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Tumor development under angiogenic signaling: a dynamical theory of tumor growth, treatment response, and postvascular dormancy.
This work poses a quantitative theory for tumor growth under angiogenic stimulator/inhibitor control that is both explanatory and clinically implementable and reveals the existence of an ultimate limitation to tumor size underAngiogenic control.
Clinical application of antiangiogenic therapy: microvessel density, what it does and doesn't tell us.
It is contended that, although microvessel density is a useful prognostic marker, it is not, by itself, an indicator of therapeutic efficacy, nor should it be used to guide the stratification of patients for therapeutic trials.
Classical Mathematical Models for Description and Prediction of Experimental Tumor Growth
The results not only have important implications for biological theories of tumor growth and the use of mathematical modeling in preclinical anti-cancer drug investigations, but also may assist in defining how mathematical models could serve as potential prognostic tools in the clinic.
PPARgamma ligands inhibit primary tumor growth and metastasis by inhibiting angiogenesis.
In in vivo studies, rosiglitazone suppresses angiogenesis in the chick chorioallantoic membrane, in the avascular cornea, and in a variety of primary tumors, suggesting that PPARgamma ligands may be useful in treating angiogenic diseases such as cancer by inhibitingAngiogenesis.
Endostatin's antiangiogenic signaling network.
Her-2-neu expression and progression toward androgen independence in human prostate cancer.
- S. Signoretti, R. Montironi, M. Loda
- Medicine, BiologyJournal of the National Cancer Institute
- 6 December 2000
Her-2-neu expression appears to increase with progression to androgen independence, and therapeutic targeting of this tyrosine kinase in prostate cancer may be warranted.
Transcriptional switch of dormant tumors to fast-growing angiogenic phenotype.
It is hypothesized that dormant tumors undergo a stable genetic reprogramming during their switch to the fast-growing phenotype, and novel dormancy-specific biomarkers such as H2BK and Eph receptor A5 (EphA5) were discovered.
Simple ODE models of tumor growth and anti-angiogenic or radiation treatment
Ionizing radiation activates the Nrf2 antioxidant response.
The results indicate that the Nrf2-ARE pathway is important to maintain resistance to irradiation, but that it operates as a second-tier antioxidant adaptive response system activated by radiation only under specific circumstances, including those that may be highly relevant to tumor response during standard clinical dose-fractionated radiation therapy.
The linear-quadratic model and most other common radiobiological models result in similar predictions of time-dose relationships.
It is shown that a broad range of radiobiological models are described by formalisms in which a perturbation calculation produces the standard LQ relationship for dose fractionation/protraction, including the same generalized time factor, G.