Abstract
In this chapter I outline some aspects that characterize biological explanations when the explananda are “functionalities”, ongoing dynamics. This sketch of a theory of explanation is tightly linked with the notion of Operational Integrating Systems, and, more generally, with all the dimensions of the Dynamic and Relational View of cancer explored in Chap. 5. We will deal with a fundamental epistemological duality constituted by, on one hand, the identification of the explanatory level according to our research interest and, on the other hand, the characterization of the system’s dynamisms we want to study. We will introduce the idea of “mesosystem” (between micro and macro) and its derivatives, arguing that reduction operates by “mesoscopic reasoning”, seeking the right explanatory level for the dynamic that needs to be understood. We will use the mesoscopic concept to reflect on why all cancer research seems to be converging on the tissue level and to derive some criteria for choosing a particular explanatory level in scientific practice. Reduction is thus methodologically adopted but it is constrained by validity conditions that are directly determined by the relational nature of the studied systems, whose elements are functionally defined by the higher level properties and ontologically dependent on them too. This is also why anti-reductionist views can play the role of defining the systems and the contexts, while reductionist views can’t. We will also deepen the crucial notions of “stability” and “specificity”, “determination” and “indetermination”. The two pairs of terms are fundamental to appreciate how our theory of explanation is deeply entangled with the operational nature of biological dynamisms.
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Notes
- 1.
The roots of this concept is found in the field of Systems Biology and of the methodological considerations presented by Noble (2006).
- 2.
Relevant considerations with respect to this issue have been also presented in Buzzoni (2015).
- 3.
This opens a philosophical reflection about the correspondence between the world and the way we know it through science. A compositional and pluralistic view of the scientific enterprise is better suited to explain why and how science works, but the philosophical implication of what is a common practice in science does not seem to be at hand yet.
- 4.
Moreover, describing functional dynamics that are nomologically dependent on the context through models, where those dynamics are reconstructed in mechanistic terms, allows us to make machines able to perform those functional properties through parts and devices that act in a mechanistic way. As noted by Agazzi, this possibility does not imply equivalence between living and non-living systems. The latter remain nevertheless ‘artificial’ because they are not able to undergo all the reciprocal relations in which natural organs are usually involved (Agazzi 1978).
- 5.
In this way, Schaffner makes explicit his original concern about the nature of theory in biology: while incorporating mechanistic explanations in his CM approach, he still takes into account the possibility that the real nature of biological theories might have been originally misconceived, avoiding the discussion of their nomological character or resolving it in mechanistic terms.
- 6.
- 7.
In the same article (2012), Schaffner is moving from coupling the term of “creeping” with “reductionism” to coupling it with “reductions”. The reason is the difference he makes with sweeping reductionism and the focus on the plurality of potential “creeping reductions” that can be performed and are exemplified in his paper. I adopt this useful distinction.
- 8.
On this point some considerations about the kind of “information” that is required in Schaffner’s definition of strong emergence can be developed: “all the information about the parts and the connections will never allow an explanation of the whole” (Schaffner 2006, p. 383) along with a discussion of the caveat about interrelations among parts included in the last part of the definition of “innocuous emergence” (ibidem, pp. 382–3).
- 9.
On this point see also footnote n. 10 of Chap. 5 and the relevance of the structure of molecular biology experiments.
- 10.
On this point of particular interest is the work done by Capp (2005). Special attention has been also devoted to the demonstration that genetic instability itself (therefore, the accumulation of mutations) follows the onset of an abnormal microenvironment, as studies seem to demonstrate the genetic instability of stem cells, when grown without control of the microenvironment (Maitra et al. 2005). The same could happen in pre-malignant cells, after the loss of the stabilizing effects from the organization of surrounding tissue. The subsequent deregulation of the DNA maintenance pathways, generated by alteration of the microenvironment, would be sufficient to generate the defects observed in cancer cells, so mutations that inactivate specific genes involved in cell differentiation may be, more generally, a consequence of the other non-mutational mechanisms, prompting the remark (already found in Chap. 1 regarding cell differentiation) that, “It may be more correct to say that cancers beget mutations than it is to say that mutations beget cancers” (Prehn 1994). Here, however, I focus on the context-dependence of the effect of mutations (i.e., specificity) once they had occurred.
- 11.
- 12.
Despite the wide-ranging debate on the question of determinism, in this study we refer to this concept only for those elements that can provide better understanding of the philosophical doctrines dominating also scientific research programs in the last century. No deterministic doctrine is a consequence only of the observation of phenomena, it is also, and above all, the result of a number of conceptual assumptions (Ferrater Mora 1994) that are not indifferent in scientific practice.
- 13.
The topic would have to be looked into in greater depth and from a broader perspective considering how, through analogous mechanisms, living systems can evolve and structure their “knowledge” of their functional state (phenotypic identity) and their environment. This would also be necessary in order to understand better how the informational dimension, contained in the genes, and that which pertains to the biological context, relate to one another. This point goes beyond the objectives that we have proposed here. It is a topic that is open to reflection concerning the peculiarity of the growth and development of living organisms.
- 14.
Such difference, that is crucial from an experimental point of view, can be further clarified analyzing different kinds of noise in biological sciences and how they are treated (cf. Bertolaso et al. 2013). It is interesting how this point meets the concern about the limitedness of the natural selection argument made by Vineis et al. (2010, cf. Section 2.8).
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Bertolaso, M. (2016). On Biological Explanations. In: Philosophy of Cancer. History, Philosophy and Theory of the Life Sciences, vol 18. Springer, Dordrecht. https://doi.org/10.1007/978-94-024-0865-2_6
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