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Open AccessJournal ArticleDOI

Tumor evolution: Linear, branching, neutral or punctuated?☆

TLDR
Data is discussed that supports the theory that most human tumors evolve from a single cell in the normal tissue, and suggests that models may change during tumor progression or operate concurrently for different classes of mutations.
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This article is published in Biochimica et Biophysica Acta.The article was published on 2017-04-01 and is currently open access. It has received 255 citations till now. The article focuses on the topics: Tumor progression.

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Posted ContentDOI

Comprehensive, integrated and phased whole-genome analysis of the primary ENCODE cell line K562

TL;DR: This comprehensive whole-genome analysis of K562 serves as a resource for future studies that utilize K562 and as the basis of advanced analyses of the rich amounts of the functional genomics data produced by ENCODE for K562.
Posted ContentDOI

Benchmarking Tools for Copy Number Aberration Detection from Single-cell DNA Sequencing Data

TL;DR: This work categorizes the methods for segmenting the genome into regions of different copy numbers into three groups, select a representative method from each group that has been commonly used in this context, and benchmark them on simulated as well as real datasets.
Journal ArticleDOI

Predicting clone genotypes from tumor bulk sequencing of multiple samples.

TL;DR: CloneFinder, LICHeE, CITUP and cloneHD inferred clone genotypes with low error for a majority of datasets in which the tumor samples contained evolutionarily-related clones, while AncesTree and Canopy did not produce results for a large number of datasets.
Journal ArticleDOI

The Many Facets of Tumor Heterogeneity: Is Metabolism Lagging Behind?

TL;DR: Historical and current views of intratumoral heterogeneity are reviewed, with an emphasis on summarizing the emerging data that begin to illuminate just how vast the spectrum of metabolic strategies a tumor can employ may be, and what this means for how to interpret other tumor characteristics, such as mutational landscape, contribution of microenvironmental influences, and treatment resistance.
Journal ArticleDOI

Evolution and Impact of Subclonal Mutations in Papillary Thyroid Cancer.

TL;DR: It is concluded that relapse in PTC does not follow a predictable evolutionary path and that subclonal mutation burden may serve as a prognostic factor, and larger studies utilizing multi-region sequencing in relapsed PTC case subjects with matching primary tissues are needed to confirm these observations.
References
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Journal ArticleDOI

Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation

TL;DR: It is proposed that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass needed to produce a new cell.
Journal ArticleDOI

A genetic model for colorectal tumorigenesis

TL;DR: A model for the genetic basis of colorectal neoplasia that includes the following salient features is presented, which may be applicable to other common epithelial neoplasms, in which tumors of varying stage are more difficult to study.
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The clonal evolution of tumor cell populations

TL;DR: Each patient's cancer may require individual specific therapy, and even this may be thwarted by emergence of a genetically variant subline resistant to the treatment, which should be directed toward understanding and controlling the evolutionary process in tumors before it reaches the late stage usually seen in clinical cancer.
Journal ArticleDOI

MET Amplification Leads to Gefitinib Resistance in Lung Cancer by Activating ERBB3 Signaling

TL;DR: It is proposed that MET amplification may promote drug resistance in other ERBB-driven cancers as well after it was found that amplification of MET causes gefitinib resistance by driving ERBB3 (HER3)–dependent activation of PI3K, a pathway thought to be specific to EGFR/ERBB family receptors.
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