Cited 4 times in
BRCA1 deficiency in triple-negative breast cancer: Protein stability as a basis for therapy
DC Field | Value | Language |
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dc.contributor.author | 조재호 | - |
dc.date.accessioned | 2023-03-22T02:38:56Z | - |
dc.date.available | 2023-03-22T02:38:56Z | - |
dc.date.issued | 2023-02 | - |
dc.identifier.issn | 0753-3322 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/193640 | - |
dc.description.abstract | Mutations in breast cancer-associated 1 (BRCA1) increase the lifetime risk of developing breast cancer by up to 51% over the risk of the general population. Many aspects of this multifunctional protein have been revealed, including its essential role in homologous recombination repair, E3 ubiquitin ligase activity, transcriptional regulation, and apoptosis. Although most studies have focused on BRCA1 deficiency due to mutations, only a minority of patients carry BRCA1 mutations. A recent study has suggested an expanded definition of BRCA1 deficiency with reduced BRCA1 levels, which accounts for almost half of all triple-negative breast cancer (TNBC) patients. Reduced BRCA1 levels can result from epigenetic modifications or increased proteasomal degradation. In this review, we discuss how this knowledge of BRCA1 function and regulation of BRCA1 protein stability can help overcome the challenges encountered in the clinic and advance current treatment strategies for BRCA1-related breast cancer patients, especially focusing on TNBC. | - |
dc.description.statementOfResponsibility | open | - |
dc.language | English, French | - |
dc.publisher | Elsevier | - |
dc.relation.isPartOf | BIOMEDICINE & PHARMACOTHERAPY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.subject.MESH | BRCA1 Protein / genetics | - |
dc.subject.MESH | BRCA1 Protein / metabolism | - |
dc.subject.MESH | DNA Repair | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Mutation | - |
dc.subject.MESH | Protein Stability | - |
dc.subject.MESH | Triple Negative Breast Neoplasms* / genetics | - |
dc.subject.MESH | Triple Negative Breast Neoplasms* / therapy | - |
dc.title | BRCA1 deficiency in triple-negative breast cancer: Protein stability as a basis for therapy | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Radiation Oncology (방사선종양학교실) | - |
dc.contributor.googleauthor | Eun Choi | - |
dc.contributor.googleauthor | Gil-Im Mun | - |
dc.contributor.googleauthor | Joohyun Lee | - |
dc.contributor.googleauthor | Hanhee Lee | - |
dc.contributor.googleauthor | Jaeho Cho | - |
dc.contributor.googleauthor | Yun-Sil Lee | - |
dc.identifier.doi | 10.1016/j.biopha.2022.114090 | - |
dc.contributor.localId | A03901 | - |
dc.relation.journalcode | J00322 | - |
dc.identifier.eissn | 1950-6007 | - |
dc.identifier.pmid | 36493696 | - |
dc.subject.keyword | BRCA1 deficiency | - |
dc.subject.keyword | Chemotherapy resistance | - |
dc.subject.keyword | Multifunction | - |
dc.subject.keyword | Proteasomal degradation | - |
dc.subject.keyword | Triple-negative breast cancer | - |
dc.contributor.alternativeName | Cho, Jae Ho | - |
dc.contributor.affiliatedAuthor | 조재호 | - |
dc.citation.volume | 158 | - |
dc.citation.startPage | 114090 | - |
dc.identifier.bibliographicCitation | BIOMEDICINE & PHARMACOTHERAPY, Vol.158 : 114090, 2023-02 | - |
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