tailieunhanh - Báo cáo y học: " A stochastic model of oncogene expression and the relevance of this model to cancer therapy"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: A stochastic model of oncogene expression and the relevance of this model to cancer therapy | Theoretical Biology and Medical Modelling BioMed Central Research Open Access A stochastic model of oncogene expression and the relevance of this model to cancer therapy Francis D Alfano Address The Harold Leever Cancer Center 1075 Chase Parkway Waterbury Connecticut 06708 USA Email Francis D Alfano - fralfano@ Corresponding author Published 31 January 2006 Received 02 December 2005 Theoretical Biology and Medical Modelling 2006 3 5 doi 1742-4682-3-5 Accepted 31 January 2006 This article is available from http content 3 1 5 2006 Alfano licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Ablation of an oncogene or of the activity of the protein it encodes can result in apoptosis and or inhibit tumor cell proliferation. Therefore if the oncogene or set of oncogenes contributing maximally to a tumor cell s survival can be identified such oncogene s are the most appropriate target s for maximizing tumor cell kill. Methods and results A mathematical model is presented that describes cellular phenotypic entropy as a function of cellular proliferation and or survival and states of transformation and differentiation. Oncogenes become part of the cellular machinery block apoptosis and differentiation or promote proliferation and give rise to new states of cellular transformation. Our model gives a quantitative assessment of the amount of cellular death or growth inhibition that result from the ablation of an oncogene s protein product. We review data from studies of chronic myelogenous leukemia and K562 cells to illustrate these principles. Conclusion The model discussed in this paper has implications for oncogene-directed therapies and their use in combination with other therapeutic .