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Control of stress signaling in stem cells: crossroads of stem cells and cancer
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Title
Control of stress signaling in stem cells: crossroads of stem cells and cancer
Issued Date
2016-10
Citation
Cho, Seung-Ju. (2016-10). Control of stress signaling in stem cells: crossroads of stem cells and cancer. Tumour biology, 37(10), 12983–12990. doi: 10.1007/s13277-016-5249-x
Type
Article
Author Keywords
Stem cellsStress modulatorAnti-growth signalsOncogenic susceptibility
Keywords
Anti-Growth SignalsCOLORECTAL-CANCERDNA-DAMAGEENDOTHELIAL PROGENITor CELLSIN-VITRO EXPANSIONLUNG-CANCEROncogenic SusceptibilityP16(INK4A) INACTIVATIONPROLIFERATIVE CAPACITYSELF-RENEWALSKELETAL-MUSCLEStem CellsStress ModulatorWIP1 PHOSPHATASE
ISSN
1010-4283
Abstract
Tumorigenesis is a relatively rare event in the human body considering the enormous number of cells composing our body and the frequent occurrence of genetic mutations in each cell. Nevertheless, the cells that happen to meet the minimum requirements can be transformed when stressed by a variety of oncogenic stimulations, then progress to form tumors. The vigorous competition between oncogenic signaling and tumor-suppressor defense is a critical determinant of cellular fate, which can be either tumorigenic transformation or cellular senescence/apoptosis depending on “who wins the battle.” Recently, a number of cancers have been reported to originate from stem cells, whose self-renewing properties are normally reduced by innate tumor suppressors. Therefore, exploring the innate mechanism by which stem cells modulate tumor suppressors to maintain their “stemness” may provide valuable clues to characterize the distinctive oncogenic susceptibility of stem cells. This review is focused on the recent advances in the field of tumorigenesis of stem cells and on the associated molecular mechanisms. © 2016, International Society of Oncology and BioMarkers (ISOBM).
URI
http://hdl.handle.net/20.500.11750/2190
DOI
10.1007/s13277-016-5249-x
Publisher
Springer
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Koo, JaeHyung구재형

Department of New Biology

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