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| Nagai,M.A.. |
| The genetic alterations observed in head and neck cancer are mainly due to oncogene activation (gain of function mutations) and tumor suppressor gene inactivation (loss of function mutations), leading to deregulation of cell proliferation and death. These genetic alterations include gene amplification and overexpression of oncogenes such as myc, erbB-2, EGFR and cyclinD1 and mutations, deletions and hypermethylation leading to p16 and TP53 tumor suppressor gene inactivation. In addition, loss of heterozygosity in several chromosomal regions is frequently observed, suggesting that other tumor suppressor genes not yet identified could be involved in the tumorigenic process of head and neck cancers. The exact temporal sequence of the genetic alterations... |
| Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Genetic alterations; Oncogene; Tumor suppressor gene; Head and neck cancer. |
| Ano: 1999 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1999000700015 |
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| Garcia,S.A.B.; Nagai,M.A.. |
| Using cDNA microarray analysis, we previously identified a set of differentially expressed genes in primary breast tumors based on the status of estrogen and progesterone receptors. In the present study, we performed an integrated computer-assisted and manual search of potential estrogen response element (ERE) binding sites in the promoter region of these genes to characterize their potential to be regulated by estrogen receptors (ER). Publicly available databases were used to annotate the position of these genes in the genome and to extract a 5’flanking region 2 kb upstream to 2 kb downstream of the transcription start site for transcription binding site analysis. The search for EREs and other binding sites was performed using several publicly available... |
| Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Breast cancer; Estrogen receptor; Gene expression; Bidirectional promoters. |
| Ano: 2011 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2011000200005 |
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