دورية أكاديمية
أعرض في EDS

Impact of DNA double-strand breaks on pancreaticobiliary maljunction carcinogenesis.

التفاصيل البيبلوغرافية
العنوان: Impact of DNA double-strand breaks on pancreaticobiliary maljunction carcinogenesis.
المؤلفون: Kuraishi Y; Department of Gastroenterology, Shinshu University School of Medicine, Matsumoto, Japan., Uehara T; Department of Laboratory Medicine, Shinshu University School of Medicine, Matsumoto, Japan. tuehara@shinshu-u.ac.jp., Muraki T; Department of Gastroenterology, North Alps Medical Center Azumi Hospital, Ikeda, Japan., Iwaya M; Department of Laboratory Medicine, Shinshu University School of Medicine, Matsumoto, Japan., Kinugawa Y; Department of Laboratory Medicine, Shinshu University School of Medicine, Matsumoto, Japan., Nakajima T; Department of Laboratory Medicine, Shinshu University School of Medicine, Matsumoto, Japan., Watanabe T; Department of Gastroenterology, Shinshu University School of Medicine, Matsumoto, Japan., Miyagawa Y; Department of Surgery, Shinshu University School of Medicine, Matsumoto, Japan., Umemura T; Department of Gastroenterology, Shinshu University School of Medicine, Matsumoto, Japan.; Department of Life Innovation, Institute for Biomedical Sciences, Shinshu University School of Medicine, Matsumoto, Japan.
المصدر: Diagnostic pathology [Diagn Pathol] 2021 Aug 09; Vol. 16 (1), pp. 72. Date of Electronic Publication: 2021 Aug 09.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: BioMed Central Country of Publication: England NLM ID: 101251558 Publication Model: Electronic Cited Medium: Internet ISSN: 1746-1596 (Electronic) Linking ISSN: 17461596 NLM ISO Abbreviation: Diagn Pathol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : BioMed Central, 2006-
مواضيع طبية MeSH: DNA Breaks, Double-Stranded*, Adenocarcinoma/*genetics , Carcinogenesis/*genetics , Gallbladder Neoplasms/*genetics , Pancreaticobiliary Maljunction/*genetics, Adenocarcinoma/metabolism ; Adenocarcinoma/pathology ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Biomarkers/metabolism ; Carcinogenesis/pathology ; Case-Control Studies ; Female ; Gallbladder Neoplasms/metabolism ; Gallbladder Neoplasms/pathology ; Histones/metabolism ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Pancreaticobiliary Maljunction/metabolism ; Pancreaticobiliary Maljunction/pathology ; Young Adult
مستخلص: Background: Pancreaticobiliary maljunction (PBM) is a condition characterized by chronic inflammation due to refluxed pancreatic juice into the biliary tract that is associated with an elevated risk of biliary tract cancer. DNA double-strand breaks (DSBs) are considered the most serious form of DNA damage. DSBs are provoked by inflammatory cell damage and are recognized as an important oncogenic event in several cancers. This study used γ-H2AX, an established marker of DSB formation, to evaluate the impact of DNA damage on carcinogenesis in PBM.
Methods: We investigated γ-H2AX expression immunohistochemically in gallbladder epithelium samples obtained from 71 PBM cases and 19 control cases.
Results: Fourteen PBM cases with gallbladder adenocarcinoma were evaluated at non-neoplastic regions. A wide range of nuclear γ-H2AX staining was detected in all PBM and control specimens. γ-H2AX expression was significantly higher in PBM cases versus controls (median γ-H2AX-positive proportion: 14.4 % vs. 4.4 %, p = 0.001). Among the PBM cases, γ-H2AX expression was significantly higher in patients with carcinoma than in those without (median γ-H2AX-positive proportion: 21.4 % vs. 11.0 %, p = 0.031).
Conclusions: DSBs occurred significantly more abundantly in the PBM gallbladder mucosa, especially in the context of cancer, indicating an involvement in PBM-related carcinogenesis.
(© 2021. The Author(s).)
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فهرسة مساهمة: Keywords: Carcinogenesis; DNA double-strand break; Gallbladder; Pancreaticobiliary maljunction; γ-H2AX
المشرفين على المادة: 0 (Biomarkers)
0 (H2AX protein, human)
0 (Histones)
تواريخ الأحداث: Date Created: 20210810 Date Completed: 20220110 Latest Revision: 20220110
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC8353780
DOI: 10.1186/s13000-021-01132-0
PMID: 34372868
قاعدة البيانات: MEDLINE
الوصف
تدمد:1746-1596
DOI:10.1186/s13000-021-01132-0