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231224s2014 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2014.07.005
|2 doi
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|a pubmed25n0801.xml
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|a (PII)S1521-6616(14)00172-7
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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| 100 |
1 |
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|a Wu, Tingyu
|e verfasserin
|4 aut
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| 245 |
1 |
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|a Interleukin 22 protects colorectal cancer cells from chemotherapy by activating the STAT3 pathway and inducing autocrine expression of interleukin 8
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|c 2014
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 04.11.2014
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|a Date Revised 13.12.2023
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2014 Elsevier Inc. All rights reserved.
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|a Resistance to chemotherapy is the major cause of colorectal cancer (CRC) treatment failure. The cytokine IL-22, which is produced by T cells and NK cells, is associated with tumorigenesis and tumor progression in cancers. However, the role of IL-22 in chemoresistance has not been investigated. We found that IL-22 levels in tumor tissues and peripheral blood were associated with chemoresistance and indicate poor prognosis for patients who received FOLFOX chemotherapy. In CRC cells, IL-22 was able to attenuate the cytotoxic and apoptosis-inducing effects of 5-FU and OXA by activating the STAT3 pathway and subsequently increasing the expression of anti-apoptotic genes. In addition, IL-22 conferred resistance to 5-FU and OXA by inducing IL-8 autocrine expression through STAT3 activation. Our findings identify IL-22 as a novel chemoresistance cytokine and may be a useful prognostic biomarker for CRC patients receiving FOLFOX chemotherapy
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Chemoresistance
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|a Interleukin 22
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|a Interleukin 8
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|a STAT3
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|a Antineoplastic Agents
|2 NLM
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|a Interleukin-8
|2 NLM
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|a Interleukins
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|a Organoplatinum Compounds
|2 NLM
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|a STAT3 Transcription Factor
|2 NLM
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|a STAT3 protein, human
|2 NLM
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|a Leucovorin
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|a Q573I9DVLP
|2 NLM
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|a Fluorouracil
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|a U3P01618RT
|2 NLM
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| 700 |
1 |
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|a Wang, Zhongchuan
|e verfasserin
|4 aut
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| 700 |
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|a Liu, Yun
|e verfasserin
|4 aut
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| 700 |
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|a Mei, Zubing
|e verfasserin
|4 aut
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|a Wang, Guanghui
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Liang, Zhonglin
|e verfasserin
|4 aut
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| 700 |
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|a Cui, Ang
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Hu, Xuguang
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Cui, Long
|e verfasserin
|4 aut
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| 700 |
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|a Yang, Yili
|e verfasserin
|4 aut
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| 700 |
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|a Liu, Chen-Ying
|e verfasserin
|4 aut
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| 773 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 154(2014), 2 vom: 30. Okt., Seite 116-26
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
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|g volume:154
|g year:2014
|g number:2
|g day:30
|g month:10
|g pages:116-26
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|u http://dx.doi.org/10.1016/j.clim.2014.07.005
|3 Volltext
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