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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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Citations
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Computational approaches for inferring tumor evolution from single-cell genomic data

TL;DR: An overview of the state-of-the-art single-cell DNA sequencing methods, technical errors that are inherent in the resulting large-scale datasets, and computational methods to overcome these errors are presented.
Journal ArticleDOI

An enhanced genetic model of colorectal cancer progression history

TL;DR: A refined tumor progression model is presented which significantly expands the understanding of the tumorigenic process of human colorectal cancer and reveals that selection is often present on subclones and that multiple evolutionary models can operate in a single tumor at different stages.
Journal ArticleDOI

Understanding genomics and the immune environment of penile cancer to improve therapy

TL;DR: Penile squamous cell carcinoma (PSCC) displays a wide range of therapeutically targetable somatic alterations, and patients with treatment-resistant advanced PSCC might benefit from combined and sequential targeted therapies.
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.
Journal ArticleDOI

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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