It appears you don't have support to open PDFs in this web browser. To view this file, Open with your PDF reader
Abstract
A distinct model of neutral evolution of rare cancer mutations is described and contrasted with models relying on the infinite sites approximation (that a specific mutation arises in only one cell at any instant). An explosion of genetic diversity is predicted at clinical cell numbers and may explain the progressive refractoriness of cancers during a clinical course. The widely used infinite sites assumption may not be applicable for clinical cancers.
You have requested "on-the-fly" machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Show full disclaimer
Neither ProQuest nor its licensors make any representations or warranties with respect to the translations. The translations are automatically generated "AS IS" and "AS AVAILABLE" and are not retained in our systems. PROQUEST AND ITS LICENSORS SPECIFICALLY DISCLAIM ANY AND ALL EXPRESS OR IMPLIED WARRANTIES, INCLUDING WITHOUT LIMITATION, ANY WARRANTIES FOR AVAILABILITY, ACCURACY, TIMELINESS, COMPLETENESS, NON-INFRINGMENT, MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. Your use of the translations is subject to all use restrictions contained in your Electronic Products License Agreement and by using the translation functionality you agree to forgo any and all claims against ProQuest or its licensors for your use of the translation functionality and any output derived there from. Hide full disclaimer
Details
1 Georgetown University Medical Center, Department of Oncology, Washington, USA (GRID:grid.411667.3) (ISNI:0000 0001 2186 0438); Georgetown University Medical Center, Department of Biostatistics, Bioinformatics, and Biomathematics, Washington, USA (GRID:grid.411667.3) (ISNI:0000 0001 2186 0438)