Clinicopathological features and immunohistochemical expression of p53, Ki-67, Mcm-2 and Mcm-5 in proliferative verrucous leukoplakia

Gouvêa, Adriele Ferreira; Vargas, Pablo Agustı́n; Coletta, Ricardo D.; Jorge, Jacks; Lopes, Márcio Ajudarte

doi:10.1111/j.1600-0714.2010.00889.x

Cited by 55 publications

(105 citation statements)

References 40 publications

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“…[26][27][28] Nasser et al 25 found p53 and Ki-67 to have low positive predictive value when expressed independently, but their dual expression could help discriminate between dysplastic and non-dysplastic leukoplakias. Gouvea et al 29 found p53 and Ki-67 expression in only a few cases of mild and moderately dysplastic proliferative verrucous leukoplakias (PVL), and their immunoexpression did not correlate with progressive epithelial alterations. This discrepancy may be explained by the fact that PVL is a distinct lesion predominating in females and having an etiology other than the use of tobacco.…”

Section: Discussionmentioning

confidence: 99%

Coexpression of p53 and Ki 67 and lack of c-erbB2 expression in oral leukoplakias in India

2012

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Oral cancer is commonly preceded by premalignant lesions and conditions. The clinician's ability to identify lesions at an increased risk of cancer development is critical for its control. The purpose of this study was to compare the expression of tumor suppressor gene p53, proliferation marker Ki-67, and oncogene c-erbB2 and to evaluate the relevance of their co-expression in the diagnosis of, and prognosis for, oral leukoplakia. In the present study, the expression of biomarkers was studied immunohistochemically in 55 cases of leukoplakia (26 without dysplasia, 29 with dysplasia) and 10 cases of normal epithelia. The Labeling Indices (LI) of p53 and Ki-67 were found to increase significantly with an increase in the grade of dysplasia. A significant correlation was also found between the LI of p53 and that of Ki-67. It was also observed that c-erbB2 expression was only cytoplasmic, indicating incomplete receptor degradation. Hence, it can be concluded from the present study that the increased expression of p53 and Ki-67 with an increase in the grade of dysplasia suggests that their co-expression may be used for the identification of high-risk lesions. Also, c-erbB2 has no pathogenetic role in early carcinogenesis in the studied population, although incomplete receptor degradation, as evidenced by cytoplasmic staining, may indicate an early change.

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Section: Discussionmentioning

confidence: 99%

Coexpression of p53 and Ki 67 and lack of c-erbB2 expression in oral leukoplakias in India

2012

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“…All patients received verbal explanations concerning the study before signing a written informed consent. In this study, 15 patients with diagnosed PVL-according to clinical and microscopical findings (Figures 1 and 2) and after numerous appointments[3,5] - and 15 control patients with no history of cancer or any oral lesion, but possessing the same demographics, were chosen from patients assisted by the Orocentro (Oral Diagnosis Clinic) of Piracicaba Dental School. Clinicopathological data were collected retrospectively from patient charts.…”

Section: Methodsmentioning

confidence: 99%

“…The rate of malignant transformation of PVL ranges from 40%-100%[1,3,5,8-12]. This variability mostly depends on the time of patient follow-up and the criteria for diagnosis of PVL[13,14].…”

Section: Introductionmentioning

confidence: 99%

“…Additionally, the p53, Ki-67, Mcm-2 and Mcm-5 proteins have been identified through immunohistochemistry to have increased expression in OSCC lesions that progressed from PVL[3,5]. PVL lesions with mild or moderate dysplasia, in addition to lesions that progressed to OSCC, had high expression of Mcm-2 and Mcm-5; such molecular indicators may be useful as markers of malignant transformation of the disease, especially Mcm-2[3,5].…”

Section: Introductionmentioning

confidence: 99%

“…PVL lesions with mild or moderate dysplasia, in addition to lesions that progressed to OSCC, had high expression of Mcm-2 and Mcm-5; such molecular indicators may be useful as markers of malignant transformation of the disease, especially Mcm-2[3,5]. Similar findings detected in other conventional dysplastic premalignant lesions and OSCC have reinforced the aggressive nature of this entity, but without clarifying the true meaning of these molecules with respect to the pathogenesis or progression of PVL[7,20].…”

Section: Introductionmentioning

confidence: 99%

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Low expression of angiotensinogen and dipeptidyl peptidase 1 in saliva of patients with proliferative verrucous leukoplakia

Flores

Santos‐Silva

Coletta

et al. 2016

WJCC

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AIMTo elucidate the profile of the salivary proteome.METHODSUnstimulated whole mouth saliva was collected from 30 volunteers [15 proliferative verrucous leukoplakia (PVL) patients and 15 controls] and proteins were submitted for mass spectrometry-based proteomics using the discovery approach, followed by analyses of variance and logistic regression tests.RESULTSA total of two hundred and eighty-three proteins were confidently identified in saliva. By combining two low abundance proteins from the PVL group, angiotensinogen (AGT) and dipeptidyl peptidase 1 (DPP1), a model for group differentiation was built with a concordance index of 94.2%, identifying both proteins as potential etiologic biomarkers for PVL.CONCLUSIONThis study suggests that both AGT and DPP1 may be involved in developmental mechanisms of PVL.

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Proliferative verrucous leukoplakia and its tumor markers: Systematic review and meta‐analysis

et al. 2018

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Background The aim was to update information on oral proliferative verrucous leukoplakia (PVL), a disease of verrucous‐like lesions with high risk of malignancy, and its biomarkers. Methods A systematic search of literature on PVL and its biomarkers showed 22 biomarkers that were investigated in 19 papers. A meta‐analysis was possible for human papillomavirus (HPV), aneuploidy, Ki‐67, and p53. Results Aneuploidy was found consistently (I2 = 0%, P = 0.61) in 92% (95% CI 80%‐99%) of the PVL cases. P53 positivity prevalence was 27% (95% CI 15%‐40%) in two available studies (I2 = 0%, P = 0.64). With HPV and Ki‐67, the most outlying studies needed to be removed and after that the pooled HPV positivity prevalence (I2 = 24%, P = 0.27) was 5% (95% CI 0%‐14%) and for Ki‐67 (I2 = 9%, P = 0.33) 14% (95% CI 6%‐26%). Conclusions With the evidence of the current literature, aneuploidy could value as a biomarker of PVL but should be further validated.

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Clinicopathological features and immunohistochemical expression of p53, Ki-67, Mcm-2 and Mcm-5 in proliferative verrucous leukoplakia

Abstract: High immunoexpression of Mcm-2 and Mcm-5 in mild and moderate dysplasia could be helpful to predict the malignant transformation of PVL.

Cited by 55 publications

References 40 publications

Coexpression of p53 and Ki 67 and lack of c-erbB2 expression in oral leukoplakias in India

Coexpression of p53 and Ki 67 and lack of c-erbB2 expression in oral leukoplakias in India

Low expression of angiotensinogen and dipeptidyl peptidase 1 in saliva of patients with proliferative verrucous leukoplakia

Proliferative verrucous leukoplakia and its tumor markers: Systematic review and meta‐analysis

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