Background: This study evaluates the existence of numerical alterations of chromosome 17 and TP53 gene deletion in gastric adenocarcinoma. The p53 protein expression was also evaluated, as well as, possible associations with clinicopathological characteristics.
Methods: Dual-color fluorescence in situ hybridization and immunostaining were performed in twenty gastric cancer samples of individuals from Northern Brazil.
Results: Deletion of TP53 was found in all samples. TP53 was inactivated mainly by single allelic deletion, varying to 7-39% of cells/case. Aneusomy of chromosome 17 was observed in 85% of cases. Chromosome 17 monosomy and gain were both observed in about half of cases. Cells with gain of chromosome 17 frequently presented TP53 deletion. The frequency of cells with two chr17 and one TP53 signals observed was higher in diffuse than in intestinal-type GC. Immunoreactivity of p53 was found only in intestinal-type samples. The frequency of cells with two chr17 and two TP53 signals found was higher in samples with positive p53 expression than in negative cases in intestinal-type GC.
Conclusion: We suggest that TP53 deletion and chromosome 17 aneusomy is a common event in GC and other TP53 alterations, as mutation, may be implicated in the distinct carcinogenesis process of diffuse and intestinal types.
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http://dx.doi.org/10.1186/1471-230X-9-55 | DOI Listing |
Hemasphere
January 2025
Department of Internal Medicine, Hematology and Oncology, and Institute of Medical Genetics and Genomics, University Hospital Brno and Medical Faculty Masaryk University Brno Czech Republic.
In chronic lymphocytic leukemia, the reliability of next-generation sequencing (NGS) to detect variants ≤10% allelic frequency (low-VAF) is debated. We tested the ability to detect 23 such variants in 41 different laboratories using their NGS method of choice. The sensitivity was 85.
View Article and Find Full Text PDFFront Genet
January 2025
First Clinical School, Liaoning University of Traditional Chinese Medicine, Shenyang, China.
Introduction: The deficiency of estrogen correlates with a range of diseases, notably Postmenopausal osteoporosis (PMO) and Parkinson's disease (PD). There is a possibility that PMO and PD may share underlying molecular mechanisms that are pivotal in their development and progression. The objective of this study was to identify critical genes and potential mechanisms associated with PMO by examining co-expressed genes linked to PD.
View Article and Find Full Text PDFJ Inflamm Res
January 2025
Department of General Surgery (Hepatopancreatobiliary Surgery), The Affiliated Hospital, Southwest Medical University, Luzhou, 646000, People's Republic of China.
Background: Nonalcoholic steatohepatitis (NASH) has recently garnered increased attention due to immune infiltration. However, the role of membrane-associated protein 17 (MAP17) in NASH remains unclear, which prompted this study to explore its relationship with immune infiltration and its regulatory mechanisms.
Methods: We employed weighted correlation network analysis (WGCNA) to construct a gene co-expression network aimed at identifying key genes associated with NASH progression.
J Obstet Gynaecol Res
January 2025
Reproductive Sciences and Technology Research Center, Department of Anatomy, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Objective: To evaluate the efficacy of a microfluidic culture system supplemented with follicular fluid meiosis-activating sterol (FF-MAS) on the maturation of immature oocytes in patients with polycystic ovarian syndrome (PCOS).
Methods: A total of 438 germinal vesicle oocytes from 163 PCOS patients were included. Oocytes were divided into five groups: (1) cultured in static drops without FF-MAS, (2) cultured in static drops with FF-MAS, (3) cultured in a microfluidic device without FF-MAS, (4) cultured in a microfluidic device with FF-MAS for the first 2 h, and (5) cultured in a microfluidic device with FF-MAS for 24 h.
BMC Cancer
January 2025
Department of Pharmacology and Public Health, Faculty of Medicine, The Hashemite University, Zarqa, 13133, Jordan.
Background: Oncogene-Induced Senescence (OIS) is a form of senescence that occurs as a consequence of oncogenic overstimulation and possibly infection by oncogenic viruses. Whether senescence plays a role in the pathogenesis of cervical cancer (CC) is not well understood. Moreover, whether cervical epithelial cells that are part of the premalignant cervical intraepithelial neoplasia (CIN), exhibit markers of OIS in Human Papillomavirus (HPV)-infected tissue, has not been investigated.
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