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Mathematical models of immune-induced cancer dormancy and the emergence of immune evasion
by Kathleen P. Wilkie, and Philip Hahnfeldt
Interface FocusVolume 3(4):20130010
August 6, 2013
©2013 by The Royal Society
Immune cytotoxicity assay data and model fits for predation decay after 0, 35, 60, 90, 120 or 365 days in dormancy.
Kathleen P. Wilkie, and Philip Hahnfeldt Interface Focus 2013;3:20130010
©2013 by The Royal Society
Bifurcation diagrams and bifurcation phase portrait for the cancer–immune dormant state.
Kathleen P. Wilkie, and Philip Hahnfeldt Interface Focus 2013;3:20130010
©2013 by The Royal Society
Simulations of immune-mediated tumour dormancy assuming the three fits to predation decay.
Kathleen P. Wilkie, and Philip Hahnfeldt Interface Focus 2013;3:20130010
©2013 by The Royal Society
Population growth curves assuming the three fits in predation decay and that the immune response is limited.
Kathleen P. Wilkie, and Philip Hahnfeldt Interface Focus 2013;3:20130010
©2013 by The Royal Society
Simulations of immune-mediated tumour dormancy assuming the three fits for decay are applied to the recruitment potential while the predation strength is constant.
Kathleen P. Wilkie, and Philip Hahnfeldt Interface Focus 2013;3:20130010
©2013 by The Royal Society
Simulations of immune-mediated tumour dormancy assuming the three fits for decay are applied to both the predation strength and the recruitment potential.
Kathleen P. Wilkie, and Philip Hahnfeldt Interface Focus 2013;3:20130010
©2013 by The Royal Society
The transition of a heterogeneous cancer population to a mostly homogeneous but resistant population can explain the observed decline in predation efficacy.
Kathleen P. Wilkie, and Philip Hahnfeldt Interface Focus 2013;3:20130010
©2013 by The Royal Society
