Sequential development of embryoblast-like memory entities in human cancer tissues: an evolutionary self-repair structure with pluripotentiality.

Hidden collective organization of cancer cells can partially or completely return to embryoid genotype-phenotype with the plasticity to transform their morphology on cell embryoblast-like memory entities by expression of dormant genes that arise from embryogenesis. After hundreds of driver mutations, cancer cells gain new abilities or attributes and recapitulate early stages of embryogenesis. Our findings document how malignant tissues reactivated ancestral storage memory and elaborate inside tumor glands spiral-pyramidal-fractal chiral crystals (Tc) as geometric attractor proteins and biomimicry the primitive cellular blastocyst embryoblast fluid-filled cavity. The resultant evolutionary embryoblast-like entity has higher survivability and spatial cephalic-caudal growth organization with pluripotentiality that carry the correct DNA instructions to repair, and regenerate. The isolation and manipulation of these order structures can guide and control the regenerative pathway mechanism in human tumors as follows: modify and reprogram the phenotype of the tumor where these entities are generated, establish a reverse primordial microscopic mold to use the swirlonic collective behavior of cellular building blocks to regenerate injured tissues, convert cancer cells to a normal phenotype through regeneration using the organizational level and scale properties of reverse genetic guidance, global control of mitotic activity and morphogenetic movements avoiding their spread and metastasis, determining a better life prognosis for patients who incubate these entities in their tumors compared to those who do not express them. An emergent self-repair order structure, biological template can develop targeted therapeutic alternatives not only in cancer but also in treatment of autoimmune, viral diseases, and in regenerative medicine and rejuvenation.

Human somatic cells acquire the plasticity to generate embryoid-like metamorphosis via the actin cytoskeleton in injured tissues.

Emergent biological responses develop via unknown processes dependent on physical collision. In hypoxia, when the tissue architecture collapses but the geometric core is stable, actin cytoskeleton filament components emerge, revealing a hidden internal order that identifies how each molecule is reassembled into the original mold, using one common connection, i.e., a fractal self-similarity that guides the system from the beginning in reverse metamorphosis, with spontaneous self-assembly of past forms that mimics an embryoid phenotype. We captured this hidden collective filamentous assemblage in progress: Hypoxic deformed cells enter into intercellular collisions, generate migratory ejected filaments, and produce self-assembly of triangular chiral hexagon complexes; this dynamic geometry guides the microenvironment scaffold in which this biological process is incubated, recapitulating embryonic morphogenesis. In all injured tissues, especially in damaged skeletal (striated) muscle cells, visibly hypertrophic intercalated actin-myosin filaments are organized in zebra stripe pattern along the anterior-posterior axis in the interior of the cell, generating cephalic-caudal polarity segmentation, with a high selective level of immunopositivity for Actin, Alpha Skeletal Muscle antibody and for Neuron-Specific Enolase expression of ectodermal differentiation. The function of actin filaments in emergent responses to tissue injury is to reconstitute, reactivate and orchestrate cellular metamorphosis, involving the re-expression of fetal genes, providing evidence of the reverse flow of genetic information within a biological system. The resultant embryoid phenotype emerges as a microscopic fractal template copy of the organization of the whole body, likely allowing the modification and reprogramming of the phenotype of the tumor in which these structures develop, as well as establishing a reverse primordial microscopic mold to collectively re-form cellular building blocks to regenerate injured tissues. Tumorigenesis mimics a self-organizing process of early embryo development. All malignant tumors produce fetal proteins, we now know from which these proteins proceed. Embryoid-like metamorphosis phenomena would represent the anatomical and functional entity of the injury stem cell niche. The sufficiently fast identification, isolation, culture, and expansion of these self-organized structures or genetically derived products could, in our opinion, be used to develop new therapeutic strategies against cancer and in regenerative medicine.