Understanding cancer from an evolutionary perspective: high-risk reprogramming of genome-damaged stem cells
Background: One of the most astounding discoveries of recent times is the recognition that cancer embodies a transition from a higher level of metazoan cell organization to a more foundational premetazoic state. This shift is steered by genes housed within the ancestral genome compartment...
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Academia.edu Journals
2024-01-01
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| Series: | Academia Medicine |
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| author | Vladimir F. Niculescu |
| author_facet | Vladimir F. Niculescu |
| author_sort | Vladimir F. Niculescu |
| collection | DOAJ |
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Background: One of the most astounding discoveries of recent times is the recognition that cancer embodies a transition from a higher level of metazoan cell organization to a more foundational premetazoic state. This shift is steered by genes housed within the ancestral genome compartment, pervasive across all metazoan genomes, encompassing humans, and governed by a premetazoic ancestral gene regulatory network. This work aims to highlight the emerging field of evolutionary cancer cell biology (ECCB), which points to the deep homology between cancer and protist life cycles tracing back to the common ancestor of amoebozoans, metazoans, and fungi (AMF). The ECCB analysis reveals the essence of the non-gametogenic germline of the AMF ancestor, which serves as a blueprint for all metazoan germlines and stem cell lineages and controls the life cycle of cancer. Every germ and stem cell lineage of humans and metazoans traces its lineage back to this Urgermline, transmitting crucial processes such as asymmetric cell cycling, differentiation, stemness, and phenomena like germ-to-soma GST and soma-to-germ transition (aka epithelial-mesenchymal transition EMT and MET) to their subsequent evolutionary descendants. Oxygen-sensitive germline and stem cells suffer DNA double-strand breaks due to stress and oxygen ranges reminiscent of ancestral hyperoxia, leading to cell senescence. Cells that can overcome senescence can proliferate as defective symmetric cell division, paving the way for malignancy and polyploid giant cancer cell cancers. Conclusions: Understanding cancer from its evolutionary origins may help break some of the logjams in cancer prevention and open up new therapeutic pathways. |
| format | Article |
| id | doaj-art-93ca825e529f404ca614ccbe19513057 |
| institution | Kabale University |
| issn | 2994-435X |
| language | English |
| publishDate | 2024-01-01 |
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| spelling | doaj-art-93ca825e529f404ca614ccbe195130572025-02-10T22:30:32ZengAcademia.edu JournalsAcademia Medicine2994-435X2024-01-011110.20935/AcadMed6168Understanding cancer from an evolutionary perspective: high-risk reprogramming of genome-damaged stem cellsVladimir F. Niculescu0Retired Scientist, Diedorf 86420, Germany. Background: One of the most astounding discoveries of recent times is the recognition that cancer embodies a transition from a higher level of metazoan cell organization to a more foundational premetazoic state. This shift is steered by genes housed within the ancestral genome compartment, pervasive across all metazoan genomes, encompassing humans, and governed by a premetazoic ancestral gene regulatory network. This work aims to highlight the emerging field of evolutionary cancer cell biology (ECCB), which points to the deep homology between cancer and protist life cycles tracing back to the common ancestor of amoebozoans, metazoans, and fungi (AMF). The ECCB analysis reveals the essence of the non-gametogenic germline of the AMF ancestor, which serves as a blueprint for all metazoan germlines and stem cell lineages and controls the life cycle of cancer. Every germ and stem cell lineage of humans and metazoans traces its lineage back to this Urgermline, transmitting crucial processes such as asymmetric cell cycling, differentiation, stemness, and phenomena like germ-to-soma GST and soma-to-germ transition (aka epithelial-mesenchymal transition EMT and MET) to their subsequent evolutionary descendants. Oxygen-sensitive germline and stem cells suffer DNA double-strand breaks due to stress and oxygen ranges reminiscent of ancestral hyperoxia, leading to cell senescence. Cells that can overcome senescence can proliferate as defective symmetric cell division, paving the way for malignancy and polyploid giant cancer cell cancers. Conclusions: Understanding cancer from its evolutionary origins may help break some of the logjams in cancer prevention and open up new therapeutic pathways.https://www.academia.edu/114293312/Understanding_cancer_from_an_evolutionary_perspective_high_risk_reprogramming_of_genome_damaged_stem_cells |
| spellingShingle | Vladimir F. Niculescu Understanding cancer from an evolutionary perspective: high-risk reprogramming of genome-damaged stem cells Academia Medicine |
| title | Understanding cancer from an evolutionary perspective: high-risk reprogramming of genome-damaged stem cells |
| title_full | Understanding cancer from an evolutionary perspective: high-risk reprogramming of genome-damaged stem cells |
| title_fullStr | Understanding cancer from an evolutionary perspective: high-risk reprogramming of genome-damaged stem cells |
| title_full_unstemmed | Understanding cancer from an evolutionary perspective: high-risk reprogramming of genome-damaged stem cells |
| title_short | Understanding cancer from an evolutionary perspective: high-risk reprogramming of genome-damaged stem cells |
| title_sort | understanding cancer from an evolutionary perspective high risk reprogramming of genome damaged stem cells |
| url | https://www.academia.edu/114293312/Understanding_cancer_from_an_evolutionary_perspective_high_risk_reprogramming_of_genome_damaged_stem_cells |
| work_keys_str_mv | AT vladimirfniculescu understandingcancerfromanevolutionaryperspectivehighriskreprogrammingofgenomedamagedstemcells |