Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/35090
Title: hTERT, MYC and TP53 deregulation in gastric preneoplastic lesions
Authors: Silva, Tanielly Cristina Raiol
Leal, Mariana Ferreira [UNIFESP]
Calcagno, Danielle Queiroz [UNIFESP]
Souza, Carolina Rosal Teixeira de
Khayat, Andre Salim
Santos, Ney Pereira Carneiro dos
Montenegro, Raquel Carvalho
Rabenhorst, Silvia Helena Barem
Nascimento, Mayara Quaresma
Assumpcao, Paulo Pimentel
Smith, Marilia de Arruda Cardoso [UNIFESP]
Burbano, Rommel Rodriguez
Universidade Federal de São Paulo (UNIFESP)
Fed Univ Para
Univ Fed Ceara
Keywords: hTERT
MYC
TP53
Gastric carcinogenesis
Precancerous lesions
Issue Date: 6-Jul-2012
Publisher: Biomed Central Ltd
Citation: Bmc Gastroenterology. London: Biomed Central Ltd, v. 12, 8 p., 2012.
Abstract: Background: Gastric cancer is a serious public health problem in Northern Brazil and in the world due to its high incidence and mortality. Despite the severity of the disease, more research is needed to better understand the molecular events involved in this intestinal-type gastric carcinogenesis process. Since precancerous lesions precede intestinal-type gastric cancer, here, we evaluated the hTERT, MYC, and TP53 mRNA and protein expression, as well as TP33 copy number, in gastric preneoplastic lesions.Methods: We evaluated 19 superficial gastritis, 18 atrophic gastritis, and 18 intestinal metaplasia from cancer-free individuals of Northern Brazil. Quantitative reverse transcription PCR was used to analyze the mRNA expression and immunohistochemical methods were used to assess protein immunoreactivity in tissue samples. the number of TP53 gene copies was investigated in gastric diseases by quantitative PCR.Results: We observed hTERT, MYC, and p53 immunoreactivity only in intestinal metaplasia samples. the immunoreactivity of these proteins was strongly associated with each other. A significantly higher MYC mRNA expression was observed in intestinal metaplasia compared to gastritis samples. Loss of TP53 was also only detected in intestinal metaplasia specimens.Conclusions: We demonstrated that hTERT, MYC, and TP53 are deregulated in intestinal metaplasia of individuals from Northern Brazil and these alterations may facilitate tumor initiation.
URI: http://repositorio.unifesp.br/handle/11600/35090
ISSN: 1471-230X
Other Identifiers: http://dx.doi.org/10.1186/1471-230X-12-85
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