ArticleHistopathology2011
Significance of p53-binding protein 1 nuclear foci in uterine cervical lesions: endogenous DNA double strand breaks and genomic instability during carcinogenesis.
Article in Histopathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Detection of genome instability by 53BP1 expression as a long-lasting health effect in human epidermis surrounding radiation-induced skin cancers.Journal of radiation research · 2024Article
- Analysis for type of 53BP1 nuclear expression by immunofluorescence as an indicator of genomic instability in oropharyngeal squamous epithelial lesions.Scientific reports · 2024Article
- Significance of P53-Binding Protein 1 as a Novel Molecular Histological Marker for Hypopharyngeal Squamous Neoplasms.Cancers · 2024Article
- A New Indicator to Differentiate Thyroid Follicular Inclusions in Cervical Lymph Nodes from Patients with Thyroid Cancer.International journal of molecular sciences · 2022Article
- Article
- 53BP1 expression as a biomarker to differentiate thyroid follicular tumors.Endocrine connections · 2021Article
- Significance of abnormal 53BP1 expression as a novel molecular pathologic parameter of follicular-shaped B-cell lymphoid lesions in human digestive tract.Scientific reports · 2021Article
- Detection of DNA damage response in nonalcoholic fatty liver disease via p53-binding protein 1 nuclear expression.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2019Article
- Human papillomavirus type 16 E6 and E7 oncoproteins interact with the nuclear p53-binding protein 1 in an in vitro reconstructed 3D epithelium: new insights for the virus-induced DNA damage response.Virology journal · 2018Article
- Expression pattern of p53-binding protein 1 as a new molecular indicator of genomic instability in bladder urothelial carcinoma.Scientific reports · 2018Article
- Discovery of microarray-identified genes associated with the progression of cervical intraepithelial neoplasia.International journal of clinical and experimental pathology · 2018Article
- Around and beyond 53BP1 Nuclear Bodies.International journal of molecular sciences · 2017Review
- TRIP12 as a mediator of human papillomavirus/p16-related radiation enhancement effects.Oncogene · 2017Article
- Significance of p53-Binding Protein 1 Nuclear Foci in Cervical Squamous Intraepithelial Lesions: Association With High-Risk Human Papillomavirus Infection and P16Cancer control : journal of the Moffitt Cancer CenterArticle
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsA defective DNA damage response can result in genomic instability (GIN) and lead to transformation to cancer. As p53-binding protein 1 (53BP1) localizes at the sites of DNA double strand breaks (DSBs) and rapidly forms nuclear foci (NF), the presence of 53BP1 NF can be considered to be an indicator of endogenous DSBs reflecting GIN. Our aim was to analyse the presence of DSBs by immunofluorescence for 53BP1 expression in a series of cervical lesions, to evaluate the significance of GIN during carcinogenesis. METHODS AND
resultsA total of 80 archival cervical tissue samples, including 11 normal, 16 cervical intraepithelial neoplasia (CIN)1, 15 CIN2, 24 CIN3 and 14 squamous cell carcinoma samples, were analysed for 53BP1 NF, human papillomavirus (HPV) infection, and p16(INK4a) overexpression. The number of 53BP1 NF in cervical cells appeared to increase with progression during carcinogenesis. The distribution of 53BP1 NF was similar to that of the punctate HPV signals as determined by in-situ hybridization and also to p16(INK4a) overexpression in CIN, suggesting an association with viral infection and replication stress.
conclusionsImmunofluorescence analysis of 53BP1 expression can be a useful tool with which to estimate the level of GIN. During cervical carcinogenesis, GIN may allow further accumulation of genomic alterations, causing progression to invasive cancer.
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