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https://doi.org/10.1038/oncsis.2017.14
| Title: | Wnt signaling in triple-negative breast cancer | Authors: | Pohl, Sö.-G Brook, N Agostino, M Arfuso, F Kumar, A.P Dharmarajan, A |
Keywords: | activating transcription factor androgen receptor beta catenin breast cancer resistance protein calcium ion DEAD box protein dishevelled protein frizzled protein glycogen synthase kinase 3 histone deacetylase inhibitor low density lipoprotein receptor related protein 5 low density lipoprotein receptor related protein 6 nicotinamide adenine dinucleotide adenosine diphosphate ribosyltransferase inhibitor protein tyrosine kinase STAT protein stress activated protein kinase ubiquitin protein ligase E3 Wnt protein actin polymerization antineoplastic activity basal like immune activated triple negative breast cancer basal like immune suppressed triple negative breast cancer cancer growth cancer recurrence cancer stem cell cancer therapy cell polarity drug use gene dosage human luminal androgen receptor triple negative breast cancer mesenchymal stem cell mesenchymal triple negative breast cancer microarray analysis postnatal development priority journal protein phosphorylation Review triple negative breast cancer Wnt signaling pathway |
Issue Date: | 2017 | Publisher: | Springer Nature | Citation: | Pohl, Sö.-G, Brook, N, Agostino, M, Arfuso, F, Kumar, A.P, Dharmarajan, A (2017). Wnt signaling in triple-negative breast cancer. Oncogenesis 6 (4) : e310. ScholarBank@NUS Repository. https://doi.org/10.1038/oncsis.2017.14 | Rights: | Attribution 4.0 International | Abstract: | Wnt signaling regulates a variety of cellular processes, including cell fate, differentiation, proliferation and stem cell pluripotency. Aberrant Wnt signaling is a hallmark of many cancers. An aggressive subtype of breast cancer, known as triple-negative breast cancer (TNBC), demonstrates dysregulation in canonical and non-canonical Wnt signaling. In this review, we summarize regulators of canonical and non-canonical Wnt signaling, as well as Wnt signaling dysfunction that mediates the progression of TNBC. We review the complex molecular nature of TNBC and the emerging therapies that are currently under investigation for the treatment of this disease. © 2017 The Author(s). | Source Title: | Oncogenesis | URI: | https://scholarbank.nus.edu.sg/handle/10635/183536 | ISSN: | 2157-9024 | DOI: | 10.1038/oncsis.2017.14 | Rights: | Attribution 4.0 International |
| Appears in Collections: | Elements Staff Publications |
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