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- Sundberg, Jonas, et al.
(författare)
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Combined Testing of p16 Tumour-suppressor Protein and Human Papillomavirus in Patients With Oral Leukoplakia and Oral Squamous Cell Carcinoma.
- 2019
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Ingår i: Anticancer research. - : Anticancer Research USA Inc.. - 1791-7530 .- 0250-7005. ; 39:3, s. 1293-1300
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Tidskriftsartikel (refereegranskat)abstract
- Oral leukoplakia (OL) is a potentially malignant oral mucosal disorder. A casual association between OL, oral squamous cell carcinoma (OSCC) and human papillomavirus (HPV) infection has been suggested, but no conclusive evidence has been presented. p16, a tumour-suppressor protein, is used as a surrogate marker for HPV infection. The aim of this study was to investigate how overexpression of p16 correlates with HPV infection in OL and in OSCC.Seventy-four patients with OL and 13 with OSCC with p16 overexpressed, were analyzed by immunohistochemistry visualizing p16 and a real-time polymerase chain reaction (PCR) assay targeting HPV types 6, 11, 16, 18, 31, 33, 35, 39, 45, 52, 56, 58 and 59.Overexpression of p16 was observed in 18% of patients with OL. None of the HPV subtypes were detected by PCR analysis in patients with OL. In the p16-positive OSCC specimens, 38% were also HPV16-positive.Overexpression of p16 was not found to be a reliable biomarker for HPV infection in patients with OL and OSCC.
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| 2. |
- Öhman, Jenny, et al.
(författare)
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Presence of CD3-Positive T-Cells in Oral Premalignant Leukoplakia Indicates Prevention of Cancer Transformation
- 2015
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Ingår i: Anticancer Research. - 0250-7005. ; 35:1, s. 311-317
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Tidskriftsartikel (refereegranskat)abstract
- Aim: Leukoplakias (LPLs) are lesions in the oral mucosa that have a potential to transform into oral squamous cell carcinoma (OSCC). As the degree of immunosurveillance may be important for this transformation to occur, the aim of this study was to determine the presence of immune cells in LPLs with dysplasia in relation to later development of OSCC. Materials and Methods: Biopsies from 16 patients with clinical diagnosis of LPL and histopathological diagnosis of hyperkeratosis with dysplasia were immunostained with antibodies to detect CD3(+) T cells, CD1a(+) LCs, Ki-67(+) and p53-expressing cells. Patients were divided into two groups: LPL with dysplasia that transformed into OSCC (LPL-dys) and that which did not (LPL-ca). Results: Quantitative analyses showed significantly lower numbers of CD3+ T-cells in LPL-ca than in LPL-dys. No significant differences were detected when comparing LPL-dys and LPL-ca regarding CD1a(+), p53(+) and Ki-67(+) cells. Conclusion: The number of CD3-expressing T-cells may be important for preventing malignant transformation of LPL.
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