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One of the most promising strategies to treat cancer is attacking it with viruses designed to exploit specific altered pathways. Here, the effects of oncolytic virotherapy on tumors having compact, papillary, and disconnected morphologies are investigated through computer simulations of a multiscale model coupling macroscopic reaction-diffusion equations for the nutrients with microscopic stochastic rules for the actions of individual cells and viruses. The interaction among viruses and tumor cells involves cell infection, intracellular virus replication, and the release of new viruses in the tissue after cell lysis. The evolution over time of both the viral load and cancer cell population, as well as the probabilities for tumor eradication, were evaluated for a range of multiplicities of infection, viral entries, and burst sizes. It was found that in immunosuppressed hosts, the antitumor efficacy of a virus is primarily determined by its entry efficiency, its replicative capacity within the tumor, and its ability to spread over the tissue. However, the optimal traits for oncolytic viruses depend critically on the tumor growth dynamics and do not necessarily include rapid replication, cytolysis, or spreading, currently assumed as necessary conditions for a successful therapeutic outcome. Our findings have potential implications on the design of new vectors for the viral therapy of cancer.

Inspired by dengue and yellow fever epidemics, we investigated the contact process (CP) in a multiscale network constituted by one-dimensional chains connected through a Barabási-Albert scale-free network. In addition to the CP dynamics inside the chains, the exchange of individuals between connected chains (travels) occurs at a constant rate. A finite epidemic threshold and an epidemic mean lifetime diverging exponentially in the subcritical phase, concomitantly with a power law divergence of the outbreak's duration, were found. A generalized scaling function involving both regular and SF components was proposed for the quasistationary analysis and the associated critical exponents determined, demonstrating that the CP on this hybrid network and nonvanishing travel rates establishes a new universality class.

Membrane ruffle fluctuations of amphibian epithelial cells A6 (CCL102) cultured in normal and upside down oriented plates have been analyzed through video microscopy. Our results reveal that their edge ruffle fluctuations exhibit a stochastic dynamics with 1/f(alpha) power spectrum over at least two decades at low frequencies and long range correlated, self-affine lateral border profiles. In a few and small areas of the membrane, probably nearby focal contacts, we found periodic oscillations which could be induced by myosin driven contraction of stress fibers. Furthermore, whereas the different gravitational orientations had none or little effect on the structure (power spectra and surface roughness) of these membrane ruffle fluctuations, their dynamic parameters were differentially affected. Indeed, the decay time of ruffles remained unchanged, but the period of lamellipodia oscillations near the focal adhesion points was significantly altered in A6 cells cultured upside down.

Recently, we have proposed a nutrient-limited model for the avascular growth of tumors including cell proliferation, motility, and death [S. C. Ferreira, Jr., M. L. Martins, and M. J. Vilela, Phys. Rev. E 65, 021907 (2002)], which qualitatively reproduces commonly observed morphologies for carcinomas in situ. In the present work, we analyze the effects of distinct chemotherapeutic strategies on the patterns, scaling, and growth laws obtained for the nutrient-limited model. Two kinds of chemotherapeutic strategies were considered, namely, those that kill cancer cells and those that block cell mitosis but allow 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.

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 determining factor in generating papillary tumor morphology.

We present a numerical study of the self-affine profiles obtained from configurations of the q-state Potts (with q=2,3, and 7) and p=10 clock models as well as from the occupation states for site percolation on the square lattice. The first and second order static phase transitions of the Potts model are located by a sharp change in the value of the roughness exponent alpha characterizing those profiles. The low temperature phase of the Potts model corresponds to flat (alpha approximately 1) profiles, whereas its high temperature phase is associated with rough (alpha approximately 0.5) ones. For the p=10 clock model, in addition to the flat (ferromagnetic) and rough (paramagnetic) profiles, an intermediate rough (0.5