Cancer stem cells: The root of tumor recurrence and metastases

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Cancer stem cells: The root of tumor recurrence and metastases. / Peitzsch, Claudia; Tyutyunnykova, Anna; Pantel, Klaus; Dubrovska, Anna.

in: SEMIN CANCER BIOL, Jahrgang 44, 06.2017, S. 10-24.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ReviewForschung

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@article{a13224d1eec949c7bbdb16ced041a849,
title = "Cancer stem cells: The root of tumor recurrence and metastases",
abstract = "Metastatic tumors are the cause of more than 90% of cancer related deaths. Metastasis formation can be considered as a culmination of the Darwinian evolutionary process within the tumor, when competition of multiple clones results in the development of cell inherent traits that favor tumor dissemination. Cancer stem cells (CSC) which possess self-renewal properties and genomic instability are considered to be an engine of tumor evolution. Cancer cells which have the capacity to colonize distant organs have the features of CSC and, in addition, exert their tumor-initiating capacity under adverse microenvironmental conditions. Recent studies support an idea that metastases can be driven by the evolved and selected subpopulations of CSC. In this review we discuss the common hallmarks of CSC and metastasis initiating cells (MIC) and prospects for the development of anti-metastatic therapy.",
keywords = "Journal Article, Review",
author = "Claudia Peitzsch and Anna Tyutyunnykova and Klaus Pantel and Anna Dubrovska",
note = "Copyright {\textcopyright} 2017 Elsevier Ltd. All rights reserved.",
year = "2017",
month = jun,
doi = "10.1016/j.semcancer.2017.02.011",
language = "English",
volume = "44",
pages = "10--24",
journal = "SEMIN CANCER BIOL",
issn = "1044-579X",
publisher = "Academic Press Inc.",

}

RIS

TY - JOUR

T1 - Cancer stem cells: The root of tumor recurrence and metastases

AU - Peitzsch, Claudia

AU - Tyutyunnykova, Anna

AU - Pantel, Klaus

AU - Dubrovska, Anna

N1 - Copyright © 2017 Elsevier Ltd. All rights reserved.

PY - 2017/6

Y1 - 2017/6

N2 - Metastatic tumors are the cause of more than 90% of cancer related deaths. Metastasis formation can be considered as a culmination of the Darwinian evolutionary process within the tumor, when competition of multiple clones results in the development of cell inherent traits that favor tumor dissemination. Cancer stem cells (CSC) which possess self-renewal properties and genomic instability are considered to be an engine of tumor evolution. Cancer cells which have the capacity to colonize distant organs have the features of CSC and, in addition, exert their tumor-initiating capacity under adverse microenvironmental conditions. Recent studies support an idea that metastases can be driven by the evolved and selected subpopulations of CSC. In this review we discuss the common hallmarks of CSC and metastasis initiating cells (MIC) and prospects for the development of anti-metastatic therapy.

AB - Metastatic tumors are the cause of more than 90% of cancer related deaths. Metastasis formation can be considered as a culmination of the Darwinian evolutionary process within the tumor, when competition of multiple clones results in the development of cell inherent traits that favor tumor dissemination. Cancer stem cells (CSC) which possess self-renewal properties and genomic instability are considered to be an engine of tumor evolution. Cancer cells which have the capacity to colonize distant organs have the features of CSC and, in addition, exert their tumor-initiating capacity under adverse microenvironmental conditions. Recent studies support an idea that metastases can be driven by the evolved and selected subpopulations of CSC. In this review we discuss the common hallmarks of CSC and metastasis initiating cells (MIC) and prospects for the development of anti-metastatic therapy.

KW - Journal Article

KW - Review

U2 - 10.1016/j.semcancer.2017.02.011

DO - 10.1016/j.semcancer.2017.02.011

M3 - SCORING: Review article

C2 - 28257956

VL - 44

SP - 10

EP - 24

JO - SEMIN CANCER BIOL

JF - SEMIN CANCER BIOL

SN - 1044-579X

ER -