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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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Cooperation among tumor cell subpopulations leads to intratumor heterogeneity

TL;DR: In this article, the authors explore how the interactions among subclone populations influence the establishment of intratumor heterogeneity (ITH), and develop quantitative theoretical models for explaining data from pancreatic cancer and glioblastoma multiforme.
Journal ArticleDOI

Mantle cell lymphoma with EBV-positive Hodgkin and Reed-Sternberg-like cells in a patient after autologous PBSCT: Phenotypically distinct but genetically related tumors.

TL;DR: The case of 70‐year‐old man with mantle cell lymphoma (MCL) carrying t(11;14) translocation that relapsed as nodal lymphoma combining MCL and classic Hodgkin lymphoma 9 years after autologous peripheral blood stem cell transplant (auto‐PBSCT) is reported.
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Intratumor Heterogeneity as a Prognostic Factor in Solid Tumors: A Systematic Review and Meta-Analysis.

TL;DR: In this paper, a meta-analysis was performed to explore whether intratumor heterogeneity (ITH) can serve as a valuable prognostic indicator in solid tumors, which revealed that high ITH associated with shorter survival time.
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Parameter, noise, and tree topology effects in tumor phylogeny inference.

TL;DR: This work examines the space of all possible tumor phylogenies under the infinite sites assumption (ISA) using several approaches for enumerating phylogenies consistent with the sequencing data and shows that an ISA-based approach can be relaxed to produce high-quality phylogenies.
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Modes of Selection in Tumors as Reflected by Two Mathematical Models and Site Frequency Spectra

TL;DR: Two Time-Continuous Markov Chain versions of the tug-of-war model are defined, including identical mutation processes but adopting different drift and selection components, and the statistics of mutation frequencies known as the Site Frequency Spectra are used, to compare the variant frequencies in DNA of sequenced HER2+ breast cancers, to those based on Model A and B simulations.
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.
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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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