Alterations of tumor suppressor gene p16 INK4a in pancreatic ductal carcinoma
| العنوان: | Alterations of tumor suppressor gene p16 INK4a in pancreatic ductal carcinoma |
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| المؤلفون: | Siddhartha Majumdar, Jyotika Attri, Radhika Srinivasan, Jaidev Wig, Bishan Dass Radotra |
| المصدر: | BMC Gastroenterology BMC Gastroenterology, Vol 5, Iss 1, p 22 (2005) |
| بيانات النشر: | Springer Science and Business Media LLC, 2005. |
| سنة النشر: | 2005 |
| مصطلحات موضوعية: | Adult, Male, Tumor suppressor gene, Adenocarcinoma, Polymerase Chain Reaction, Pancreatic cancer, medicine, Carcinoma, Humans, Gene silencing, Gene Silencing, lcsh:RC799-869, Promoter Regions, Genetic, Cyclin-Dependent Kinase Inhibitor p16, Polymorphism, Single-Stranded Conformational, Aged, Staining and Labeling, business.industry, Genes, p16, Homozygote, Gastroenterology, General Medicine, DNA Methylation, Middle Aged, Cell cycle, medicine.disease, Immunohistochemistry, Mutation, DNA methylation, Cancer research, lcsh:Diseases of the digestive system. Gastroenterology, Female, business, Gene Deletion, Research Article, Carcinoma, Pancreatic Ductal |
| الوصف: | Background Cell cycle inhibitor and tumor suppressor gene p16 / MTS-1 has been reported to be altered in a variety of human tumors. The purpose of the study was to evaluate primary pancreatic ductal adenocarcinomas for potentially inactivating p16 alterations. Methods We investigated the status of p16 gene by polymerase chain reaction (PCR), nonradioisotopic single strand conformation polymorphism (SSCP), DNA sequencing and hypermethylation analysis in 25 primary resected ductal adenocarcinomas. In addition, we investigated p16 protein expression in these cases by immunohistochemistry (IHC) using a monoclonal antibody clone (MS-887-PO). Results Out of the 25 samples analyzed and compared to normal pancreatic control tissues, the overall frequency of p16 alterations was 80% (20/25). Aberrant promoter methylation was the most common mechanism of gene inactivation present in 52% (13/25) cases, followed by coding sequence mutations in 16% (4/25) cases and presumably homozygous deletion in 12% (3/25) cases. These genetic alterations correlated well with p16 protein expression as complete loss of p16 protein was found in 18 of 25 tumors (72%). Conclusion These findings confirm that loss of p16 function could be involved in pancreatic cancer and may explain at least in part the aggressive behaviour of this tumor type. |
| تدمد: | 1471-230X |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2fa3b16c62ab948f37b8f73baa926865Test https://doi.org/10.1186/1471-230x-5-22Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....2fa3b16c62ab948f37b8f73baa926865 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 1471230X |
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