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dc.contributor.author Cho, Seung-Ju -
dc.contributor.author Koo, JaeHyung -
dc.contributor.author Chun, Kwang-Hoon -
dc.contributor.author Cha, Hyuk-Jin -
dc.date.available 2017-07-05T08:33:35Z -
dc.date.created 2017-04-10 -
dc.date.issued 2016-10 -
dc.identifier.issn 1010-4283 -
dc.identifier.uri http://hdl.handle.net/20.500.11750/2190 -
dc.description.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). -
dc.language English -
dc.publisher Springer -
dc.title Control of stress signaling in stem cells: crossroads of stem cells and cancer -
dc.type Article -
dc.identifier.doi 10.1007/s13277-016-5249-x -
dc.identifier.scopusid 2-s2.0-84979656477 -
dc.identifier.bibliographicCitation Tumour biology, v.37, no.10, pp.12983 - 12990 -
dc.description.isOpenAccess FALSE -
dc.subject.keywordAuthor Stem cells -
dc.subject.keywordAuthor Stress modulator -
dc.subject.keywordAuthor Anti-growth signals -
dc.subject.keywordAuthor Oncogenic susceptibility -
dc.subject.keywordPlus Anti-Growth Signals -
dc.subject.keywordPlus COLORECTAL-CANCER -
dc.subject.keywordPlus DNA-DAMAGE -
dc.subject.keywordPlus ENDOTHELIAL PROGENITor CELLS -
dc.subject.keywordPlus IN-VITRO EXPANSION -
dc.subject.keywordPlus LUNG-CANCER -
dc.subject.keywordPlus Oncogenic Susceptibility -
dc.subject.keywordPlus P16(INK4A) INACTIVATION -
dc.subject.keywordPlus PROLIFERATIVE CAPACITY -
dc.subject.keywordPlus SELF-RENEWAL -
dc.subject.keywordPlus SKELETAL-MUSCLE -
dc.subject.keywordPlus Stem Cells -
dc.subject.keywordPlus Stress Modulator -
dc.subject.keywordPlus WIP1 PHOSPHATASE -
dc.citation.endPage 12990 -
dc.citation.number 10 -
dc.citation.startPage 12983 -
dc.citation.title Tumour biology -
dc.citation.volume 37 -
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Department of New Biology Brain-Immune Axis Laboratory 1. Journal Articles

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