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DC Field | Value | Language |
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dc.citation.endPage | 21063 | - |
dc.citation.number | 51 | - |
dc.citation.startPage | 21058 | - |
dc.citation.title | PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | - |
dc.citation.volume | 109 | - |
dc.contributor.author | Park, Jiyoung | - |
dc.contributor.author | Sarode, Venetia R. | - |
dc.contributor.author | Euhus, David | - |
dc.contributor.author | Kittler, Ralf | - |
dc.contributor.author | Scherer, Philipp E. | - |
dc.date.accessioned | 2023-12-22T04:36:41Z | - |
dc.date.available | 2023-12-22T04:36:41Z | - |
dc.date.created | 2014-10-13 | - |
dc.date.issued | 2012-12 | - |
dc.description.abstract | Poor outcomes in diabetic patients are observed across a range of human tumors, suggesting that cancer cells develop unique characteristics under diabetic conditions. Cancer cells exposed to hyperglycemic insults acquire permanent aggressive traits of tumor growth, even after a return to euglycemic conditions. Comparative genome-wide mapping of hyperglycemia-specific open chromatin regions and concomitant mRNA expression profiling revealed that the neuregulin-1 gene, encoding an established endogenous ligand for the HER3 receptor, is activated through a putative distal enhancer. Our findings highlight the targeted inhibition of NRG1-HER3 pathways as a potential target for the treatment breast cancer patients with associated diabetes. | - |
dc.identifier.bibliographicCitation | PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, v.109, no.51, pp.21058 - 21063 | - |
dc.identifier.doi | 10.1073/pnas.1214400109 | - |
dc.identifier.issn | 0027-8424 | - |
dc.identifier.scopusid | 2-s2.0-84871361983 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/7142 | - |
dc.identifier.url | http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84871361983 | - |
dc.identifier.wosid | 000313123700064 | - |
dc.language | 영어 | - |
dc.publisher | NATL ACAD SCIENCES | - |
dc.title | Neuregulin 1-HER axis as a key mediator of hyperglycemic memory effects in breast cancer | - |
dc.type | Article | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordAuthor | PANIC-ATTAC | - |
dc.subject.keywordAuthor | FAIRE-seq | - |
dc.subject.keywordAuthor | metabolic imprinting | - |
dc.subject.keywordPlus | GROWTH-FACTOR RECEPTOR | - |
dc.subject.keywordPlus | IN-VIVO | - |
dc.subject.keywordPlus | MOUSE MODEL | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | PROLIFERATION | - |
dc.subject.keywordPlus | TRASTUZUMAB | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | INHIBITORS | - |
dc.subject.keywordPlus | HEREGULIN | - |
dc.subject.keywordPlus | CHROMATIN | - |
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