Estudo genético do gene p16 pela técnica de PCR-SSCP e expressão de proteína p16 em melanomas de mucosa oral e melanomas cutâneos

Hsieh, Ricardo; Sousa, Fabrício Bitú; Firmiano, Aline; Nunes, Fábio Daumas; Magalhães, Marina Helena Cury Gallottini; Sotto, Mírian Nacagami

doi:10.1590/s0365-05962006000500005

Cited by 5 publications

(8 citation statements)

References 22 publications

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“…Other authors, however, have not found a correlation between melanoma thickness and the loss of p16 expression 13 . In a recent study of several clinicopathologic types of melanoma, no relationship was found between p16 expression, revealed by immunohistochemistry, and lesion thickness 30 . Such contradictory results may be related to the fact that p16 inactivation is not a strictly timed event in melanoma tumorigenesis 31 .…”

Section: Discussionmentioning

confidence: 97%

“…Such contradictory results may be related to the fact that p16 inactivation is not a strictly timed event in melanoma tumorigenesis 31 . Other possible explanations for the conflicting results could be the use of different methods to demonstrate p16 expression, such as p16 monoclonal 13,27,30 and polyclonal 17,28,29 antibodies, immunohistochemistry, 13,27–30 and flow cytometric analysis 17 …”

Section: Discussionmentioning

confidence: 99%

“…13 In a recent study of several clinicopathologic types of melanoma, no relationship was found between p16 expression, revealed by immunohistochemistry, and lesion thickness. 30 Such contradictory results may be related to the fact that p16 inactivation is not a strictly timed event in melanoma tumorigenesis. 31 Other possible explanations for the conflicting results could be the use of different methods to demonstrate p16 expression, such as p16 monoclonal 13,27,30 and polyclonal 17,28,29 antibodies, immunohistochemistry, 13,[27][28][29][30] and flow cytometric analysis.…”

Section: Discussionmentioning

confidence: 99%

“…30 Such contradictory results may be related to the fact that p16 inactivation is not a strictly timed event in melanoma tumorigenesis. 31 Other possible explanations for the conflicting results could be the use of different methods to demonstrate p16 expression, such as p16 monoclonal 13,27,30 and polyclonal 17,28,29 antibodies, immunohistochemistry, 13,[27][28][29][30] and flow cytometric analysis. 17 The maintenance of p16 expression in ALM, even in thick and ulcerated lesions, suggests that p16 expression per se may not represent a marker of pRb pathway disturbance in ALM tumorigenesis.…”

Section: Discussionmentioning

confidence: 99%

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Expression of p16 protein in acral lentiginous melanoma

2009

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Expression of p16 protein in acral lentiginous melanoma

2009

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“…Both steps were developed in a four minute interval each. The positive control was performed with human tonsil (for Ki-67) and dermal nevocellular nevus (for p16) 14 . For negative control, we substituted primary antibody by phosphate buffered saline in the reaction.…”

Section: Immunohistochemical Analysismentioning

confidence: 99%

Expression of Ki-67 and P16 INK4a in chemically-induced perioral squamous cell carcinomas in mice.

Alves

Ribeiro

Lima

et al. 2016

Rev. Col. Bras. Cir.

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Objective: to evaluate the influence of INK4a proteins immunohistochemical expressions on the clinical and morphological parameters of perioral squamous cell carcinoma induced with 9,10-dimethyl-1,2-benzanthracene (DMBA) in mice. Methods: we topically induced the lesions in the oral commissure of ten Swiss mice for 20 weeks, determining the time to tumors onset and the average tumor volume up to 26 weeks. In histopathological analysis, the variables studied were histological malignancy grade and the immunohistochemical expression of INK4a proteins. The correlation between variables was determined by application of the Spearman correlation test. Results: the mean time to onset of perioral lesions was 21.1 ± 2.13 weeks; mean tumor volume was 555.91 ± 205.52 mm3. Of the induced tumors, 80% were classified as low score and 20% high score. There was diffuse positivity for Ki-67 in 100% of lesions -Proliferation Index (PI) of 50.1 ± 18.0. There was a strong direct correlation between Ki-67 immunoreactivity and tumor volume (R = 0.702) and a low correlation with the malignancy score (R = 0.486). The P16INK4a protein expression was heterogeneous, showing a weak correlation with tumor volume (R = 0.334). There was no correlation between the immunohistochemical expression of the two proteins studied. Conclusion: in an experimental model of DMBA-induced perioral carcinogenesis, tumor progression was associated with the tumor proliferative fraction (Ki-67 positive cells) and with tumor histological grading, but not with P16 INK4a expression.Keywords: Carcinogenesis. 9,10-Dimetil-1,2-benzanthracene. Immunohistochemistry. Ki-67 Antigen. Genes, p16. MTSI, CDK4I or CDKN2) located on chromosome 9p, locus 21, involved in cell cycle progression blocking process. It is inactive in a wide range human malignancies. The loss of p16 INK4a immunoexpression has been observed in the early stages of oral carcinogenesis and has been considered a molecular event of significant value in the prognostic analysis of such tumors 9,10 . This study evaluated the influence of Ki-67 and p16 proteins immunohistochemical expression on morphological parameters (mean tumor volume and histological malignancy grade) of DMBA-induced perioral SCC in mice. In addition, it sought to verify the existence of correlation between the immunoreactivity of p16 and Ki-67 proteins. METHODSThe development of the study had the approval of the Ethics in Research Committee of the Universidade Tiradentes -Aracaju / SE, with protocol number 191208. Animals and chemical carcinogenesis induction procedureWe used ten Swiss mice without distinction between gender, from the vivarium of the Universidade Tiradentes, with a body mass of about 150 ± 30g (Average age 100 days).We induced the oral lesions in the mice left oral commissure by the topical application of 9,10-dimethyl-1,2-benzanthracene (DMBA), diluted to 0.5% in acetone, on a weekly basis in three alternate days for 20 weeks 11 . After this period, the animals were kept under observation for six weeks, and we duly regis...

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Expressão da proteína p16, ciclina D1, CDK4 e proteína do retinoblastoma no melanoma acral lentiginoso

Hsieh¹

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À minha orientadora Profa. Dra. Mirian Nacagami Sotto, por incentivar o meu progresso acadêmico e confiar no meu potencial; pela sua paciência, ajuda e dedicação durante todo este projeto, por toda sua dedicação à pesquisa, pela qual eu me inspiro. Agradeço a confiança e apoio nos bons momentos e também nas horas mais difíceis, e por estar sempre presente durante todas as etapas deste percurso, desde a iniciação científica até a pós-graduação, como professora e orientadora dedicada. À Profa. Dra. Sílvia Vanessa Lourenço, por incentivar e ensinar o papel importante da pesquisa. Agradeço a confiança e apoio, desde a iniciação científica até a pós-graduação, como professora dedicada e como amiga. Ao Prof. Dr. Fernando Augusto Soares, Professor Titular da disciplina de Patologia Geral da FOUSP, pela ajuda no fornecimento e padronização dos anticorpos utilizados neste trabalho. À Aline Firmiano, por sua dedicação, apoio e auxilio na execução e realização deste trabalho. À Sabrina Hitomi Uyekita e ao Fábio Rodrigues Gonçalves de Carvalho, grandes amigos, colegas de graduação, de iniciação científica e de pósgraduação. Obrigado pela amizade, apoio, ajuda e incentivo ao longo destes anos. A todos os colegas do Instituto de Medicina Tropical (IMT), pela ajuda e cooperação e pelo ótimo ambiente que desfrutei ao longo destes anos. Aos funcionários da Divisão de Dermatologia do HC-FMUSP por toda a ajuda e contribuição neste trabalho. Aos meus pais pelo amor, apoio incondicional, educação, compreensão, ajuda nos momentos mais complicados e confiança nas minhas decisões. A CAPES pelo incentivo à pesquisa através contemplação da bolsa de Mestrado (Portaria CAPES No. 52/002).

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Estudo genético do gene p16 pela técnica de PCR-SSCP e expressão de proteína p16 em melanomas de mucosa oral e melanomas cutâneos

Cited by 5 publications

References 22 publications

Expression of p16 protein in acral lentiginous melanoma

Expression of p16 protein in acral lentiginous melanoma

Expression of Ki-67 and P16 INK4a in chemically-induced perioral squamous cell carcinomas in mice.

Expressão da proteína p16, ciclina D1, CDK4 e proteína do retinoblastoma no melanoma acral lentiginoso

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