We are analyzing https://link.springer.com/article/10.1007/s10555-013-9435-7.

Title:
Genetic and non-genetic instability in tumor progression: link between the fitness landscape and the epigenetic landscape of cancer cells | Cancer and Metastasis Reviews
Description:
Genetic instability is invoked in explaining the cell phenotype changes that take place during cancer progression. However, the coexistence of a vast diversity of distinct clones, most prominently visible in the form of non-clonal chromosomal aberrations, suggests that Darwinian selection of mutant cells is not operating at maximal efficacy. Conversely, non-genetic instability of cancer cells must also be considered. Such mutation-independent instability of cell states is most prosaically manifest in the phenotypic heterogeneity within clonal cell populations or in the reversible switching between immature “cancer stem cell-like” and more differentiated states. How are genetic and non-genetic instability related to each other? Here, we review basic theoretical foundations and offer a dynamical systems perspective in which cancer is the inevitable pathological manifestation of modes of malfunction that are immanent to the complex gene regulatory network of the genome. We explain in an accessible, qualitative, and permissively simplified manner the mathematical basis for the “epigenetic landscape” and how the latter relates to the better known “fitness landscape.” We show that these two classical metaphors have a formal basis. By combining these two landscape concepts, we unite development and somatic evolution as the drivers of the relentless increase in malignancy. Herein, the cancer cells are pushed toward cancer attractors in the evolutionarily unused regions of the epigenetic landscape that encode more and more “dedifferentiated” states as a consequence of both genetic (mutagenic) and non-genetic (regulatory) perturbations—including therapy. This would explain why for the cancer cell, the principle of “What does not kill me makes me stronger” is as much a driving force in tumor progression and development of drug resistance as the simple principle of “survival of the fittest.”
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Keywords {🔍}

google, scholar, pubmed, cas, cancer, cell, cells, research, biology, nature, support, stem, government, journal, huang, nonus, review, instability, genetic, states, sciences, gene, reviews, article, progression, landscape, human, academy, national, epigenetic, resistance, proceedings, molecular, nongenetic, systems, regulatory, drug, united, america, tumor, kauffman, plasticity, doijcell, expression, transition, phenotype, development, evolution, networks, genetics,

Topics {✒️}

chemotherapy-induced epithelial–mesenchymal transition hyperthermia-induced nuclear translocation epithelial–mesenchymal transition phenotype mitogen-activated protein kinases month download article/chapter chromosome-specific segmentation revealed complex multi-stable systems slow-cycling melanoma cells mutation-independent driving force mesenchymal transition contributes privacy choices/manage cookies genetic instability related mutation-independent instability epithelial cell plasticity wnt-mediated regulation trail-induced apoptosis full article pdf related subjects reversible processes irreversible clonal chromosome aberrations suggest molecular underpinnings genetic regulatory networks ovarian carcinoma cells cell lineage determination continuous tumor growth gene network dynamics breast cancer cells clonal chromosomal aberrations cell regulatory networks stem cell plasticity human metastatic sarcoma cancer stem cells boolean network models stem cell traits chinese hamster cells mammalian progenitor cells european economic area inevitable pathological manifestation permissively simplified manner evolutionarily unused regions perturbations—including therapy dogmatic canonical rules histone lysine demethylases harvard university press single catastrophic event cisplatin-induced activation evade p-glycoprotein tumour stem cells human cancers express stochastic gene expression

Questions {❓}

Adult stem cell plasticity: fact or artifact?
Cancer stem cells: controversial or just misunderstood?
Cancer stem cells: mirage or reality?
Cancer: a matter of life cycle?
Cellular heterogeneity: do differences make a difference?
Efficiency of carcinogenesis: is the mutator phenotype inevitable?
How are genetic and non-genetic instability related to each other?
Neo-Darwinism, the modern synthesis and selfish genes: are they of use in physiology?
Putting together the pieces: evolutionary mechanisms at work within genomes: can we suggest molecular underpinnings of punctuated equilibria and the Cambrian explosion?
Stem cell plasticity?

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