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Prediction of lung cancer patients' response to combined chemo-radiotherapy using a personalized hybrid model

Wołkowicz Sebastian, Fujarewicz Krzysztof, Kurpas Monika, Łakomiec Krzysztof, Śmieja Jarosław, Suwiński Rafał, Świerniak Andrzej

Mathematica Applicanda

2019

Vol. 47, no. 2

219--228

The paper presents a novel approach to prediction of the combined therapy outcome for non-small lung cancer patients. A hybrid model is proposed, consisting of two parts. The first one is a mathematical model of tumor response to therapy, whose parameters are expressed as a linear functions of data from mass spectrometry of patient blood plasma samples. These linear functions constitute the second component of the hybrid model. A comparison of clinical and simulation-based survival curves is used to evaluate the quality of the model.

W pracy przedstawiono oryginalne podejście do przewidywania łącznego wyniku terapii u pacjentów z niedrobnokomórkowym rakiem płuc. Zaproponowano model hybrydowy, składający się z dwóch części. Pierwsza z nich to matematyczny model odpowiedzi guza na terapię, którego parametry wyrażone są jako liniowe funkcje wyników spektrometrii masowej osocza krwi pobranego od pacjentów. Równania te stanowią drugi składnik modelu hybrydowego. Do oceny jakości modelu zostało wykorzystane porównanie krzywych przeżycia wyznaczonych dla danych klinicznych i uzyskanych za pomocą symulacji modelu.

Regulation of p53 by siRNA in radiation treated cells: Simulation studies

Puszyński K., Jaksik R., Świerniak A.

International Journal of Applied Mathematics and Computer Science

2012

Vol. 22, no. 4

1011-1018

Ionizing radiation activates a large variety of intracellular mechanisms responsible for maintaining appropriate cell functionality or activation of apoptosis which eliminates damaged cells from the population. The mechanism of such induced cellular death is widely used in radiotherapy in order to eliminate cancer cells, although in some cases it is highly limited by increased cellular radio-resistance due to aberrations in molecular regulation mechanisms of malignant cells. Despite the positive correlation between the radiation dose and the number of apoptotic cancer cells, radiation has to be limited because of extensive side effects. Therefore, additional control signals whose role will be to maximize the cancer cells death-ratio while minimizing the radiation dose and by that the potential side effects are worth considering. In this work we present the results of simulation studies showing possibilities of single gene regulation by small interfering RNA (siRNA) that can increase radio-sensitivity of malignant cells showing aberrations in the p53 signaling pathway, responsible for DNA damage-dependant apoptosis. By blocking the production of the p53 inhibitor Mdm2, radiation treated cancer cells are pushed into the apoptotic state on a level normally achievable only with high radiation doses. The presented approach, based on a simulation study originating from experimentally validated regulatory events, concerns one of the basic problems of radiotherapy dosage limitations, which, as will be shown, can be partially avoided by using the appropriate siRNA based control mechanism.