Human papillomavirus-associated increase in p16INK4A expression in penile lichen sclerosus and squamous cell carcinoma

Prowse, David M.; Ktori, Elena; Chandrasekaran, Dhivya; Prapa, A.; Baithun, Suhail

doi:10.1111/j.1365-2133.2007.08305.x

Cited by 74 publications

(71 citation statements)

References 35 publications

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“…Within their series there was only one case of verrucous carcinoma, and it was HPV6-positive, however, this tumour did not express p16 INK4A protein, exhibit p16 INK4A promoter methylation or BMI-1 staining, which suggests additional mechanism of p16 INK4A inactivation. Study by two of the authors of this paper 20 confirmed the inverse correlation between HPV16/18 and p16 INK4A in usual type squamous cell carcinomas and penile lichen sclerosus. We found the same correlation in our usual type samples but not in verrucous, which again suggests the connection to HPV infection only in usual type carcinoma.…”

Section: Discussionsupporting

confidence: 68%

“…Validated samples were tested for the presence of HPV DNA by a broadspectrum HPV PCR method using SPF10 primers, which amplify a 65-bp fragment of the L1 open reading frame and HPV genotypes identified by the INNO-LiPA line probe assay (Innogenetics NV, Ghent, Belgium). 20 As a positive control, a known HPV-positive cervical cancer sample was used. Mouse tissue served as negative control.…”

Section: Hpv Analysismentioning

confidence: 99%

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HPV infection and immunochemical detection of cell-cycle markers in verrucous carcinoma of the penis

et al. 2009

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Penile verrucous carcinoma is a rare disease and little is known of its aetiology or pathogenesis. In this study we examined cell-cycle proteins expression and correlation with human papillomavirus infection in a series of 15 pure penile verrucous carcinomas from a single centre. Of 148 penile tumours, 15 (10%) were diagnosed as pure verrucous carcinomas. The expression of the cell-cycle-associated proteins p53, p21, RB, p16 INK4A and Ki67 were examined by immunohistochemistry. Human papillomavirus infection was determined by polymerase chain reaction to identify a wide range of virus types. The expression of p16 INK4A and Ki67 was significantly lower in verrucous carcinoma than in usual type squamous cell carcinoma, whereas the expression of p53, p21 and RB was not significantly different. p53 showed basal expression in contrast to usual type squamous cell carcinoma. Human papillomavirus infection was present in only 3 out of 13 verrucous carcinomas. Unique lowrisk, high-risk and mixed viral infections were observed in each of the three cases. In conclusion, lower levels of p16 INK4A and Ki67 expressions differentiate penile verrucous carcinoma from usual type squamous cell carcinoma. The low Ki67 index reflects the slow-growing nature of verrucous tumours. The low level of p16 INK4A expression and human papillomavirus detection suggests that penile verrucous carcinoma pathogenesis is unrelated to human papillomavirus infection and the oncogenes and tumour suppressor genes classically altered by virus infection.

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Section: Discussionsupporting

confidence: 68%

Section: Hpv Analysismentioning

confidence: 99%

HPV infection and immunochemical detection of cell-cycle markers in verrucous carcinoma of the penis

et al. 2009

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“…Maehama and colleagues [33] reported that they found 10.6% of positive for HPV in women with normal cytology smear, using PCR technique. Based on that report, we expected to find some expression of p16 protein in this group of patients, which may not have happened because of the small number of cases studied, or non-viral integration in the genome of the host [16,18].…”

Section: Discussionmentioning

confidence: 99%

“…The Ki-67 is a marker of protein, non-histonic of cell proliferation, and is expressed in all phases of the cell cycle, except in G0 [18,19]. This protein has a function of growth in human tumor, and expression of its marker could suggest the degree of malignancy [20][21][22].…”

Section: Ki-67mentioning

confidence: 99%

The Use of Molecular Markers (p16, Ki-67 and E-Cadherin) in Uterine Cervical Biopsies

Munhoz¹,

Rodrigues²,

Pedregosa³

et al. 2009

TOPATJ

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Abstract:Introduction: Cervical cancer is related to the Human Papillomavirus (HPV). The E7 viral DNA sequence induces the start of DNA synthesis of infected cell, releasing protein p16. The sequence E6 inhibits apoptosis, with prolonged survival of cells heavily damaged and changed, with inhibition of p53 protein and increasing of protein Ki-67. In those injured cells, the molecules are reduced to join the cell membrane, the type E-cadherin. Aim:To study the expression of p16 protein in: normal epithelium cervical, cervical lesions, pre-invasive (CIN) persistent and no persistent lesions and invasive carcinoma of the cervix and to correlate with the expression of Ki-67 and Ecadherin.Patients and Methods: 54 uterine cervix biopsies were selected and submitted to immunohistochemical study, with biomarkers p16, Ki-67 and E-cadherin.Results: 1 CIN I (27.9%) and CIN II (47.9%) had lower expression of p16 than in CIN III (73.5%) and invasive carcinoma (72.7%) (p < 0.0005). For Ki-67, invasive carcinoma (57.8%), had a higher expression when compared to CIN I (35.6%), CIN II (51.9%) and CIN III (40.9%) (p = 0.005). E-cadherin expression in invasive carcinoma (46.2%) was lower than in CIN III (56.0%), CIN II (77.4%) and CIN I (82.2%) (p < 0.0005) and, normal epithelium had the greatest E-cadherin expression (89.1%). In persistent and no persistent CIN there was no difference in the expression of the biomarkers, with p16 presenting p = 0.50, Ki-67, p = 0.91 and the E-cadherin a p = 0.43 value. Conclusions:The use of p16, Ki-67 and E-cadherin biomarkers in cervical biopsies with difficult diagnosis could help in the early diagnosis of malignant lesions and support adequate treatment, 2. There is no association between the diagnosis of the biopsy and the persistence of the cervical lesion and, 3. The used biomarkes don't differentiate between persistent CIN and no persistent lesions.

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“…Cells with anti-p16 antibody-stained nuclei and/or cytoplasm were considered as positive, irrespective of the intensity of the staining. The grading of the immunohistochemical expression was assessed, according to the method of Prowse et al [29], by grading the intensity (0, negative; 1, low intensity; 2, mild range; and 3, high intensity) and the percentage of positively stained cells (1, low percentage coverage, <30%; 2, mild percentage coverage, 30-60%; and 3, high percentage coverage, more than 60%). The combined score total was calculated as the sum of the intensity and percentage coverage scores.…”

Section: Preparationmentioning

confidence: 99%

Inhibition of DMBA‐induced Oral Squamous Cells Carcinoma Growth by Brazilian Red Propolis in Rodent Model

Ribeiro

Alves

Santos

et al. 2015

Basic Clin Pharma Tox

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Abstract:We investigated the effect of oral administration of hydroalcoholic extract of Brazilian red propolis (HERP) on DMBA-induced oral squamous cell carcinomas (OSCC) in rodents. The chemical components of the HERP were assessed by high-performance liquid chromatography (HPLC). Carcinogenesis was topically induced in the lower lip of 25 rats using 9,10-dimethyl-1,2-benzanthracene (DMBA); the tumour was treated with saline (TUM1) and Tween 80 (TUM2) as well as HERP at 10, 50 and 100 mg/kg (HERP10, HERP50 and HERP100, respectively) for 20 weeks. Topical application of saline and oral administration of 100 mg/kg HERP was used in five rats as a control group (CTR). After 26 weeks, the histological malignancy grading and immunohistochemical expression of INK4A were assessed in the tumours/tissue samples. The compounds identified were propyl gallate, daidzein, catechin, epicatechin, formononetin and biochanin A. Formononetin, daidzein and biochanin A showed concentration of 23.29, 0.38 and 0.67 mg/g of HERP, respectively. HERP at doses of 50 and 100 mg/ kg inhibited 40% of OSCC growth and promoted a 3-week delay in development of clinically detectable tumours. Epithelial dysplasia was observed in all samples with no clinical tumour, except in CTR. No significant difference in the immunoexpression of INK4A was observed between HERP-treated and saline/Tween 80-treated groups (p > 0.05). Our results suggest that HERP exerts chemopreventive activity on the progression of DMBA-induced epithelial dysplasia to OSCC in an experimental model of labial carcinogenesis; however, this effect is not associated with Ki-67 and p16INK4A immunoexpression.Propolis is a natural, resinous hive product that honeybees manufacture by mixing their own waxes and salivary secretions with resins collected from cracks in tree barks and leaf buds [1]. Propolis samples from different regions of Brazil display different colours and chemical compositions, depending on the local flora at the site of collection [2]. Brazilian green propolis, derived from Baccharis dracunculifolia (Asteraceae) [3], is the most popular and well-studied Brazilian propolis.In the last few years, a red variety of Brazilian propolis has been described and characterized by various authors [4][5][6], demonstrating that the botanical origin influences directly its chemical composition. Isoflavones are chemical constituents usually identified in ethanolic extracts of red propolis, being formononetin, daidzein and biochanin A more often found [5,7].Brazilian

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Human papillomavirus-associated increase in p16INK4A expression in penile lichen sclerosus and squamous cell carcinoma

Cited by 74 publications

References 35 publications

HPV infection and immunochemical detection of cell-cycle markers in verrucous carcinoma of the penis

HPV infection and immunochemical detection of cell-cycle markers in verrucous carcinoma of the penis

The Use of Molecular Markers (p16, Ki-67 and E-Cadherin) in Uterine Cervical Biopsies

Inhibition of DMBA‐induced Oral Squamous Cells Carcinoma Growth by Brazilian Red Propolis in Rodent Model

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