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Critical Reviews™ in Oncogenesis
SJR: 0.946 SNIP: 0.503 CiteScore™: 2

ISSN Imprimir: 0893-9675
ISSN En Línea: 2162-6448

Critical Reviews™ in Oncogenesis

DOI: 10.1615/CritRevOncog.v18.i1-2.30
pages 19-42

Cell Fusion In Tumor Development: Accelerated Genetic Evolution

Ty Harkness
Departments of Biomedical Engineering, University of Wisconsin-Madison
Beth A. Weaver
Cell and Regenerative Biology; Carbone Cancer Center, University of Wisconsin at Madison, Madison, Wisconsin
Caroline M. Alexander
Carbone Cancer Center; Laboratory for Optical and Computational Instrumentation, Cardiovascular Physiology Core Facility, University of Wisconsin at Madison
Brenda M. Ogle
Material Sciences Program; Laboratory for Optical and Computational Instrumentation, Cardiovascular Physiology Core Facility; Department of Biomedical Engineering,University of Wisconsin-Madison


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.

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