Dynamics of chronic myeloid leukaemia

By F. Michor, T. Hughes, Yoh Iwasa, S. Branford, N. Shah, C. Sawyers, Martin A. Nowak. Nature, 2005

845 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Cancer stem cells: an old idea--a paradigm shift. (2006, neutral): “with kinetics predicted by a stem cell model (66).”
Lessons from the cancer genome. (2013, positive): “There is cause for optimism: mathematical modeling suggests that resistance may often be due to pre-existing mutations in the tumor cell population (Michor et al., 2005).”
Cancer Evolution: Mathematical Models and Computational Inference (2014, background): “The different rates of cellular proliferation in stem cells and differentiating cells can also explain the biphasic response to imatinib treatment in chronic myeloid leukemia as well as the rates of relapse due to resistance mutations (Michor et al. 2005).”
Genetic Progression and the Waiting Time to Cancer (2007, background): “The former scenario would suggest a much smaller effective population size, an important variable for modeling the evolution of cancer [4,22,35–37].”
The biology of CML blast crisis. (2004, result): “The above model is in keeping with a mathematic model of chronic phase CML kinetics based on quantitative PCR of Bcr-Abl in 163 patients.(69) The best-fitting model had an initial rapid drop of 3 logs of disease, followed by a slow decline.”