hTERT, MYC and TP53 deregulation in gastric preneoplastic lesions
- Equal contributors
1 Laboratório de Citogenética Humana, Instituto de Ciências Biológicas, Universidade Federal do Pará, CEP: 66073-000, Belém, PA, Brazil
2 Disciplina de Genética, Departamento de Morfologia e Genética, Universidade Federal de São Paulo, Rua Botucatu 740, CEP 04023-900, São Paulo, SP, Brazil
3 Unidade de Alta Complexidade em Oncologia, Hospital Universitário João de Barros Barreto, Universidade Federal do Pará, CEP: 60673-000, Belém, PA, Brazil
4 Laboratório de Genética Molecular, Departamento de Patologia e Medicina Forense, Escola de Medicina, Universidade Federal do Ceará, CEP: 60020-181, Fortaleza, CE, Brazil
BMC Gastroenterology 2012, 12:85 doi:10.1186/1471-230X-12-85Published: 6 July 2012
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.
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.
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.
We demonstrated that hTERT, MYC, and TP53 are deregulated in intestinal metaplasia of individuals from Northern Brazil and these alterations may facilitate tumor initiation.