| Origin of metastases: Subspecies of cancers generated by intrinsic karyotypic variations. | |
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MedLine Citation:
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PMID: 22377695 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Conventional mutation theories do not explain (1) why the karyotypes of metastases are related to those of parental cancers, but not to those of metastases of other cancers, and (2) why cancers metastasize at rates that often far exceed those of conventional mutations. To answer these questions, we advance here the theory that metastases are autonomous subspecies of cancers, rather than mutations. Since cancers are species with intrinsically flexible karyotypes, they can generate new subspecies by spontaneous karyotypic rearrangements. This phylogenetic theory predicts that metastases are karyotypically related to parental cancers but not to others. Testing these predictions on metastases from two pancreatic cancers, we found (1) Metastases had individual karyotypes and phenotypes. The karyotypes of metastases were related to, but different from, those of parental cancers in 11 out of 37 and 26 out of 49 parental chromosomal units. Chromosomal units are defined as intact chromosomes with cancer-specific copy numbers and marker chromosomes that are > 50% clonal. (2) Metastases from the two different cancers did not share chromosomal units. Testing the view that multi-chromosomal rearrangements occur simultaneously in cancers, as opposed to sequentially, we found spontaneous non-clonal rearrangements with as many new chromosomal units as in authentic metastases. We conclude that metastases are individual autonomous species differing from each other and parental cancers in species-specific karyotypes and phenotypes. They are generated from parental cancers by multiple simultaneous karyotypic rearrangements, much like new species. The species-specific individualities of metastases explain why so many searches for commonalities have been unsuccessful. |
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Authors:
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Peter Duesberg; Christine Iacobuzio-Donahue; Jackie Brosnan; Amanda McCormack; Daniele Mandrioli; Lewis Chen |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-3-15 |
Journal Detail:
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Title: Cell cycle (Georgetown, Tex.) Volume: 11 ISSN: 1551-4005 ISO Abbreviation: - Publication Date: 2012 Mar |
Date Detail:
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Created Date: 2012-3-1 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101137841 Medline TA: Cell Cycle Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Department of Molecular and Cell Biology; Donner Laboratory; University of California at Berkeley; Berkeley, CA USA. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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