دورية أكاديمية

Proteogenomic Characterization of Ovarian HGSC Implicates Mitotic Kinases, Replication Stress in Observed Chromosomal Instability.

التفاصيل البيبلوغرافية
العنوان: Proteogenomic Characterization of Ovarian HGSC Implicates Mitotic Kinases, Replication Stress in Observed Chromosomal Instability.
المؤلفون: McDermott JE; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354, USA.; Department of Molecular Microbiology and Immunology, Oregon Health & Science University, Portland, OR 97201, USA.; These authors contributed equally., Arshad OA; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354, USA.; These authors contributed equally., Petyuk VA; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354, USA., Fu Y; Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA., Gritsenko MA; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354, USA., Clauss TR; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354, USA., Moore RJ; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354, USA., Schepmoes AA; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354, USA., Zhao R; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354, USA., Monroe ME; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354, USA., Schnaubelt M; Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA., Tsai CF; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354, USA., Payne SH; Department of Biology, Brigham Young University, Provo, UT 84602, USA., Huang C; Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston, TX 77030, USA.; Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA., Wang LB; The McDonnell Genome Institute, Washington University in St. Louis, St Louis, MO 63108, USA., Foltz S; The McDonnell Genome Institute, Washington University in St. Louis, St Louis, MO 63108, USA., Wyczalkowski M; The McDonnell Genome Institute, Washington University in St. Louis, St Louis, MO 63108, USA., Wu Y; The McDonnell Genome Institute, Washington University in St. Louis, St Louis, MO 63108, USA., Song E; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354, USA., Brewer MA; Department of Obstetrics and Gynecology, University of Connecticut, Farmington, CT 06030, USA., Thiagarajan M; Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA., Kinsinger CR; Office of Cancer Clinical Proteomics Research, National Cancer Institute, Bethesda, MD 20892, USA., Robles AI; Office of Cancer Clinical Proteomics Research, National Cancer Institute, Bethesda, MD 20892, USA., Boja ES; Office of Cancer Clinical Proteomics Research, National Cancer Institute, Bethesda, MD 20892, USA., Rodriguez H; Office of Cancer Clinical Proteomics Research, National Cancer Institute, Bethesda, MD 20892, USA., Chan DW; Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA., Zhang B; Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston, TX 77030, USA.; Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA., Zhang Z; Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA., Ding L; The McDonnell Genome Institute, Washington University in St. Louis, St Louis, MO 63108, USA., Smith RD; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354, USA., Liu T; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354, USA., Rodland KD; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354, USA.; Department of Cell, Developmental, and Cancer Biology, Oregon Health & Science University, Portland, OR 97201, USA.; Lead Contact.
مؤلفون مشاركون: Clinical Proteomic Tumor Analysis Consortium
المصدر: Cell reports. Medicine [Cell Rep Med] 2020 Apr 21; Vol. 1 (1). Date of Electronic Publication: 2020 Apr 10.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 101766894 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2666-3791 (Electronic) Linking ISSN: 26663791 NLM ISO Abbreviation: Cell Rep Med
أسماء مطبوعة: Original Publication: [Cambridge, MA] : Cell Press, [2020]-
مواضيع طبية MeSH: Cystadenocarcinoma, Serous*/genetics , Cystadenocarcinoma, Serous*/metabolism , Cystadenocarcinoma, Serous*/mortality , Ovarian Neoplasms*/genetics , Ovarian Neoplasms*/metabolism , Ovarian Neoplasms*/mortality, Chromosomal Instability/*physiology , DNA Replication/*genetics , Phosphotransferases/*genetics, Adult ; Aged ; Aged, 80 and over ; Cell Cycle Checkpoints/genetics ; Cohort Studies ; DNA Damage ; Fallopian Tube Neoplasms/genetics ; Fallopian Tube Neoplasms/metabolism ; Fallopian Tube Neoplasms/mortality ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Middle Aged ; Mitosis/genetics ; Phosphotransferases/metabolism ; Proteogenomics ; Transcriptome ; Tumor Suppressor Protein p53/genetics
مستخلص: In the absence of a dominant driving mutation other than uniformly present TP53 mutations, deeper understanding of the biology driving ovarian high-grade serous cancer (HGSC) requires analysis at a functional level, including post-translational modifications. Comprehensive proteogenomic and phosphoproteomic characterization of 83 prospectively collected ovarian HGSC and appropriate normal precursor tissue samples (fallopian tube) under strict control of ischemia time reveals pathways that significantly differentiate between HGSC and relevant normal tissues in the context of homologous repair deficiency (HRD) status. In addition to confirming key features of HGSC from previous studies, including a potential survival-associated signature and histone acetylation as a marker of HRD, deep phosphoproteomics provides insights regarding the potential role of proliferation-induced replication stress in promoting the characteristic chromosomal instability of HGSC and suggests potential therapeutic targets for use in precision medicine trials.
Competing Interests: DECLARATION OF INTERESTS The authors declare no competing interests.
التعليقات: Erratum in: Cell Rep Med. 2020 Aug 25;1(5):. (PMID: 32954372)
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معلومات مُعتمدة: P41 GM103493 United States GM NIGMS NIH HHS; U24 CA160019 United States CA NCI NIH HHS; U24 CA160036 United States CA NCI NIH HHS; U24 CA210955 United States CA NCI NIH HHS
المشرفين على المادة: 0 (Tumor Suppressor Protein p53)
EC 2.7.- (Phosphotransferases)
تواريخ الأحداث: Date Created: 20200613 Date Completed: 20220222 Latest Revision: 20220222
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC7289043
DOI: 10.1016/j.xcrm.2020.100004
PMID: 32529193
قاعدة البيانات: MEDLINE
الوصف
تدمد:2666-3791
DOI:10.1016/j.xcrm.2020.100004