Comprehensive Data of P53 R282 Gene Mutation with Human Papillomaviruses (HPV)-Associated Oral Squamous Cell Carcinoma (OSCC)
| Autor: | Tipaya Ekalaksananan, Jureeporn Chuerduangphui, Natcha Patarapadungkit, Chamsai Pientong, Supannee Promthet, Patravoot Vatanasapt, Weerayut Wongjampa, Pensiri Phusingha |
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| Rok vydání: | 2019 |
| Předmět: |
Male
0301 basic medicine Cancer Research Gene mutation medicine.disease_cause Pathology and Forensic Medicine law.invention Lesion 03 medical and health sciences Exon 0302 clinical medicine law Allele-specific oligonucleotide Humans Medicine Typing Polymerase chain reaction Squamous Cell Carcinoma of Head and Neck business.industry Papillomavirus Infections HPV infection General Medicine medicine.disease stomatognathic diseases 030104 developmental biology Oncology Head and Neck Neoplasms 030220 oncology & carcinogenesis Mutation Cancer research Female Tumor Suppressor Protein p53 medicine.symptom business Carcinogenesis |
| Zdroj: | Pathology & Oncology Research. 26:1191-1199 |
| ISSN: | 1532-2807 1219-4956 |
| Popis: | Alterations of the P53 gene and human papillomavirus (HPV) infection are associated with development of oral squamous cell carcinoma (OSCC). We aimed to identify mutation of P53 exon 8 codon 282 in OSCC and correlate these with HPV infection as well as histopathological grade of OSCC. Samples of known HPV infection status were studied including oral lesion cells, formalin-fixed paraffin embedded (FFPE) tissues from OSCC and exfoliated oral cells of matched age-sex controls. P53 exon 8 mutation was detected using the polymerase chain reaction (PCR). Mutation of codon 282 was identified by allele-specific oligonucleotide typing (ASO) using EvaGreen real-time PCR. The PCR products were analyzed by gel electrophoresis and melting curve analysis. Mutation of P53 exon 8 was seen in 81.7% and 69.6% of FFPE OSCC tissues and oral lesion cells, respectively. This was significantly higher than in controls (16.7%). Frequency of mutation did not differ between HPV-positive samples (62.5% and 81.8% in oral lesion cells and FFPE tissue samples, respectively) and HPV-negative samples (73.3% and 81.5% in oral lesion cells and FFPE tissue samples, respectively). This finding is similar to P53 codon 282 mutation that was found only in FFPE tissues (35.0%) and oral lesion cells (32.6%) from both HPV-positive and negative OSCC. Interestingly, frequency of mutation was higher in well-differentiated OSCC with HPV-infection (28.1%) than without HPV (14.8%). This result demonstrated a mutation hot spot in P53 associated with oral carcinogenesis and might be useful to guide chemotherapeutic modality for HPV-associated OSCC in northeast Thailand. |
| Databáze: | OpenAIRE |
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