The cancer aneuploidy paradox : In the light of evolution

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dc.contributor.authorSalmina, Kristine
dc.contributor.authorHuna, Anda
dc.contributor.authorKalējs, Mārtiņš
dc.contributor.authorPjanova, Dace
dc.contributor.authorScherthan, Harry
dc.contributor.authorCragg, Mark S.
dc.contributor.authorĒrenpreisa, Jekaterina
dc.contributor.institutionBiomehānikas zinātniskā laboratorija
dc.date.accessioned2021-04-16T14:05:01Z
dc.date.available2021-04-16T14:05:01Z
dc.date.issued2019-01-01
dc.descriptionPublisher Copyright: © 2019 by the authors. Licensee MDPI, Basel, Switzerland. Copyright: Copyright 2019 Elsevier B.V., All rights reserved.
dc.description.abstractAneuploidy should compromise cellular proliferation but paradoxically favours tumour progression and poor prognosis. Here, we consider this paradox in terms of our most recent observations of chemo/radio-resistant cells undergoing reversible polyploidy. The latter perform the segregation of two parental groups of end-to-end linked dyads by pseudo-mitosis creating tetraploid cells through a dysfunctional spindle. This is followed by autokaryogamy and a homologous pairing preceding a bi-looped endo-prophase. The associated RAD51 and DMC1/γ- H2AX double-strand break repair foci are tandemly situated on the AURKB/REC8/kinetochore doublets along replicated chromosome loops, indicative of recombination events. MOS-associated REC8-positive peri-nucleolar centromere cluster organises a monopolar spindle. The process is completed by reduction divisions (bi-polar or by radial cytotomy including pedogamic exchanges) and by the release of secondary cells and/or the formation of an embryoid. Together this process preserves genomic integrity and chromosome pairing, while tolerating aneuploidy by by-passing the mitotic spindle checkpoint. Concurrently, it reduces the chromosome number and facilitates recombination that decreases the mutation load of aneuploidy and lethality in the chemo-resistant tumour cells. This cancer life-cycle has parallels both within the cycling polyploidy of the asexual life cycles of ancient unicellular protists and cleavage embryos of early multicellulars, supporting the atavistic theory of cancer.en
dc.description.statusPeer reviewed
dc.format.extent22
dc.format.extent4681542
dc.identifier.citationSalmina, K, Huna, A, Kalējs, M, Pjanova, D, Scherthan, H, Cragg, M S & Ērenpreisa, J 2019, 'The cancer aneuploidy paradox : In the light of evolution', Genes, vol. 10, no. 2, 83. https://doi.org/10.3390/genes10020083
dc.identifier.doi10.3390/genes10020083
dc.identifier.issn2073-4425
dc.identifier.urihttps://dspace.rsu.lv/jspui/handle/123456789/3830
dc.identifier.urlhttp://www.scopus.com/inward/record.url?scp=85061937762&partnerID=8YFLogxK
dc.language.isoeng
dc.relation.ispartofGenes
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectAneuploidy
dc.subjectAutokaryogamy
dc.subjectCancer
dc.subjectChromothripsis
dc.subjectCleavage embryo
dc.subjectDisabled spindle
dc.subjectMeio-mitosis
dc.subjectRecombination on kinetochores
dc.subjectReduction
dc.subjectSomatic pairing
dc.subject3.1 Basic medicine
dc.subject3.2 Clinical medicine
dc.subject1.1. Scientific article indexed in Web of Science and/or Scopus database
dc.subjectGenetics
dc.subjectGenetics(clinical)
dc.subjectSDG 3 - Good Health and Well-being
dc.titleThe cancer aneuploidy paradox : In the light of evolutionen
dc.type/dk/atira/pure/researchoutput/researchoutputtypes/contributiontojournal/article

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