Cited 16 times in
Genomic profiling of the residual disease of advanced high-grade serous ovarian cancer after neoadjuvant chemotherapy
DC Field | Value | Language |
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dc.contributor.author | 김현수 | - |
dc.contributor.author | 배수진 | - |
dc.contributor.author | 백순명 | - |
dc.contributor.author | 이용재 | - |
dc.contributor.author | 이정윤 | - |
dc.contributor.author | 이한나 | - |
dc.date.accessioned | 2020-04-13T16:43:26Z | - |
dc.date.available | 2020-04-13T16:43:26Z | - |
dc.date.issued | 2020 | - |
dc.identifier.issn | 0020-7136 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/175482 | - |
dc.description.abstract | The goal of our study was to demonstrate the spectrum of genomic alterations present in the residual disease of patients with advanced high-grade serous ovarian cancer (HGSOC) after neoadjuvant chemotherapy (NAC), including matched pretreatment biopsies. During the study period between 2006 and 2017, we collected pre-NAC and post-NAC tumor tissue samples from patients with advanced HGSOC. We performed combined next-generation sequencing and immunohistochemistry to identify actionable targets and pathway activation in post-NAC residual tumors. We also examined whether post-NAC profiling of residual HGSOC identified targetable molecular lesions in the chemotherapy-resistant component of tumors. Among 102 post-NAC samples, 41 (40%) of patients had mutations in homologous recombination repair (HRR) genes (HRR deficiency). Patients with HRR mutations had higher tumor mutation burdens (p < 0.001) and higher alterations in the PI3K-AKT-mTOR pathway (p = 0.004) than patients without these HRR mutations. Nevertheless, we found no significant differences in progression-free survival (p = 0.662) and overall survival (OS; p = 0.828) between the two groups. Most patients (91%) had alterations in at least one of the targetable pathways, and those patients with cell cycle (p = 0.004) and PI3K-AKT-mTOR signaling (p = 0.005) pathway alterations had poorer OS (Bonferroni-corrected threshold = 0.0083, 0.05/6). We showed the genomic landscape of tumor cells remaining in advanced HGSOC after NAC. Once validated, these data can help inform biomarker-driven adjuvant studies in targeting residual tumors to improve the outcomes of patients with advanced HGSOC after NAC. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.language | English | - |
dc.publisher | Wiley-Liss | - |
dc.relation.isPartOf | INTERNATIONAL JOURNAL OF CANCER | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.subject.MESH | Adult | - |
dc.subject.MESH | Aged | - |
dc.subject.MESH | Antineoplastic Combined Chemotherapy Protocols/pharmacology* | - |
dc.subject.MESH | Antineoplastic Combined Chemotherapy Protocols/therapeutic use | - |
dc.subject.MESH | Biopsy | - |
dc.subject.MESH | Cell Cycle/genetics | - |
dc.subject.MESH | Cystadenocarcinoma, Serous/genetics* | - |
dc.subject.MESH | Cystadenocarcinoma, Serous/mortality | - |
dc.subject.MESH | Cystadenocarcinoma, Serous/therapy | - |
dc.subject.MESH | Cytoreduction Surgical Procedures/methods | - |
dc.subject.MESH | Disease Progression | - |
dc.subject.MESH | Drug Resistance, Neoplasm/genetics | - |
dc.subject.MESH | Female | - |
dc.subject.MESH | Genomics | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Middle Aged | - |
dc.subject.MESH | Mutation/drug effects | - |
dc.subject.MESH | Neoadjuvant Therapy/methods | - |
dc.subject.MESH | Neoplasm, Residual | - |
dc.subject.MESH | Ovarian Neoplasms/genetics* | - |
dc.subject.MESH | Ovarian Neoplasms/mortality | - |
dc.subject.MESH | Ovarian Neoplasms/therapy | - |
dc.subject.MESH | Ovariectomy/methods | - |
dc.subject.MESH | Ovary/drug effects | - |
dc.subject.MESH | Ovary/pathology* | - |
dc.subject.MESH | Phosphatidylinositol 3-Kinases/metabolism | - |
dc.subject.MESH | Progression-Free Survival | - |
dc.subject.MESH | Proto-Oncogene Proteins c-akt/metabolism | - |
dc.subject.MESH | Retrospective Studies | - |
dc.subject.MESH | Signal Transduction/drug effects | - |
dc.subject.MESH | Signal Transduction/genetics | - |
dc.subject.MESH | Survival Analysis | - |
dc.subject.MESH | TOR Serine-Threonine Kinases/metabolism | - |
dc.title | Genomic profiling of the residual disease of advanced high-grade serous ovarian cancer after neoadjuvant chemotherapy | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Pathology (병리학교실) | - |
dc.contributor.googleauthor | Yong J. Lee | - |
dc.contributor.googleauthor | Dachan Kim | - |
dc.contributor.googleauthor | Jung E. Shim | - |
dc.contributor.googleauthor | Su‐Jin Bae | - |
dc.contributor.googleauthor | Yu‐Jin Jung | - |
dc.contributor.googleauthor | Sora Kim | - |
dc.contributor.googleauthor | Hanna Lee | - |
dc.contributor.googleauthor | So H. Kim | - |
dc.contributor.googleauthor | Su B. Jo | - |
dc.contributor.googleauthor | Jung‐Yun Lee | - |
dc.contributor.googleauthor | Hyun‐Soo Kim | - |
dc.contributor.googleauthor | Soonmyung Paik | - |
dc.identifier.doi | 10.1002/ijc.32729 | - |
dc.contributor.localId | A01114 | - |
dc.contributor.localId | A05344 | - |
dc.contributor.localId | A01823 | - |
dc.contributor.localId | A05165 | - |
dc.contributor.localId | A04638 | - |
dc.contributor.localId | A03275 | - |
dc.relation.journalcode | J01092 | - |
dc.identifier.eissn | 1097-0215 | - |
dc.identifier.pmid | 31603993 | - |
dc.identifier.url | https://onlinelibrary.wiley.com/doi/full/10.1002/ijc.32729 | - |
dc.subject.keyword | genomic profiling | - |
dc.subject.keyword | high-grade serous carcinoma | - |
dc.subject.keyword | ovarian cancer | - |
dc.subject.keyword | residual disease | - |
dc.contributor.alternativeName | Kim, Hyun-Soo | - |
dc.contributor.affiliatedAuthor | 김현수 | - |
dc.contributor.affiliatedAuthor | 배수진 | - |
dc.contributor.affiliatedAuthor | 백순명 | - |
dc.contributor.affiliatedAuthor | 이용재 | - |
dc.contributor.affiliatedAuthor | 이정윤 | - |
dc.contributor.affiliatedAuthor | 이한나 | - |
dc.citation.volume | 146 | - |
dc.citation.number | 7 | - |
dc.citation.startPage | 1851 | - |
dc.citation.endPage | 1861 | - |
dc.identifier.bibliographicCitation | INTERNATIONAL JOURNAL OF CANCER, Vol.146(7) : 1851-1861, 2020 | - |
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