Related papers: Computational modelling of cancer evolution by mul…
Cancer is a complex disease driven by dynamic regulatory shifts that cannot be fully captured by individual molecular profiling. We employ a data-driven approach to construct a coarse-grained dynamic network model based on hallmark…
The emergence of a predominant phenotype within a cell population is often triggered by a rare accumulation of DNA mutations in a single cell. For example, tumors may be initiated by a single cell in which multiple mutations cooperate to…
Individual cells exhibit specific proliferative responses to changes in microenvironmental conditions. Whether such potential is constrained by the cell density throughout the growth process is however unclear. Here, we identify a…
Cancers remain the lead cause of disease-related, pediatric death in North America. The emerging field of complex systems has redefined cancer networks as a computational system with intractable algorithmic complexity. Herein, a tumor and…
Some clinical and pre-clinical data suggests that treating some tumors at a mild, patient-specific dose might delay resistance to treatment and increase survival time. A recent mathematical model with sensitive and resistant tumor cells…
We present a model for the interaction dynamics of lymphocytes-tumor cells population. This model reproduces all known states for the tumor. Futherly,we develop it taking into account periodical immunotheraphy treatment with cytokines…
When confronted with an undesired cell population, such as bacterial infections or tumors, we seek the most effective treatment, designed to eliminate the population as rapidly as possible. A common practice is to monitor the cells…
Angiogenesis is a key process in the tumoral growth which allows the cancerous tissue to impact on its vasculature in order to improve the nutrient's supply and the metastatic process. In this paper, we introduce a model for the density of…
Quasispecies theory predicts that there is a critical mutation probability above which a viral population will go extinct. Above this threshold the virus loses the ability to replicate the best adapted genotype, leading to a population…
The forest of mutations associated to a multitype branching forest is obtained by merging together all vertices of its clusters and by preserving connections between them. We first show that the forest of mutations of any mulitype branching…
The emergence of acquired drug resistance in cancer represents a major barrier to treatment success. While research has traditionally focused on genetic sources of resistance, recent findings suggest that cancer cells can acquire transient…
The transition from a normal to cancerous cell requires a number of highly specific mutations that affect cell cycle regulation, apoptosis, differentiation, and many other cell functions. One hallmark of cancerous genomes is genomic…
The process of programmed cell death, namely apoptosis, is a natural mechanism that regulates healthy tissue, multicellular structures, and homeostasis. An improved understanding of apoptosis can significantly enhance our knowledge of…
Signaling pathways serve to communicate information about extracellular conditions into the cell, to both the nucleus and cytoplasmic processes to control cell responses. Genetic mutations in signaling network components are frequently…
Although the survival rate of cancer patients has significantly increased due to advances in anti-cancer therapeutics, one of the major side effects of these therapies, particularly radiotherapy, is the potential manifestation of…
How multicellular life forms evolved out from unicellular ones constitutes a major problem in our understanding of the evolution of our biosphere. A recent set of experiments involving yeast cell populations has shown that selection for…
Cancer results from a sequence of genetic and epigenetic changes which lead to a variety of abnormal phenotypes including increased proliferation and survival of somatic cells, and thus, to a selective advantage of pre-cancerous cells. The…
Two models of circulating tumor cell (CTC) dynamics have been proposed to explain the phenomenon of tumor 'self-seeding', whereby CTCs repopulate the primary tumor and accelerate growth: Primary Seeding, where cells from a primary tumor…
Extreme mutation rates in microbes and cancer cells can result in error-induced extinction (EEX), where every descendant cell eventually acquires a lethal mutation. In this work, we investigate critical birth-death processes with $n$…
We propose a simple dynamic model of cancer development that captures carcinogenesis and subsequent cancer progression. A central idea of the model is to include the immune system as an extinction threshold, similar to the strong Allee…