Related papers: Critically assessing atavism, an evolution-centere…
Theoretical reasoning suggests that human cancer may result from knocking down the genetic constraints evolved for maintenance of the metazoan multicellularity, which, however, requires a critical test. Using xenograft-based experimental…
It is proposed that cancer results from the breakdown of universal control mechanisms which developed in mutual association as part of the historical process that brought individual cells together into multi-cellular communities. By…
The fitness of somatic cells of metazoan, the ability of proliferation and survival, depends on microenvironment. In somatic evolution, a mutated cell in a tissue clonally expands abnormally because of its high fitness as normal cells in a…
Environmental and genetic mutations can transform the cells in a co-operating healthy tissue into an ecosystem of individualistic tumour cells that compete for space and resources. Various selection forces are responsible for driving the…
Cancer results from genetic alterations that disturb the normal cooperative behavior of cells. Recent high-throughput genomic studies of cancer cells have shown that the mutational landscape of cancer is complex and that individual cancers…
An endogenous molecular-cellular network for both normal and abnormal functions is assumed to exist. This endogenous network forms a nonlinear stochastic dynamical system, with many stable attractors in its functional landscape. Normal or…
Tumors are defined by their intense proliferation, but sometimes cancer cells turn senescent and stop replicating. In the stochastic cancer model in which all cells are tumorigenic, senescence is seen as the result of random mutations,…
Cancer is viewed as a multistep process whereby a normal cell is transformed into a cancer cell through the acquisition of mutations. We reduce the complexities of cancer progression to a simple set of underlying rules that govern the…
Cancer progression involves the sequential accumulation of genetic alterations that cumulatively shape the tumour phenotype. In prostate cancer, tumours can follow divergent evolutionary trajectories that lead to distinct subtypes, but the…
Cancer is increasingly perceived as a systems-level, network phenomenon. The major trend of malignant transformation can be described as a two-phase process, where an initial increase of network plasticity is followed by a decrease of…
Metastasis, the spread of cancer cells from a primary tumor to secondary location(s) in the human organism, is the ultimate cause of death for the majority of cancer patients. That is why, it is crucial to understand metastases evolution in…
We discuss the mathematical modelling of two of the main mechanisms which pushed forward the emergence of multicellularity: phenotype divergence in cell differentiation, and between-cell cooperation. In line with the atavistic theory of…
We present a general computational theory of cancer and its developmental dynamics. The theory is based on a theory of the architecture and function of developmental control networks which guide the formation of multicellular organisms.…
Predictive modeling of the evolutionary dynamics of cancer is a challenge issue in computational cancer biology. In this paper, we propose a general mathematical model framework for the evolutionary dynamics of cancer with plasticity and…
Human language emerged abruptly. Diverse body forms evolved suddenly. Seed-bearing plants spread rapidly. How do complex evolutionary innovations arise so quickly? Resolving alternative claims remains difficult. The great events of the past…
We study the effect of intratumor heterogeneity in the likelihood of cancer cells moving from a primary tumor to other sites in the human body, generating a metastatic process. We model different scenarios of competition between tumor cells…
Cancer progression is an evolutionary process that is driven by mutation and selection in a population of tumor cells. We discuss mathematical models of cancer progression, starting from traditional multistage theory. Each stage is…
Most human tumors result from the accumulation of multiple genetic and epigenetic alterations in a single cell. Mutations that confer a fitness advantage to the cell are known as driver mutations and are causally related to tumorigenesis.…
Despite their potential to address crucial bottlenecks in computing architectures and contribute to the pool of biological inspiration for engineering, pathological biological mechanisms remain absent from computational theory. We hereby…
Any process in which competing solutions replicate with errors and numbers of their copies depend on their respective fitnesses is the evolutionary optimization process. As during carcinogenesis mutated genomes replicate according to their…