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.About:
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.read more
Citations
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Single-cell DNA and RNA sequencing reveals the dynamics of intra-tumor heterogeneity in a colorectal cancer model
Hanako Ono,Arai Yasuhito,Eisaku Furukawa,Daichi Narushima,Tetsuya Matsuura,Hiromi Nakamura,Daisuke Shiokawa,Momoko Nagai,Toshio Imai,Koshi Mimori,Koji Okamoto,Yoshitaka Hippo,Tatsuhiro Shibata,Mamoru Kato +13 more
TL;DR: An evolutionary dynamics of single-cell RNA and DNA changes in tumor progression is revealed, giving insights into the mesenchymal-epithelial transformation of tumor cells at metastasis in colorectal cancer.
Journal ArticleDOI
Breast cancer heterogeneity through the lens of single-cell analysis and spatial pathologies
TL;DR: In this article, the authors discuss the insights gained through single-cell analysis and spatial pathologies on breast cancer heterogeneity, which may help facilitate the development of novel therapies and improve outcomes for patients.
Posted ContentDOI
Power and pitfalls of computational methods for inferring clone phylogenies and mutation orders from bulk sequencing data
TL;DR: Overall, CloneFinder, MACHINA, and LICHeE showed the highest overall accuracy, but none of the methods performed well for all simulated datasets and conditions.
Journal ArticleDOI
Towards multi-omics characterization of tumor heterogeneity: a comprehensive review of statistical and machine learning approaches.
TL;DR: A comprehensive review of diverse approaches to characterize tumor heterogeneity based on three different omics layers: genome, epigenome and transcriptome can be useful for the analysis of multi-omics profiles produced by many large-scale consortia.
Journal ArticleDOI
Breast cancer heterogeneity through the lens of single-cell analysis and spatial pathologies
Cihan Papan,Elena A. Lapp +1 more
TL;DR: In this article , the authors discuss the insights gained through single-cell analysis and spatial pathologies on breast cancer heterogeneity, which may help facilitate the development of novel therapies and improve outcomes for patients.
References
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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
Eric R. Fearon,Bert Vogelstein +1 more
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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Intratumor heterogeneity and branched evolution revealed by multiregion sequencing.
Marco Gerlinger,Andrew Rowan,Stuart Horswell,James Larkin,David Endesfelder,Eva Grönroos,Pierre Martinez,Nicholas Matthews,Aengus Stewart,Patrick S. Tarpey,Ignacio Varela,Benjamin Phillimore,Sharmin Begum,Neil Q. McDonald,Adam Butler,David T. Jones,Keiran Raine,Calli Latimer,Claudio R. Santos,Mahrokh Nohadani,Aron Charles Eklund,Bradley Spencer-Dene,Graham Clark,Lisa Pickering,Gordon Stamp,Martin Gore,Zoltan Szallasi,Zoltan Szallasi,Julian Downward,P. Andrew Futreal,Charles Swanton +30 more
TL;DR: Intratumor heterogeneity can lead to underestimation of the tumor genomics landscape portrayed from single tumor-biopsy samples and may present major challenges to personalized-medicine and biomarker development.
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
Jeffrey A. Engelman,Kreshnik Zejnullahu,Tetsuya Mitsudomi,Youngchul Song,Courtney Hyland,Joon Oh Park,Neal I. Lindeman,Christopher-Michael Gale,Xiaojun Zhao,James J. Christensen,Takayuki Kosaka,Alison J. Holmes,Andrew M. Rogers,Federico Cappuzzo,Tony Mok,Charles Lee,Bruce E. Johnson,Lewis C. Cantley,Pasi A. Jänne +18 more
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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Marco Gerlinger,Andrew Rowan,Stuart Horswell,James Larkin,David Endesfelder,Eva Grönroos,Pierre Martinez,Nicholas Matthews,Aengus Stewart,Patrick S. Tarpey,Ignacio Varela,Benjamin Phillimore,Sharmin Begum,Neil Q. McDonald,Adam Butler,David T. Jones,Keiran Raine,Calli Latimer,Claudio R. Santos,Mahrokh Nohadani,Aron Charles Eklund,Bradley Spencer-Dene,Graham Clark,Lisa Pickering,Gordon Stamp,Martin Gore,Zoltan Szallasi,Zoltan Szallasi,Julian Downward,P. Andrew Futreal,Charles Swanton +30 more