3). This view would thus expand on a previous biophysical concept postulating (molecular) entropy

as a key driving force for carcinogenesis [51] and, moreover, be in line with observations on the (prognostically adverse) structural entropy of lung tumors [52] and the entropic accumulation of splicing defects in various carcinomas [53]. Figure 3 Schematic representation of the increase in entropy (S) associated with premalignant, subcellular changes over time and its potential reversal. More specifically, S gradually increases from the state of oncoprotein metastasis (OPM) in conjunction with oncoprotein (OP)-tumor suppressor protein (TSP) complex formations (OP × TSP) to the state of (epigenetic) tumor suppressor gene (TSG) promoter hypermethylations (hyperCH3) and again to the state of LY2109761 in vivo TSG loss of heterozygosity (LOH) defects, whereby each of their neutralization requires a corresponding amount of energy (E) or negative entropy, respectively,

intrinsic to a given dose of a therapeutic compound (Rx). In this context, it should be specified that the (premalignant) stages of an OPM encompassing OP-TSP complex formations and of its epigenetic equivalent may be subject to a relatively high degree of spontaneous reversibility through PD0325901 mouse natural mechanisms of cancer surveillance. As a result, these premalignant processes might be reversed-in a dose-dependent fashion corresponding to distinct energy (or negative entropy) values (Fig. 3) – by antagonistic quantum states induced e.g. by therapeutic cell-permeable peptides in

conjunction with the growth-suppressive function of endogenous proteins that these peptides may recruit through physical interactions [17, 43, 54]. In accordance with this view, it has been shown for a series of antineoplastic compounds including peptides that the inhibition of cell cycle progression ensuing from the disruption of protein-protein interactions requires a lower dose of the respective anticancer agent as compared to that at which (programmed) cell death (e.g. by nuclear fragmentation) occurs in cancer cells. Moreover, the energetic or quantum states of untreated vs. treated (pre)malignant cells should be explored by physical methods, thus considerably expanding on measurements of quantum states in elements used by living systems such as shown for photosynthetic reactions [55, 56]. almost These envisioned advances may not only be decisive for the further refinement and increased precision of diagnosis and therapy of cancer disease, e.g. by means of sequential mapping and targeting of neoplastic “”fields”" [5, 17, 51], but also further substantiate the insights of Delbrück et al. at the interface between biology and physics [57], ultimately making it likely that quantum biology will come of age in the foreseeable future. References 1. Nowell P, Hungerford D: A minute chromosome in human chronic granulocytic leukemia [abstract]. Science 1960, 132:1497. 2.