Evaluation of the expression of Bmi-1 stem cell marker in sinonasal melanomas and its correlation with the expression of cell cycle proteins

Abstract Background Sinonasal melanomas (SNM) are aggressive neoplasms, which present distinct clinicopathological and molecular aspects when compared to cutaneous melanomas (CM). B-cell-specific moloney murine leukemia virus integration site-1 (Bmi-1) is a stem cell marker involved in the regulatio...

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Main Authors: Harim Tavares dos Santos, Juliana de Souza do Nascimento, Fernanda Meireles, João Figueira Scarini, Erika Said Egal, Victor Angelo Montalli, Felipe Paiva Fonseca, Fernanda Viviane Mariano, Albina Altemani
Format: Article
Language:English
Published: BMC 2019-03-01
Series:Surgical and Experimental Pathology
Subjects:
Online Access:http://link.springer.com/article/10.1186/s42047-019-0034-y
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author Harim Tavares dos Santos
Juliana de Souza do Nascimento
Fernanda Meireles
João Figueira Scarini
Erika Said Egal
Victor Angelo Montalli
Felipe Paiva Fonseca
Fernanda Viviane Mariano
Albina Altemani
author_facet Harim Tavares dos Santos
Juliana de Souza do Nascimento
Fernanda Meireles
João Figueira Scarini
Erika Said Egal
Victor Angelo Montalli
Felipe Paiva Fonseca
Fernanda Viviane Mariano
Albina Altemani
author_sort Harim Tavares dos Santos
collection DOAJ
description Abstract Background Sinonasal melanomas (SNM) are aggressive neoplasms, which present distinct clinicopathological and molecular aspects when compared to cutaneous melanomas (CM). B-cell-specific moloney murine leukemia virus integration site-1 (Bmi-1) is a stem cell marker involved in the regulation of the cell cycle and has been found to be expressed in 70% of CM and 100% of benign nevi. Regarding the cell cycle, Bmi-1 is known to be an upstream repressor of p16, which is a tumor suppressor encoded by the INK4a/Arf locus. Considering this, the aim of this study is to evaluate the immunohistochemical expression of Bmi-1 in a series of SNM and its correlation with the expression of cell cycle proteins (p16 and Ki-67, a nuclear antigen of proliferating cells). Methods In 16 cases of SNM, nuclear expression of Bmi-1 and nuclear and cytoplasmic of p16 was classified as: absent, low (> 5 to < 50% of cells) and high (≥50%). Ki-67 proliferation index was represented by the ratio positive cells/ total cells. Results Histologically, all cases presented varying amount of necrosis and 75% contained undifferentiated cells. Bmi-1 was detected in 6 cases (37.5%) with high level of expression in 2; p16 expression was seen in 10 cases (62.5%) with high level in 7. The frequency of p16 expression did not differ significantly between tumors with or without Bmi-1 expression. Ki-67 index ranged from 8 to 22%. Neither Bmi-1 nor p16 expression showed correlation with Ki-67 index. Bmi-1 negative tumors presented more extensive necrosis (71.4%); no association between Bmi-1 expression and undifferentiated phenotype was observed. Conclusions In our SNM series, low immunohistochemical expression of Bmi-1 was a common phenomenon favoring the hypothesis that mucosal melanoma possibly presents molecular pathways different from the cutaneous counterpart. In SNM, Bmi-1 and p16 expression levels did not correlate with each other or with the cell proliferative index.
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spelling doaj.art-edafb7fb237c4682a4e17af52b4307302022-12-21T23:41:40ZengBMCSurgical and Experimental Pathology2520-84542019-03-01211710.1186/s42047-019-0034-yEvaluation of the expression of Bmi-1 stem cell marker in sinonasal melanomas and its correlation with the expression of cell cycle proteinsHarim Tavares dos Santos0Juliana de Souza do Nascimento1Fernanda Meireles2João Figueira Scarini3Erika Said Egal4Victor Angelo Montalli5Felipe Paiva Fonseca6Fernanda Viviane Mariano7Albina Altemani8Centro Universitário AgesUniversidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba, Departamento de Patologia OralUniversidade Estadual de Campinas, Faculdade de Ciências Médicas, Departamento de Anatomia PatológicaUniversidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba, Departamento de Patologia OralUniversidade Estadual de Campinas, Faculdade de Ciências Médicas, Departamento de Anatomia PatológicaInstituto e Centro de Pesquisa São Leopoldo Mandic, Departamento de Patologia OralUniversidade Federal de Minas Gerais, Faculdade de Odontologia, Departamento de Cirurgia e Patologia OralUniversidade Estadual de Campinas, Faculdade de Ciências Médicas, Departamento de Anatomia PatológicaUniversidade Estadual de Campinas, Faculdade de Ciências Médicas, Departamento de Anatomia PatológicaAbstract Background Sinonasal melanomas (SNM) are aggressive neoplasms, which present distinct clinicopathological and molecular aspects when compared to cutaneous melanomas (CM). B-cell-specific moloney murine leukemia virus integration site-1 (Bmi-1) is a stem cell marker involved in the regulation of the cell cycle and has been found to be expressed in 70% of CM and 100% of benign nevi. Regarding the cell cycle, Bmi-1 is known to be an upstream repressor of p16, which is a tumor suppressor encoded by the INK4a/Arf locus. Considering this, the aim of this study is to evaluate the immunohistochemical expression of Bmi-1 in a series of SNM and its correlation with the expression of cell cycle proteins (p16 and Ki-67, a nuclear antigen of proliferating cells). Methods In 16 cases of SNM, nuclear expression of Bmi-1 and nuclear and cytoplasmic of p16 was classified as: absent, low (> 5 to < 50% of cells) and high (≥50%). Ki-67 proliferation index was represented by the ratio positive cells/ total cells. Results Histologically, all cases presented varying amount of necrosis and 75% contained undifferentiated cells. Bmi-1 was detected in 6 cases (37.5%) with high level of expression in 2; p16 expression was seen in 10 cases (62.5%) with high level in 7. The frequency of p16 expression did not differ significantly between tumors with or without Bmi-1 expression. Ki-67 index ranged from 8 to 22%. Neither Bmi-1 nor p16 expression showed correlation with Ki-67 index. Bmi-1 negative tumors presented more extensive necrosis (71.4%); no association between Bmi-1 expression and undifferentiated phenotype was observed. Conclusions In our SNM series, low immunohistochemical expression of Bmi-1 was a common phenomenon favoring the hypothesis that mucosal melanoma possibly presents molecular pathways different from the cutaneous counterpart. In SNM, Bmi-1 and p16 expression levels did not correlate with each other or with the cell proliferative index.http://link.springer.com/article/10.1186/s42047-019-0034-ySinonasal melanomaBmi-1p16Immunohistochemical expression
spellingShingle Harim Tavares dos Santos
Juliana de Souza do Nascimento
Fernanda Meireles
João Figueira Scarini
Erika Said Egal
Victor Angelo Montalli
Felipe Paiva Fonseca
Fernanda Viviane Mariano
Albina Altemani
Evaluation of the expression of Bmi-1 stem cell marker in sinonasal melanomas and its correlation with the expression of cell cycle proteins
Surgical and Experimental Pathology
Sinonasal melanoma
Bmi-1
p16
Immunohistochemical expression
title Evaluation of the expression of Bmi-1 stem cell marker in sinonasal melanomas and its correlation with the expression of cell cycle proteins
title_full Evaluation of the expression of Bmi-1 stem cell marker in sinonasal melanomas and its correlation with the expression of cell cycle proteins
title_fullStr Evaluation of the expression of Bmi-1 stem cell marker in sinonasal melanomas and its correlation with the expression of cell cycle proteins
title_full_unstemmed Evaluation of the expression of Bmi-1 stem cell marker in sinonasal melanomas and its correlation with the expression of cell cycle proteins
title_short Evaluation of the expression of Bmi-1 stem cell marker in sinonasal melanomas and its correlation with the expression of cell cycle proteins
title_sort evaluation of the expression of bmi 1 stem cell marker in sinonasal melanomas and its correlation with the expression of cell cycle proteins
topic Sinonasal melanoma
Bmi-1
p16
Immunohistochemical expression
url http://link.springer.com/article/10.1186/s42047-019-0034-y
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