Abstract
In the present manuscript we propose a lattice free multiscale model for avascular tumor growth that takes into account the biochemical environment, mitosis, necrosis, cellular signaling and cellular mechanics. This model extends analogous approaches by assuming a function that incorporates the biochemical energy level of the tumor cells and a mechanism that simulates the behavior of cancer stem cells. Numerical simulations of the model are used to investigate the morphology of the tumor at the avascular phase. The obtained results show similar characteristics with those observed in clinical data in the case of the Ductal Carcinoma In Situ (DCIS) of the breast.
Highlights
In 2014 in the US, there is an estimation of 1,665,540 new diagnosed cancer cases and 585,720 deaths
In the present manuscript we propose a lattice free multiscale model for avascular tumor growth that takes into account the biochemical environment, mitosis, necrosis, cellular signaling and cellular mechanics
At this scale we introduce the concept of a function that encounters the chemical energy level of each cell in Adenosine 5-triphosphate (ATP)
Summary
In 2014 in the US, there is an estimation of 1,665,540 new diagnosed cancer cases and 585,720 deaths. In cancers of epithelial origin, namely carcinomas, this colony is delimited by a basement membrane that isolates the neoplastic cells At this phase, the tumor is called carcinoma in situ and has no metastatic potential. Once the tumor cells enter the blood vessels they can be transported via the circulation to other organs, where they can exit from the circulation, engraft in the new environment and start to grow again to produce a metastatic or secondary tumor. In this manuscript we consider only the early stages of cancer development, while the tumor remains in an avascular state. This mutated stem cell named cancer stem cell travels inside the tissue like normal stem cells, producing cancer cells
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