Full metadata record
DC Field | Value | Language |
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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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