This correspondence to Gene&Diseases calls attention to the controversy between proponents of genetic modification in carcinogenesis and supporters of non-mutational oncogenesis.Data from molecular cancer research...This correspondence to Gene&Diseases calls attention to the controversy between proponents of genetic modification in carcinogenesis and supporters of non-mutational oncogenesis.Data from molecular cancer research and findings from evolutionary cancer cell biology support the latter claim and provide no rationale for the mutational origin of sporadic cancers.It is more conceivable that the general susceptibility of asymmetric cell division(ACD)phenotypes to oxygen leads to irreparable DNA defects and dysregulated defective symmetric cell division(DscD)phenotypes.展开更多
From an evolutionary perspective,the human cancer genome is based on an ancient gene module developed by the common ancestor of the Amoebozoa,Metazoa,and Fungi(AMF).^(1)The transition phase to multicellularity(premeta...From an evolutionary perspective,the human cancer genome is based on an ancient gene module developed by the common ancestor of the Amoebozoa,Metazoa,and Fungi(AMF).^(1)The transition phase to multicellularity(premetazoan period)was a rather long period of evolu-tionary attempts and failures.During this time,suppressor genes were evolved to deactivate the G+S cell system inherited from the AMF ancestor.展开更多
The comment of Ivanovic and Vlaski-Lafarge on my article“Cancer genes and cancer stem cells in tumorigenesis:Evolutionary deep homology and controversies”opens up a welcome discussion on the evolutionary history of ...The comment of Ivanovic and Vlaski-Lafarge on my article“Cancer genes and cancer stem cells in tumorigenesis:Evolutionary deep homology and controversies”opens up a welcome discussion on the evolutionary history of cancer.The authors have appreciative words about my work,for which I am very grateful.At this point,I would like to contribute a few words on polyploidy,cancer genes,age,and colonial organization.展开更多
In the past,contradictory statements have been made about the age of cancer genes.While phylostratigraphic studies suggest that cancer genes emerged during the transitional period from unicellularians(UC)to early meta...In the past,contradictory statements have been made about the age of cancer genes.While phylostratigraphic studies suggest that cancer genes emerged during the transitional period from unicellularians(UC)to early metazoans(EM),life cycle studies suggest that they arose earlier.This controversy could not be resolved.Phylostratigraphic methods use data from somatic tumor gene collections containing or lacking polyploidy genes(PGCC genes)and compare them to genes from evolutionary node taxa.I analyze whether the selected taxa are suitable to resolve the above contradiction or not.Both cancer and amoebae life cycles have a reproductive asexual germline that produces germline stem cells(GSCs)and somatic cell lines that cannot.When the germline loses its reproductive function,the soma-to-germ transition forms a new reproductive germline.The reproductive polyploidy of cancer is homologous to the reproductive polyploidy of unicellular cysts.PGCCs repair DNA defects,reorganize the involved genome architecture and produce new GSCs.The present study refutes the dogma of the early metazoan origin of cancer.Cancer has a unicellular life cycle that was adopted by early metazoans to rescue themselves from evolutionary dead ends.Early metazoans controlled the unicellular life cycle through suppressor and anti-suppressor genes that could suspend or reactivate it.They are the archetypes of tumor suppressor genes and oncogenes.Cells of mammalians and humans that reach a similar impasse as early metazoans can reactivate the conserved life cycle of unicellularians.展开更多
文摘This correspondence to Gene&Diseases calls attention to the controversy between proponents of genetic modification in carcinogenesis and supporters of non-mutational oncogenesis.Data from molecular cancer research and findings from evolutionary cancer cell biology support the latter claim and provide no rationale for the mutational origin of sporadic cancers.It is more conceivable that the general susceptibility of asymmetric cell division(ACD)phenotypes to oxygen leads to irreparable DNA defects and dysregulated defective symmetric cell division(DscD)phenotypes.
文摘From an evolutionary perspective,the human cancer genome is based on an ancient gene module developed by the common ancestor of the Amoebozoa,Metazoa,and Fungi(AMF).^(1)The transition phase to multicellularity(premetazoan period)was a rather long period of evolu-tionary attempts and failures.During this time,suppressor genes were evolved to deactivate the G+S cell system inherited from the AMF ancestor.
文摘The comment of Ivanovic and Vlaski-Lafarge on my article“Cancer genes and cancer stem cells in tumorigenesis:Evolutionary deep homology and controversies”opens up a welcome discussion on the evolutionary history of cancer.The authors have appreciative words about my work,for which I am very grateful.At this point,I would like to contribute a few words on polyploidy,cancer genes,age,and colonial organization.
文摘In the past,contradictory statements have been made about the age of cancer genes.While phylostratigraphic studies suggest that cancer genes emerged during the transitional period from unicellularians(UC)to early metazoans(EM),life cycle studies suggest that they arose earlier.This controversy could not be resolved.Phylostratigraphic methods use data from somatic tumor gene collections containing or lacking polyploidy genes(PGCC genes)and compare them to genes from evolutionary node taxa.I analyze whether the selected taxa are suitable to resolve the above contradiction or not.Both cancer and amoebae life cycles have a reproductive asexual germline that produces germline stem cells(GSCs)and somatic cell lines that cannot.When the germline loses its reproductive function,the soma-to-germ transition forms a new reproductive germline.The reproductive polyploidy of cancer is homologous to the reproductive polyploidy of unicellular cysts.PGCCs repair DNA defects,reorganize the involved genome architecture and produce new GSCs.The present study refutes the dogma of the early metazoan origin of cancer.Cancer has a unicellular life cycle that was adopted by early metazoans to rescue themselves from evolutionary dead ends.Early metazoans controlled the unicellular life cycle through suppressor and anti-suppressor genes that could suspend or reactivate it.They are the archetypes of tumor suppressor genes and oncogenes.Cells of mammalians and humans that reach a similar impasse as early metazoans can reactivate the conserved life cycle of unicellularians.
