Chemotherapy may be delivered based on an integrated view of tumour dynamics

被引:13
作者
Ribba, B. [1 ,2 ]
You, B. [1 ,2 ,3 ]
Tod, M. [1 ,2 ]
Girard, P. [1 ,2 ]
Tranchand, B. [1 ,2 ,4 ]
Trillet-Lenoir, V. [1 ,2 ,3 ]
Freyer, G. [1 ,2 ,3 ]
机构
[1] Univ Lyon, F-69003 Lyon, France
[2] Univ Lyon 1, Fac Med Lyon Sud, CTO, EA3738, F-69600 Oullins, France
[3] Hosp Civils Lyon, Ctr Hosp Lyon Sud, Med Oncol Serv, F-69310 Pierre Benite, France
[4] Ctr Anticancereux Leon Berard, F-69008 Lyon, France
关键词
MATHEMATICAL-MODEL; COLORECTAL-CANCER; GROWTH; DRUGS;
D O I
10.1049/iet-syb.2008.0104
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The aim here was to explore the potential of pharmacokinetic (PK)/pharmacodynamic (PD) and physiopathological parameters in explaining the primary effects of an anti-cancer treatment that targets cells in a specific cell cycle phase. The authors applied a theoretical multi-scale disease model of tumour growth that integrates cancer processes at the cellular and tissue scales. The mathematical model at the cell level relies on a dynamic description of cell cycle regulation while the model at the tissue level is based on fluid mechanics considerations. Simulations show that the number of target cells oscillates as the tumour grows after a first cycle of chemotherapy. Both treatment effect and tumour growth processes drive these oscillations. Nonetheless, results indicate that parameters related to physiopathological processes may have greater relevance than classical drug-related parameters in determining the efficacy of a chemotherapy treatment protocol. Physiopathological parameters, in particular those related to cell cycle regulation, may be integrated in PK/PD models aimed at optimising the delivery of phase-specific cytotoxic treatments.
引用
收藏
页码:180 / U1
页数:12
相关论文
共 19 条
[1]   RANDOMNESS, SYNCHRONY AND POPULATION PERSISTENCE [J].
AGUR, Z .
JOURNAL OF THEORETICAL BIOLOGY, 1985, 112 (04) :677-693
[2]   A cell cycle automaton model for probing circadian patterns of anticancer drug delivery [J].
Altinok, Atilla ;
Levi, Francis ;
Goldbeter, Albert .
ADVANCED DRUG DELIVERY REVIEWS, 2007, 59 (9-10) :1036-1053
[3]   On the closure of mass balance models for tumor growth [J].
Ambrosi, D ;
Preziosi, L .
MATHEMATICAL MODELS & METHODS IN APPLIED SCIENCES, 2002, 12 (05) :737-754
[4]   Where next for gefitinib in patients with lung cancer? [J].
Blackhall, Fiona ;
Ranson, Malcolm ;
Thatcher, Nick .
LANCET ONCOLOGY, 2006, 7 (06) :499-507
[5]   The Restriction Point of the Cell Cycle [J].
Blagosklonny, Mikhail V. ;
Pardee, Arthur B. .
CELL CYCLE, 2002, 1 (02) :103-110
[6]   A THEORETICAL-ANALYSIS OF INTERVAL DRUG DOSING FOR CELL-CYCLE-PHASE-SPECIFIC DRUGS [J].
COJOCARU, L ;
AGUR, Z .
MATHEMATICAL BIOSCIENCES, 1992, 109 (01) :85-97
[7]   The effect of hyperbaric oxygen therapy on tumour growth in a mouse model of colorectal cancer liver metastases [J].
Daruwalla, Jurstine ;
Christophi, Chris .
EUROPEAN JOURNAL OF CANCER, 2006, 42 (18) :3304-3311
[8]   Dose calculation of anticancer drugs: A review of the current practice and introduction of an alternative [J].
Gurney, H .
JOURNAL OF CLINICAL ONCOLOGY, 1996, 14 (09) :2590-2611
[9]   Modelling the molecular circuitry of cancer [J].
Hahn, WC ;
Weinberg, RA .
NATURE REVIEWS CANCER, 2002, 2 (05) :331-341
[10]   The hallmarks of cancer [J].
Hanahan, D ;
Weinberg, RA .
CELL, 2000, 100 (01) :57-70