TL;DR: The switch between the tetrameric and dimeric form of M2-PK allows tumor cells to survive in environments with varying oxygen und nutrient supply.

TL;DR: The properties and putative relationship of these two amino acid exchangers are discussed in the context of their demonstrated utility in cancer biology, including cellular growth and survival signaling and integrated links to the mammalian target-of-rapamycin (mTOR) kinase.

TL;DR: Three-dimensional tissue culture models have an invaluable role in tumour biology today providing some very important insights into cancer biology and are currently being exploited by many branches of biomedical science with therapeutically oriented studies becoming the major focus of research.

TL;DR: It has become apparent that 3D cell culture offers a more realistic micro- and local-environment where the functional properties of cells can be observed and manipulated that is not possible in animals.

TL;DR: Analysis of the multistage skin cancer model in mice reveals that a diverse array of signals can selectively impair or enhance clonal expansion of Ras mutant cells into a visible neoplasm, indicating that tumor cells have an inherent reduced capacity to buffer against perturbations.

TL;DR: Understanding the mechanisms leading to chromosomal instability has major translational significance, since it is undoubtedly a major cause of tumor evasion of therapy.

TL;DR: This article addresses how centrosomal changes are initiated and how they may lead to spindle multipolarity and how the structure of the spindle changes that leads to increased numbers of spindle poles and abnormal partitioning of the chromosomes in mitosis.

TL;DR: It is suggested that cancer-stromal interaction can best be investigated by three-dimensional (3D) co-culture models with the results validated by clinical specimens, and showed that 3D culture promoted bone formation in vitro.

TL;DR: This paper addresses the problem of applying the concept of clonal selection to genetically unstable cells and presents an alternative perspective based on the principles of molecular evolution that explains genetic instability in terms of competition between genetic strategies and draws lines to basic aspects of evolutionary biology.

TL;DR: A carcinogenesis model in which the development of a field with genetically altered cells plays a central role is supported, which is of monoclonal origin and expands non-invasively superseding normal epithelium.

TL;DR: This article addresses the problem of whether ESFT reflect the phenotype of the tumor stem cell that is blocked in differentiation by the activity of the EWS-ets gene fusion or if the oncogene imposes an incomplete differentiation program on a pluripotent precursor cell.

TL;DR: The role of cyclin E as a prognostic marker and predictive factor in breast cancer management and the potential to use this marker as a target for therapy are discussed.

TL;DR: It is not yet possible to assess whether or not genomic instability is a prerequisite for carcinogenesis, but experimental data have shown genomic instability in some cancers, but the authors do not yet knowWhether or not hypermutation initiates and drives tumorigenesis.

TL;DR: This review compares the G --> T spectra induced by PAH o-quinones and diol epoxides with those in lung cancer and shows that the main "shaper" of the latter is selection, not mutagenesis.

TL;DR: Although Barrett's esophagus is an ideal model for the study of neoplastic clonal evolution, similar studies may be carried out in a wide variety of human neoplasms, providing insights for clinical management, including rates of progression to cancer and emergence of resistance to interventions.

TL;DR: Colorectal cancers may have chromosomal instability, microsatellite instability, or the CpG island methylator phenotype, which is associated with a unique mutational or epigenetic "signature" identifiable in the tumor cells, and there are important conceptual and clinical implications of each.

TL;DR: Numerical chromosome changes and ploidy shifts allow the simultaneous alteration of multiple cancer-relevant genes, thereby reducing the number of independent genomic events necessary for carcinogenesis and the need for postulating genomic instability as a necessity in cancer development.

TL;DR: A combination of three-dimensional in vitro and in vivo methods for the investigation of tumor cell migration are suggested and the knowledge has been reached so far is summarized.

TL;DR: This chapter will provide an overview of investigations that have characterized how the tissue microenvironment can regulate the incipient development of squamous cell carcinoma.

TL;DR: The application of transgenic methods to the study of this sarcoma-associated FUS-DDIT3 gene fusion has provided insights into their functions in vivo, and suggested mechanisms by which lineage selection may be achieved.

TL;DR: A stochastic dynamical model of cell renewal of epithelial tissue (colonic crypts) which explicitly includes asymmetric indefinite divisions of stem cells and symmetric, finite divisions of daughter cells is presented and it is found that the hierarchical structure of crypts plays a protective role against accumulation of double-mutants.

TL;DR: Observations on p53-mutant keratinocyte clones in epidermal sheets of UVB-irradiated mice reveal that mutant stem cells are normally restrained within their stem cell compartment, and chronic UVB exposure drives clonal expansion by a non-mutational mechanism, which deletes DNA-damaged cells in unmutated stem cell compartments but will preferentially spare death-resistant p53.

TL;DR: 3D-extravasation assays are valuable tools for the identification of genes, which are the key players at switchboards of the intracellular signaling pathways, and lead to unravel molecular parameters which descripe distinct clinical phenotypes of cancer and work as prognosticators, predictors of therapy and new therapy targets.

TL;DR: It is clear that genetic lesions themselves provide valuable information in the treatment of patients with cancer and those genetic lesions can be exploited successfully as therapeutic targets, whether the mechanisms resulting in the accumulation of genetic lesionscan be translated and used clinically remains to be seen.

TL;DR: Therapeutic targeting of ubiquitin or ubiquitilated proteins may reduce the malignant potential of cancer cells.

TL;DR: Evidence against a need for junctional communication supports membrane stabilization with restoration of Mg(2+) regulation as the mechanism of normalization.