Cell fusion in tumor development: Accelerated genetic evolution

Ty Harkness, Beth A. Weaver, Caroline M. Alexander, Brenda M. Ogle

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

The majority of human tumor cells have highly aberrant karyotypes, typically ascribed to errors during tumor cell division, potentially linked to a failure of DNA repair, or telomeric insufficiency. Here we discuss another option, that of cell fusion which can lead to the re-assortment of chromosomes during post-fusion mitosis. The observation of hyperdiploid cells has a long history in cancer genetics, but the concept of cell fusion has been difficult to test in practice. Here, we examine the role of cell fusion during normal development, and relate that to potential cellular fusion partners for primary tumor cells. In particular, we describe the potential for stromal partner fusion during metastatic mobilization. The evidence for genetic and cytoplasmic diversity in heterotypic fusion partners is described, together with the new tools available to help the evaluation of this process as a tumor driver.

Original languageEnglish (US)
Pages (from-to)19-42
Number of pages24
JournalCritical Reviews in Oncogenesis
Volume18
Issue number1-2
DOIs
StatePublished - Mar 28 2013

Fingerprint

Molecular Evolution
Cell Fusion
Neoplasms
Genetic Phenomena
Polyploidy
Karyotype
Mitosis
DNA Repair
Cell Division
Chromosomes
History
Observation

Keywords

  • Chromosomal instability
  • Metastasis
  • Multipolar mitosis
  • Polyploidy
  • Reprogramming

Cite this

Cell fusion in tumor development : Accelerated genetic evolution. / Harkness, Ty; Weaver, Beth A.; Alexander, Caroline M.; Ogle, Brenda M.

In: Critical Reviews in Oncogenesis, Vol. 18, No. 1-2, 28.03.2013, p. 19-42.

Research output: Contribution to journalArticle

Harkness, Ty ; Weaver, Beth A. ; Alexander, Caroline M. ; Ogle, Brenda M. / Cell fusion in tumor development : Accelerated genetic evolution. In: Critical Reviews in Oncogenesis. 2013 ; Vol. 18, No. 1-2. pp. 19-42.
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