensured by duplications of the TP53 tumor-suppressor gene in elephants, overproduction of high molecular mass hyaluronan in the naked mole rats, interferonmediated concerted cell death in the blind mole rat and reduced growth hormone (GH)–insulin-like growth factor-1 (IGF1) signaling and microRNA (miRNA) changes in bats. Despite its value, robust cancer prevalence data on animals are surprisingly limited. Our research, at the interface of oncology, physiology, genetic, cellular and evolutionary biology, aims to unravel the cross-species diversity of cancer resistance, and highlight future avenues in the identification of efficient tumour-suppressor mechanisms. These findings will have huge potential to be translated to human patients through evolutionary medicine. Moreover, our results are expected to provide key information about cancer in wildlife, which is a top-priority due to the accelerated anthropogenic change of the past decades that might favor cancer progression in wild populations.

***

Fridolin Gross (ImmunoConcept, CNRS & Univ. Bordeaux, France)

Cancer and Complexity

What do biomedical researchers mean when they say that cancer is complex? Often what they mean is that cancer is a group of diseases that have defied efforts to cure or control. In this case, “complexity” does not refer to an intrinsic property of any particular object, but rather to a biomedical (or societal) problem. In some cases, however, what is meant is that a particular instance of cancer can be understood as a complex system. Such claims can in turn be interpreted in various ways, and it is not clear whether the implied notion of complexity actually accomplishes anything useful. To better understand the potential role of “complexity” in the context of cancer, I will attempt to place it within the general conceptual framework of biological complexity that I have recently developed. This framework applies the technical notion of “effective complexity” to descriptions of phenomena and their underlying mechanisms, and establishes a spectrum between two extremes that I call “emergent complexity” and “mechanical complexity,” respectively. This conceptual work is useful in particular because the prospects of particular strategies for understanding and managing it may depend on where cancer falls on this spectrum.

***

Lucie Laplane (IHPST, CNRS & Univ. Panthéon-Sorbonne; Gustave Roussy, France) (Philosophy of cancer: clonality)

Revisiting the clonal evolution model

Tumors are made up of heterogeneous cells. This heterogeneity makes cancer cells difficult to target and contributes to therapeutic avoidance and relapses. The clonal evolution model describes the dynamical processes of emergence, growth, decline or disappearance of clones constituting a tumor in space and time. Understanding these dynamics helps avoiding certain pitfalls (such as the selection of resistant clones) and lead to innovative therapeutic strategies taking these dynamics into account, such as adaptive therapies. However, the very concept of a clone is more ambiguous than it appears. I will start by showing that the notion of clone is necessarily relative (relating to the choice of traits used to identify and track clones), that its use is polysemous, and that the traditional conception of the clone is no longer in line with the data, nor with the emerging tools available to study clonal evolution. These mismatches might infringe scientific and clinical progress. A conceptual shift is thus needed to overcome these obstacles, and I will propose some solutions to both clarify the concept and make it more operational.

***

Maël Lemoine (ImmunoConcept, CNRS & Univ. Bordeaux, France)

What does it mean to say that ‘aging causes cancer’?

It is often claimed that ‘aging causes cancer’ and that a good strategy to prevent or cure cancer is to target some processes of aging (the ‘geroscience’ agenda). Yet the meaning of the initial claim is unclear. This is because aging and cancer are understood alternatively in interaction (what they cause to one another) and in extension (what they share with one another). Instead, I propose to investigate whether organismal senescence, the general property of organisms that age as opposed to those that don’t, is a necessary condition for cancer to be possible. This requires first to question the received view that cancer and ‘successful aging’ simply are opposite trajectories: indeed, what is to be understood, is why exactly cancer becomes possible, in most cases, only after an organism has “aged” enough, and whether this indeed makes it a necessary condition. ‘Organismal senescence’ could be characterized as a drift in tissue homeostasis rather than by the passive accumulation of damage. Then, I show that as far as we know, only senescent animals (i.e., bilaterians) can have cancer, but that it requires a specific form of organismal senescence for cancer to be possible, as some senescent organisms never (C. elegans) or rarely (naked-mole rat) have cancer. In the end, I propose a short reinterpretation of the hot topics of cancer geroscience in the light of this new conceptual framework.

***

Thomas Pradeu (ImmunoConcept, CNRS & Univ. Bordeaux, France)

Reconceptualizing the interactions between the immune system and cancer

The field of cancer immunology is thriving, with major empirical and clinical results. Yet it is built on a relatively traditional conception of the immune system. In this talk, I show how recent reconceptualizations and extensions of immunity may prompt a new and much richer understanding of the interactions between cancer and the immune system.

***

Rodrigue Rossignol (INSERM & Univ. Bordeaux, France) (Cancer & metabolism)

Mitochondria in cancer: a malignant symbiosis?

***

Isabelle Sagot (Institute for Genetics and Cell Bilogy, IBGC, CNRS & Univ. Bordeaux, France)

On a definition of cellular quiescence

For a long period, cellular quiescence was considered as a “sleeping” inactive default state with a poorly acknowledged biological relevance. Yet, an increasing amount of literature is progressively revealing that quiescence is central in many biological processes, such as organism development or tissue maintenance and for major human pathologies such as cancer. In fact, cellular quiescence is captivating, as it is diverse and multifaceted. But, by the way: what is a quiescent cell?

***

Bernhard Strauss (Univ. Cambridge, Department of Biochemistry, UK)

“Rethinking Cancer” – when are we done? How conceptual progress in explaining cancer might inform research practice and novel treatment approaches

Despite the persistent dominance of the somatic mutation paradigm in current experimental and therapeutic approaches, alternative conceptual frameworks are being increasingly considered and applied in basic and clinical cancer research. In addition, the systematic study of the theoretical underpinnings of cancer research over the past decade by philosophers of science has greatly enhanced and clarified our understanding of the role of theory in this field. However, this has also led to the view that various conceptual frameworks that support different research programs would be equally valid in dealing with the complex biological phenomenon that cancer is. Such a stance of conceptual relativism or perspectivism, will most likely fail to guide innovation in experimental and therapeutic practice in a constructive manner. I propose here that the recent convergence of conceptual innovations and of results in basic and clinical research clearly point toward several gaps in our mechanistic understanding of cancer that can be well defined, and need addressing at the tissue and organism levels to make more progress with therapy.

 

Selected speakers

Nicholas Binney (University of Exeter, United Kingdom)

Liquid Biopsy, Multi-Cancer Diagnosis and the Evaluation of Medical Tests

This paper explores how the new technology of liquid biopsy may shape the ontology of cancer, and the epistemic implications of this shifting ontology for diagnostic test evaluation. Traditionally, cancer has been encountered as a growth, located in one of the patient’s tissues. The tissue of origin has framed the classification and diagnosis of specific types of cancer. This traditional approach to oncology tended to treat patients with the same histological diagnosis as interchangeable for most intents and purposes. Liquid biopsy is a new technology, which uses liquid samples, such as blood or saliva, to test for circulating tumor cells or circulating tumor genetic material. Tumors shed cells and genetic material into the circulation as they grow, and this can provide information about genetic and epigenetic heterogeneity of patients with the same histological diagnosis. However, liquid biopsies can also be used in other, more philosophically radical ways. Medical researchers are exploring the possibility that liquid biopsies can be used to screen apparently healthy people for multiple forms of cancer at once. Such tests (e.g. CancerSEEK, GRAIL, PanSeer and DELFI) are called ”multi-cancer” tests. Such tests are ontologically interesting for several reasons. Firstly, their use runs counter to the prevailing narrative of precision medicine: that medical progress will come with the stratification of patient groups, targeting ever smaller groups of patients. These tests are designed to detect groups of patients that are larger than the group of patients with the same histological diagnosis. Perhaps this is an example of imprecision medicine. Secondly, their use opens the possibility of encountering cancers without identifying a growth, which may diminish the importance of the histological diagnosis to cancer ontology. These ontological considerations have epistemic consequences for the evaluation of multi-cancer tests. Traditionally, the evaluation of medical tests has been highly focused on diagnostic accuracy. However, if patients are much more heterogeneous than this, so that patients with the same disease status have different prognosis, respond to different treatments, etc., then tests can be useful even if they are not accurate.

***

Benjamin Chin-Yee (Western University, Canada)

Minimal Residual Disease: Premises Before Promises

Minimal or measurable residual disease (MRD) is a concept increasingly employed in oncology research and practice which straddles the boundary between biomarker and surrogate endpoint. In hematology-oncology, MRD refers to a lower limit of detection of malignant cells or molecular markers, with ”MRD positive” versus ”MRD negative” status often touted as a key biomarker and one of the most important predictors of disease relapse in several cancers. As a result, MRD status is not only used as a biomarker to assess prognosis and guide therapy but also as a surrogate outcome measure in clinical trials in oncology. The concept of MRD intersects with issues in the ontology of cancer explored by philosophers of biology and medicine, including debates over cancer stem cell (CSC) biology and processes of tumour evolution (Germain, 2012; Lean and Plutynski, 2016; Laplane, 2018). However, a philosophical analysis of MRD with a specific focus on ontological and epistemological issues arising in translating this concept from research to practice is currently lacking. This paper analyzes a series of ontological, epistemological and methodological challenges with MRD, critically examining its expanding use as a biomarker and surrogate endpoint in hematology-oncology.

***

Matthieu Duchmann (The Puissant Lab, INSERM, France)

Parallel evolution of signaling mutations in Core-binding factor acute myeloid leukemia.

Somatic mutations occur during cancer initiation and progression. Intra-tumoral genetic heterogeneity is a key feature of cancer and is dynamic during evolution. In acute myeloid leukemia (AML) clonal architecture can be linear or branched. A linear architecture is characterized by a sequential acquisition of mutations in one ancestral clone, each new subclone stemming from the precedent one. Branched architecture is characterized by the occurrence of two independent mutations in one ancestral clone. When these two mutations affect the same biological pathway, this specific branched architecture is called ”parallel evolution”, as it lead to the coexistence of two clones functionally related. Core-binding Factor (CBF) AML is a subtype of leukemia characterized by an initiating translocation involving RUNX1 or CBFB genes, two components of the CBF complex that important in normal hematopoiesis. Additional genetic events are necessary for CBF AML progression, including mutations in tyrosine kinase receptor (TKR) and downstream signaling effector genes including RAS pathway. We previously reported in a large cohort of CBF patients treated by intensive chemotherapy that one third of patients had multiple TKR/RAS mutations on bulk targeted sequencing of diagnostic samples. This feature was associated with an independent poorer prognosis after treatment by chemotherapy owing to higher rates of relapses. The aim of this talk is to better understand the relationship between clonal architecture and chemoresistance, using CBF AML as a model.

***

Jean Feunteun (Institut Gustave Roussy / Université Paris-Saclay, Villejuif, France)

Tumor cell malignancy: a complex trait built through recip-rocal interactions between tumor cells and tissue-body system.

Since the discovery of oncogenes and tumor suppressor genes in the late past century, cancer research has been overwhelmingly focused on the genetics and biology of tumor cells and hence has addressed mostly cell-autonomous processes. From the perspective of geneticists, tumors arise from the transformation of cells initiated by cell autonomous oncogenic events and the emergence of a tumor in situ and the possible dissemination of metastases is determined by additional oncogenic events.
Several seminal observations have highlighted the role of non-cell autonomous effectors in tumor growth and metastasis. But, given that both cell autonomous and non-autonomous events are present at diagnosis, it is in fact impossible to know if the malignant transformation is initiated by cell autonomous oncogenic events or by non-cell autonomous conditions generated by alterations of the tissue-body ecosystem.
This presentation aims at resetting cancer geneticists’ short sightedness to incorporate the fact that tumor cell malignancy should no longer be considered as an exclusive property of cells carrying oncogenic driver events, but rather as a complex trait (in the genetic sense), built in through reciprocal interactions between tumor cells and tissue-body ecosystem.

***

Simon Okholm (ImmunoConcept, CNRS & Univ. Bordeaux, France)

Rapamycin: an anti-aging treatment or cancer suppression?

The mTOR-modulating drug known as rapamycin is today considered one of leading biomedical compounds capable of slowing down the aging process in humans, yet the nature of cancer is deeply intertwined in this treatments geroprotective potential. This pro-longevity spurred a lot of public and scientific interest in rapamycin as potentially being the first pharmacological drug to curb multiple age-related diseases and improve various aging phenotypes. However, rapamycin’s geroprotective effects were soon called into question: The longevity effects observed could alternatively be explained by rapamycin’s ability to postpone one particular and highly prominent age-related disease in laboratory mice, namely neoplastic diseases rather than targeting the aging. Now, a decade later and more than 30 mouse studies on rapamycin, scientists are still debating and advancing new arguments for why the longevity effects produced by rapamycin are either due to suppressing the life-limiting effects of cancers in particular or the aging process in general.
So far, no systematic analysis of all arguments advanced for each side have been carried out with the explicit aim to evaluate its semantic, its epistemological, and the ontological issues it raises. To carry this out, we first need to understand what rapamycin is, its history, and how the drug works on a molecular level, namely by targeting nutrient-sensing hub known as mTOR network. Hereafter we can turn to scrutinize the arguments advanced by each side of the debate for their plausibility. Our argument will be that while each side has brought up some valuable arguments, there nevertheless might be one unexplored option to experimentally test the central crux of the debate: Feeding rapamycin to cancer-resistant so-called ‘super p53 mice’ to see if their longevity effects are ‘additive’ of one another as has been suggested or if no additional lifespan extension is shown, thereby suggesting that cancer might explain rapamycin’s geroprotective effects.

***

Jonathan Sholl (ImmunoConcept, CNRS & Univ. Bordeaux, France)

Learning from the intersection of cancer metabolism and nutrient regulation.

Philosophers of cancer have explored a variety of issues concerning cancer biology, e.g., causality, complexity, reductionism, cancer models, notions like ‘stemness’, the explanatory role of genetics and evolution, etc. So far, there have been no systematic analyses of the nutrient dysregulations found in tumoral metabolism. Interestingly, while the supposed ‘reprogramming’ of metabolism is considered an ‘emerging’ cancer hallmark, there is no clear consensus as to what exactly constitutes this phenotypic shift. There is thus much philosophical work to be done here. My suggestion is to place cancer metabolism within the broader context of regulatory physiology – how cells and organisms respond to variations in nutrient availability and maintain internal nutrient levels. Bringing these areas together, I raise questions in both directions: how can some of the changes characterizing cancer metabolism provide insights into cellular and organismal nutrient regulation and how does this nutrient regulation in turn clarify the nature and complexity of cancer biology? Interestingly, exploring these questions will contribute to recent philosophical-scientific debates about cancer as a case of multilevel selection and the evidence in favor of this view. While nutrition and tumor metabolism remain largely unexplored by philosophers of cancer, by showing ways in which regulatory physiology and oncology can be mutually illuminating, I hope to entice philosophers to explore the potential links between nutrient (dys)regulation and cancer formation.

 

 

 

 

Call for abstracts

The organizing committee welcomes abstracts for 20 minutes’ oral presentations on subjects that explore a problem with a conceptual, theoretical, methodological and/or philosophical approach and directly address questions relevant to cancer research.

Examples of questions that this workshop will raise include:

  • How is the complexity of cancer addressed in scientific and medical practices?
  • Is there an underlying logic of cancer?
  • What are the epistemic implications of different approaches to cancer?
  • How are questions about the ontology of cancer related to methodological issues?
  • To what extent are questions concerning the nature of cancer intertwined with issues concerning diagnostics and/or treatments?
  • How are new approaches, such as cancer genomics, organoids, and organ-on-chip technologies, influencing cancer research?

The call is open to philosophers, scientists, medical doctors, and more generally to everyone interested in the analysis of conceptual, theoretical, and methodological problems of cancer biology.

Abstract submission: Abstracts should be between 1000-1500 words long and must be submitted via https://philofcancer.sciencesconf.org/ by October 17th, 2021.

Notifications will be sent by November 2nd, 2021.

If you have any question, please contact cluijten@immuconcept.org

 

 

Organizing committee

Fridolin Gross (ImmunoConcept, CNRS & University of Bordeaux, France)

Lucie Laplane (IHPST, CNRS & University Paris 1; Gustave Roussy Cancer Center, France)

Maël Lemoine (ImmunoConcept, CNRS & University of Bordeaux; IHPST, CNRS & University Paris 1, France)

Corinne Luijten (ImmunoConcept, CNRS & University of Bordeaux, France)

Thomas Pradeu (ImmunoConcept, CNRS & University of Bordeaux; IHPST, CNRS & University Paris 1, France)

 

 

Scientific committee

 

Patronage Committee in Bordeaux

Bertrand Daignan-Fornier (Research Director in Genetics at CNRS, Head of IBGC lab, Bordeaux)

Julie Déchanet-Merville (Research Director in Immunology at CNRS, Head of ImmunoConcept lab, Bordeaux)

Jean-Luc Feugeas (Researcher in Applied Mathematics, Center for Intense Lasers and Applications, Bordeaux)

Guy Kantor (Professor of Medical Oncology and Radiotherapy, Institut Bergonié, Bordeaux)

Nicolas Larmonier (Professor of Immunology, Head of the research axis Cancer Immunology and Immunotherapies at ImmunoConcept, Bordeaux)

Simone Mathoulin-Pelissier (Professor, Head of ISPED Bordeaux Population Health, Member of Cancer & Environment Team, & Deputy Director of SIRIC Brio)

Jean-François Moreau (Professor Emeritus of Immunology, Univ. Bordeaux, Pellegrin Hospital & ImmunoConcept, Bordeaux).

Violaine Moreau (Research Director at INSERM, BaRITON, Bordeaux Research in Translational Oncology, Bordeaux)

Maya Saleh (Professor of Oncoimmunology at ImmunoConcept, Bordeaux)

Isabelle Sagot (Research Director at CNRS, IBGC, Bordeaux)

Frédéric Saltel (Research Director at INSERM, BaRITON, Bordeaux Research in Translational Oncology, Bordeaux)

David Santamaria (Group leader, Novel mediators in lung oncogenesis, IECB, Bordeaux)

Pierre Soubeyran (Head of research of Institut Bergonié, Comprehensive Cancer Center in Bordeaux, and Professor of Medical Oncology at the University of Bordeaux)

Martin Teichmann (Professor, Head of Transcription and Tumor Laboratory, University of Bordeaux)

Christine Varon (Professor, BaRITON, Bordeaux Research in Translational Oncology, Bordeaux)

Details

Start:
6 December | 10 h 45 min
End:
8 December | 16 h 20 min
Event Categories:
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Venue

Bordeaux Campus Victoire
Amphi Sigalas, 3ter Place de la Victoire
Bordeaux, 33000 France
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