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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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The Genetics of Uveal Melanoma: Overview and Clinical Relevance.

TL;DR: In this article, it has been shown that uveal melanoma differs fundamentally from non-uveal melanomas and is an independent genetic subtype and has a low mutational burden compared to other tumours.
Journal ArticleDOI

The Genetic Evolution of Metastasis

TL;DR: In this paper , the authors discuss how these insights could inform clinical decision-making and uncover rational antimetastasis treatment strategies and discuss how they could be used to improve clinical decision making.
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Life Entrapped in a Network of Atavistic Attractors: How to Find a Rescue

TL;DR: A potentially universal model of cancer transformation and development supported by a proposed new model of cellular functionality evolution is presented and the methods of fighting cancer resulting from unified cell bioenergetics and the two presented models are considered.
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Single-cell RNA sequencing and bioinformatics as tools to decipher cancer heterogenicity and mechanisms of drug resistance.

TL;DR: In this paper, the role of single-cell RNA sequencing technologies in addressing cancer heterogeneity and cell lineage-dependent drug resistance is discussed, as well as their role in addressing carcinogenesis and drug resistance.
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.
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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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