Figure 1.

Theoretical compilation on tumor evolution. Based on bibliographic data and isolated schemes, according to Heng and Heng (16), Casotti et al. (19), Niculescu (34), Niculescu (35), Erenpreisa et al. (48), Uthamacumaran (49), and Russo et al. (50). Cancer evolution involves a somatic lineage characteristic, immersed in proliferation following mitotic, amitotic and endoreplication cycles. However, this process reaches a cellular limit that leads to senescence which can bridge to a mitotic catastrophe followed by apoptosis with or without anastasis, but with a connection to mitotic slippage capable of guiding polyploidization. Polyploidization seems to act as a central connective hub for cell fusion mechanisms, syncytium formation, and cell-in-cell structures. Through this, a germline phase prone to the perpetuation of genomic, epigenomic, and quantum chaos for descendants is reached through depolyploidization. What might be imagined to be entirely random, a system dynamism through continuous self-organization also provides resistance to extinction. And have a phylogenetic regression to unicellular traits under an evolutionary access to ancient regulatory genetic networks and transcriptional regulatory complexes capable of providing singularities, such as bursting/fragmentation, budding mechanisms and formation of supergiant nurse cells, promoting cellular diversity according to intra- and intertumoral heterogeneity, breaking the barriers of the Hayflick limit, which is sustained by a common G + S ancestral cellular system from amoebozoans, metazoans, and fungi (AMF). From this perspective, cancer modulation is present through a mechanistic compilation of balanced processes on a profound systemic dynamism of genome, epigenome, and quantum chaos, and regulation of the biological, physiological, pathological, and normal circadian clock, requiring a robust therapeutic approach through lenses of personalized and adaptive approaches for effective modulation and mastery of cancer cells.