|
|
|
|
|
| Brenna,S.M.F.; Zeferino,L.C.; Pinto,G.A.; Souza,R.A.; Andrade,L.A.L.; Vassalo,J.; Martinez,E.Z.; Syrjänen,K.J.. |
| The c-myc protein is known to regulate the cell cycle, and its down-regulation can lead to cell death by apoptosis. The role of c-myc protein as an independent prognostic determinant in cervical cancer is controversial. In the present study, a cohort of 220 Brazilian women (mean age 53.4 years) with FIGO stage I, II and III (21, 28 and 51%, respectively) cervical squamous cell carcinomas was analyzed for c-myc protein expression using immunohistochemistry. The disease-free survival and relapse-rate were analyzed using univariate (Kaplan-Meier) survival analysis for 116 women who completed the standard FIGO treatment and were followed up for 5 years. Positive c-myc staining was detected in 40% of carcinomas, 29% being grade 1, 9% grade 2, and 2% grade 3.... |
| Tipo: Info:eu-repo/semantics/article |
Palavras-chave: C-myc; Oncogene; Cervical cancer; Prognosis. |
| Ano: 2002 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2002000400003 |
| |
|
|
| Primo,Luiza M. F.; Teixeira,Leonardo K.. |
| Abstract Precise replication of genetic material is essential to maintain genome stability. DNA replication is a tightly regulated process that ensues faithful copies of DNA molecules to daughter cells during each cell cycle. Perturbation of DNA replication may compromise the transmission of genetic information, leading to DNA damage, mutations, and chromosomal rearrangements. DNA replication stress, also referred to as DNA replicative stress, is defined as the slowing or stalling of replication fork progression during DNA synthesis as a result of different insults. Oncogene activation, one hallmark of cancer, is able to disturb numerous cellular processes, including DNA replication. In fact, extensive work has indicated that oncogene-induced replication... |
| Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Cancer; Cell cycle; DNA replication; Oncogene; Replication stress. |
| Ano: 2020 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572020000200301 |
| |
|
|
| 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 |
| |
|
| |
|
|
| Amarante-Mendes,G.P.; Green,D.R.. |
| Apoptosis is a fundamental biological phenomenon in which the death of a cell is genetically and biochemically regulated. Different molecules are involved in the regulation of the apoptotic process. Death receptors, coupled to distinct members of the caspases as well as other adapter molecules, are involved in the initiation of the stress signals (The Indictment). Members of the Bcl-2 family control at the mitochondrial level the decision between life and death (The Judgement). The effector caspases are responsible for all morphological and biochemical changes related to apoptosis including the "eat-me" signals perceived by phagocytes and neighboring cells (The Execution). Finally, apoptosis would have little biological significance without the recognition... |
| Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Apoptosis; Cell death; Caspase; Mitochondria; Bcl-2; Oncogene. |
| Ano: 1999 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1999000900001 |
| |
|
|
|
