arXiv subjects

M. J. Vilela

Publications and source records attributed to M. J. Vilela.

3 recordsLinked to original sources

arXiv2003

Fighting cancer with virus

One of the most promising strategies to treat cancer is attacking it with viruses. Virus can kill tumor cells specifically or act as carriers that deliver normal genes into cancer cells. A model for virus therapy of cancer is investigated and some of its predictions are in agreement with results obtained from experimental tumors. Furthermore, the model reveals an oscillatory (periodic or aperiodic) response of tumor cells and virus populations which may difficult clinical prognosis. These results suggest the need for new \textit{in vivo} and \textit{in vitro} experiments aiming to detect this oscillatory response.

cond-mat.stat-mech↗

arXiv2002

Morphology transitions induced by chemotherapy in carcinomas "in situ"

Recently, we have proposed a nutrient-limited model for the avascular growth of tumors including cell proliferation, motility and death \cite{jr}, that, qualitatively reproduces commonly observed morphologies for carcinomas {\it in situ}. In the present work, we analyze the effects of distinct chemotherapeutic strategies on the patterns, scaling and growth laws obtained for such nutrient-limited model. Two kinds of chemotherapeutic strategies were considered, namely, those that kill cancer cells and those that block cell mitosis but allows the cell to survive for some time. Depending on the chemotherapeutic schedule used, the tumors are completely eliminated, reach a stationary size or grow following power laws. The model suggests that the scaling properties of the tumors are not affected by the mild cytotoxic treatments, although a reduction in growth rates and an increase in invasiveness are observed. For the strategies based on antimitotic drugs a morphological transition in which compact tumors become more fractal under aggressive treatments was seen.

cond-mat↗

arXiv2001

A reaction-diffusion model for the growth of avascular tumor

A nutrient-limited model for avascular cancer growth including cell proliferation, motility and death is presented. The model qualitatively reproduces commonly observed morphologies for primary tumors, and the simulated patterns are characterized by its gyration radius, total number of cancer cells, and number of cells on tumor periphery. These very distinct morphological patterns follow Gompertz growth curves, but exhibit different scaling laws for their surfaces. Also, the simulated tumors incorporate a spatial structure composed of a central necrotic core, an inner rim of quiescent cells and a narrow outer shell of proliferating cells in agreement with biological data. Finally, our results indicate that the competition for nutrients among normal and cancer cells may be a determinant factor in generating papillary tumor morphology.

cond-mat.stat-mech↗