Cell-cell fusion is the rate-limiting step in causation and progression of clinically significant cancers

Cancer Genetics and Cytogenetics

Volumn 185, Issue 2, 2008, Pages 113-

  Parris, George E ^a  

^a NONE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CANCER GROWTH; CARCINOGENESIS; CELL FUSION; CHROMOSOME; GENE MUTATION; GENOME; HUMAN; KARYOTYPE; LETTER; METASTASIS; PRIORITY JOURNAL; SOMATIC CELL;

CAUSALITY; CELL FUSION; DISEASE PROGRESSION; HUMANS; NEOPLASMS;

EID: 49849101583     PISSN: 01654608     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.cancergencyto.2008.05.008     Document Type: Letter

References (6)

1. Fabarius A., Li R., Yerganian G., Hehlmann R., and Duesberg P. Specific clones of spontaneously evolving karyotypes generate individuality of cancers. Cancer Genet Cytogenet 180 (2008) 89-99
2. Parris G.E. Clinically significant cancer evolves from transient mutated and/or aneuploid neoplasia by cell fusion to form unstable syncytia that give rise to ecologically viable parasite species. Med Hypotheses 65 (2005) 846-850
3. Duelli D., and Lazebnik Y. Cell-to-cell fusion as a link between viruses and cancer. Nat Rev Cancer 7 (2007) 968-976
4. Parris G.E. The cell clone ecology hypothesis and the cell fusion model of cancer progression and metastasis: history and experimental support. Med Hypotheses 66 (2006) 76-83
5. Pawelek J.M., and Chakraborty A.K. Fusion of tumour cells with bone marrow-derived cells: a unifying explanation for metastasis. Nat Rev Cancer 5 (2008) 377-386
6. Thompson S.L., and Compton D.A. Examining the link between chromosomal instability and aneuploidy in human cells. J Cell Biol 180 (2008) 665-672