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aCLS cancers: genomic and epigenetic changes transform the cell of origin of cancer into a tumorigenic pathogen of unicellular organization and lifestyle

Research article Created on 05 Nov 2019

Authors

Vladimir F. Niculescu

Abstract

Paper accepted by GENE (Elsevier) 2019, Vol. 274

At least 1/3 of all acquired solid cancers produce unusual cyst-like structures  (CLSs , PGCCs) with simultaneous loss of p53 function. However, p53 deficiency or accumulated mutations are not the causes of aCLS cancers. The cause is the reversal to unicellularity of a metabolic stressed cell by activating silenced transition switches and ancestral gene networks inherited from early Metazoans. After reprogramming and transformation the cell-of-origin of cancer bypasses mitosis and forms the polyploid pCLS, the homemade pathogen of aCLS cancers. pCLS's daughter cells (microcells) generate the pretumorigenic cancer stem cell pool (pCSCs) that start in turn the unicellular cancer cell lineage containing reproductive and somatic sublines. While the reproductive subline gives rise to new autonomous aCLSs by asymmetric division and cyclic differentiation, the somatic subline grows aCLS free.  In the course of cancer evolution, some of the somatic mutants convert to stem cell precursors (SCPs). Somatic SCPs transfer part of somatic mutations and epimutations to the genome of newly formed reproductive clones. In this way, subsequent generations of tumorigenic and metastatic CSCs are being produced. aCLS cancer development is neither chaotic nor deregulated it follows unicellular development patterns. The unicellular program is controlled by mechanisms from early eukaryotic evolution.

Keywords:  cancer, unicellular, reproductive and somatic cell lines, stem cells (CSCs), somatic stem cell precursors (SCPs); protist stem cells

Abbreviations: CLS, cyst-like structure;  pCLS, primary pretumorigenic cyst-like structure; aCLS, autonomous cyst-like structure; giCLS, genotoxic induced cyst-like structure;  PGCC, polyploid giant cancer cell; CSC, cancer stem cell; UG, unicellular genes; MG, multicellular; genes; MG:UG gene conflicts; ACD, autonomous cyst differentiation (protists); ICD, induced cyst differentiation (protists);  MUT,  multicellular-unicellular transition switch;  SCP, somatic stem cell precursors; SRT, somatic - reproductive transition; OCB, oxygen consuming bacteria

Further details

HIGHLIGHTS 

·      Ancestral MU switches reverse the cell-of-origin into a unicellular life form (pCLS)

·      The reversal to unicellularity occurs through genomic  and  epigenetic rearrangements

·      The pCLS starts an archaic life cycle that differentiates numerous aCLSs

       The pCLS/aCLS progeny generates CSC pools that form reproductive and somatic cells


·      Cancer evolution means the transition from pretumorigenic to malignant life cycles.

 

 

 

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