What is the mechanism of the tumor-to-tumor carcinogenesis theory in heterogenic tumors?
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The tumor-to-tumor carcinogenesis theory in heterogenic tumors involves various mechanisms proposed in different studies. One theory suggests that cancer heterogeneity arises from epigenetic sources, leading to the emergence of multiple phenotypic states and kinetic paths from normal to cancer states, reflecting wider protein concentration fluctuations and weaker stability . Another hypothesis introduces the neosis paradigm, where cells escape senescence through neosis, producing a population of Tumor Repopulating Raju Cells (TRRCs) with transient stem cell properties, contributing to tumor heterogeneity . Additionally, the feedback loop model proposes that mutated genes act in a cell-heteronomous fashion, interacting reciprocally with stromal cells to form the cancer phenotype, contrary to the somatic mutation theory . Furthermore, the dysdedifferentiation process in metazoans, influenced by epigenetic mechanisms, can lead to a neoplastic phenotype, emphasizing the role of epigenetic changes in carcinogenesis .
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Open access•Posted Content 4 Citations | The neosis paradigm of carcinogenesis (NPC) proposes that tumor cells escape senescence via neosis, producing Tumor Repopulating Raju Cells (TRRCs) with transient stem cell properties, contributing to tumor heterogeneity. |
Open access•Posted Content | Not addressed in the paper. |
Open access 01 Jan 2003 | Not addressed in the paper. |
5 Citations | The "feedback loop model" suggests that tumor-stromal cell interactions, altered intercellular communication, and anomalous signal processing contribute to tumor development in a cell-heteronomous manner. |
30 Citations | The tumor-to-tumor carcinogenesis theory in heterogenic tumors is driven by epigenetic influences on gene regulation dynamics, leading to diverse phenotypic states and increased instability within the cancer cells. |
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