MYC and gastric adenocarcinoma carcinogenesis

被引:88
作者
Calcagno, Danielle Queiroz
Leal, Mariana Ferreira [1 ]
Assumpcao, Paulo Pimentel [2 ]
Cardoso Smith, Marilia de Arruda [1 ]
Burbano, Rommel Rodriguez [3 ]
机构
[1] Univ Fed Sao Paulo, Dept Morphol & Genet, Div Genet, BR-04023900 Sao Paulo, Brazil
[2] Fed Univ Para, Joao de Barros Barreto Univ Hosp, BR-66073000 Belem, Para, Brazil
[3] Fed Univ Para, Dept Biol, Lab Citogenet Humana, Inst Ciencias Biol, BR-66075900 Belem, Para, Brazil
基金
巴西圣保罗研究基金会;
关键词
MYC; Gastric adenocarcinoma; Gastric preneoplastic lesions; Gastric carcinogenesis; Helicobacter pylori;
D O I
10.3748/wjg.14.5962
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
MYC is an oncogene involved in cell cycle regulation, cell growth arrest, cell adhesion, metabolism, ribosome biogenesis, protein synthesis, and mitochondrial function. It has been described as a key element of several carcinogenesis processes in humans. Many studies have shown an association between MYC deregulation and gastric cancer. MYC deregulation is also seen in gastric preneoplastic lesions and thus it may have a role in early gastric carcinogenesis. Several studies have suggested that amplification is the main mechanism of MYC deregulation in gastric cancer. In the present review, we focus on the deregulation of the MYC oncogene in gastric adenocarcinorna carcinogenesis, including its association with Helicobacterpylori (Hpylorl) and clinical applications. (c) 2008 The WIG Press. All rights reserved.
引用
收藏
页码:5962 / 5968
页数:7
相关论文
共 86 条
[1]   Numerical aberrations of chromosome 8 detected by conventional cytogenetics and fluorescence in situ hybridization in individuals from northern Brazil with gastric adenocarcinoma [J].
Assumpcao, Paulo Pimentel ;
Ishak, Geraldo ;
Chen, Elizabeth Suchi ;
Takeno, Sylvia Satomi ;
Leal, Mariana Ferreira ;
Guimaraes, Adriana Costa ;
Calcagno, Danielle Queiroz ;
Khayat, Andre Salim ;
Demachki, Sarnia ;
de Arruda Cardoso Smith, Marilia ;
Burbano, Rommel Rodriguez .
CANCER GENETICS AND CYTOGENETICS, 2006, 169 (01) :45-49
[2]  
Assumpção Paulo Pimentel de, 2006, Int. J. Morphol., V24, P335, DOI 10.4067/S0717-95022006000400007
[3]  
AssumpcAo PP, 2005, ATUALIZACAO CANC GAS, P95
[4]   MAD - A HETERODIMERIC PARTNER FOR MAX THAT ANTAGONIZES MYC TRANSCRIPTIONAL ACTIVITY [J].
AYER, DE ;
KRETZNER, L ;
EISENMAN, RN .
CELL, 1993, 72 (02) :211-222
[5]  
Baffa R, 2000, CLIN CANCER RES, V6, P1372
[6]   THE HUMAN C-MYC-ONCOGENE - STRUCTURAL CONSEQUENCES OF TRANSLOCATION INTO THE IGH LOCUS IN BURKITT-LYMPHOMA [J].
BATTEY, J ;
MOULDING, C ;
TAUB, R ;
MURPHY, W ;
STEWART, T ;
POTTER, H ;
LENOIR, G ;
LEDER, P .
CELL, 1983, 34 (03) :779-787
[7]   RETROVIRUSES AND CANCER GENES [J].
BISHOP, JM .
ADVANCES IN CANCER RESEARCH, 1982, 37 :1-32
[8]   Lack of sustained regression of c-MYC-induced mammary adenocarcinomas following brief or prolonged MYC inactivation [J].
Boxer, RB ;
Jang, JW ;
Sintasath, L ;
Chodosh, LA .
CANCER CELL, 2004, 6 (06) :577-586
[9]   Myc represses transcription through recruitment of DNA methyltransferase corepressor [J].
Brenner, C ;
Deplus, R ;
Didelot, C ;
Loriot, A ;
Viré, E ;
De Smet, C ;
Gutierrez, A ;
Danovi, D ;
Bernard, D ;
Boon, T ;
Pelicci, PG ;
Amati, B ;
Kouzarides, T ;
de Launoit, Y ;
Di Croce, L ;
Fuks, F .
EMBO JOURNAL, 2005, 24 (02) :336-346
[10]  
Burbano RR, 2006, ANTICANCER RES, V26, P2909