Carcinogenesis and Morphogenetic Field
The Somatic Mutation Theory of carcinogenesis encompasses significant inconsistencies and, as now admitted by its own supporters, can hardly explain the emergence of tissue-based processes, like cancer. The increasingly burden of unexplained paradoxes and shortfalls is driving the current carcinogenesis theory toward a blind alley. Ignoring these paradoxes is unsustainable. By avoiding facing these conundrums the scientific community is depriving itself of the opportunity to achieve real progress in this important biomedical field. To remedy this situation, cancer research should be reframed by embracing new theoretical perspectives, taking the cells-microenvironment interplay as the privileged etiopathogenic level of observation, and by assuming radically different premises as such provided by The Tissue Organization Field Theory (TOFT), according to which cancer arises as a consequence of altered cross-talk among cells and their microenvironment, involving both biophysical and molecular cues Indeed, the cell-stroma interaction plays a pivotal role in both cancer onset and prevention, by providing a set of biophysical and biochemical cues, which drive cell towards neoplastic transformation, eventually leading to metastasis. However, experimental and clinical evidences suggest that cancers can be induced to become quiescent, differentiate, die or form completely normal tissues, if provided with the correct set of complex signals, as conveyed by embryonic tissues or other microenvironmental cues. These data suggest that by manipulating cancer microenvironment may help in opening new avenues for therapeutic solutions.
Our lab is especially committed in investigating how both cytoskeleton (CSK) and nucleoskeleton (NSK) – thought to convey mechano-based signals from the microenvironment to the cell biochemical and genetic pathways – changes in cancer cells. Namely, we are focusing on how architecture of both CSK and NSK undergo relevant modifications during phenotypic transition (during cell differentiation and in cells acquiring an invasive property) and cancer ‘reversion’, induced by the morphogenetic field or anti-tumoral drugs.