January 7, 2011 | Philip J. Stephens, Chris D. Greenman, Beijuan Fu, Fengtang Yang, Graham R. Bignell, Laura J. Mudie, Erin D. Pleasance, King Wai Lau, David Bearle, Lucy A. Stebbings, Stuart McLaren, Meng-Lay Lin, David J. McBride, Ignacio Varela, Serena Nik-Zainal, Catherine Leroy, Mingming Jia, Andrew Menzies, Adam P. Butler, Jon W. Teague, Michael A. Quail, John Burton, Harold Swerdlow, Nigel P. Carter, Laura A. Morsberger, Christine Iacobuzio-Donahue, George A. Follows, Anthony R. Green, Adrienne M. Flanagan, Michael R. Stratton, P. Andrew Futreal, Peter J. Campbell
The study introduces a phenomenon termed "chromothripsis," where tens to hundreds of genomic rearrangements occur in a single cellular crisis, leading to a highly improbable genomic landscape. This process is characterized by frequent oscillations between two copy number states and is observed in at least 2%–3% of all cancers, particularly in bone cancers. The authors argue that chromothripsis can generate genomic consequences that promote cancer development, such as the creation of double-minute chromosomes and disruption of tumor suppressor genes. The mechanisms underlying chromothripsis are discussed, including potential causes like ionizing radiation and telomere attrition. The findings suggest that chromothripsis can provide a significant selective advantage to the affected clone, accelerating the evolution toward cancer.The study introduces a phenomenon termed "chromothripsis," where tens to hundreds of genomic rearrangements occur in a single cellular crisis, leading to a highly improbable genomic landscape. This process is characterized by frequent oscillations between two copy number states and is observed in at least 2%–3% of all cancers, particularly in bone cancers. The authors argue that chromothripsis can generate genomic consequences that promote cancer development, such as the creation of double-minute chromosomes and disruption of tumor suppressor genes. The mechanisms underlying chromothripsis are discussed, including potential causes like ionizing radiation and telomere attrition. The findings suggest that chromothripsis can provide a significant selective advantage to the affected clone, accelerating the evolution toward cancer.