Cancers rely on multiple, heterogeneous processes at different scales, pertaining to many biomedical fields. Therefore, understanding cancer is necessarily an interdisciplinary task that requires placing specialised experimental and clinical research into a broader conceptual, theoretical, and methodological framework. Without such a framework, oncology will collect piecemeal results, with scant dialogue between the different scientific communities studying cancer. We argue that one important way forward in service of a more successful dialogue is through greater integration of applied sciences (experimental and clinical) with conceptual and theoretical approaches, informed by philosophical methods. By way of illustration, we explore six central themes: (i) the role of mutations in cancer; (ii) the clonal evolution of cancer cells; (iii) the relationship between cancer and multicellularity; (iv) the tumour microenvironment; (v) the immune system; and (vi) stem cells. In each case, we examine open questions in the scientific literature through a philosophical methodology and show the benefit of such a synergy for the scientific and medical understanding of cancer.

Plasticity is an important feature of modern cancer research. However, the level at which we should consider it remains an open question. Such debate is not new in the field of cancer and can be exemplified by the different models explaining carcinogenesis. Those models mostly explain cell transformation through the deregulation of the internal circuitry. In the last years, those models dramatically increased our knowledge and led to a series of short-term successes in terms of therapeutics. However, cancer drug resistance inevitably arises. Recently, studies on the so-called tumor microenvironment enriched the cell-centered perspective but it also enlarged the complexity of cancer etiology in particular for advanced diseases. Here, we suggest that the plastic and multi-sites specific nature of cancer combined with our incapacity to promise cure should push towards a new perspective where early clinical actions, instead of late ones, should be heralded as the priority of cancer research and care.

La principale théorie étiologique du cancer est génétique. Cependant, cette théorie présente d’importantes limites : elle ne permet pas de comprendre l’apparition et la progression de la maladie et les succès cliniques restent limités. Face à ces limites, certains biologistes ont plaidé en faveur d’un changement de théorie. L’objectif de cet article est d’analyser les conséquences des modifications de la théorie étiologique du cancer dans le domaine thérapeutique. Nous analyserons d’abord la manière dont le concept de microenvironnement tumoral permet de formuler au moins deux nouvelles théories sur l’étiologie du cancer pour lesquelles les événements génétiques ne sont plus considérés comme la principale et unique cause de la carcinogenèse. Puis, grâce à l’analyse de deux exemples, nous démontrerons que ne plus considérer la maladie comme le résultat uniquement de mutations génétiques modifie son explication causale et permet de nouvelles stratégies thérapeutiques.

No abstract