Early genetic changes involved in low-grade astrocytic tumor development

被引:13
作者
Arjona, Dolores
Rey, Juan Antonio
Taylor, Shirley M.
机构
[1] Virginia Commonwealth Univ, Dept Microbiol & Immunol, Richmond, VA 23298 USA
[2] Virginia Commonwealth Univ, Massey Canc Ctr, Richmond, VA 23298 USA
[3] Hosp Univ La Paz, Unidad Invest, Lab Oncognet Mol, E-28046 Madrid, Spain
关键词
low-grade astrocytomas; gene amplification; gene mutation; LOH; promoter hypermethylation;
D O I
10.2174/156652406778195017
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Astrocytomas represent the most common form of glial tumors. The most malignant grade of these tumors, glioblastoma multiforme, may arise as a malignant progression from low-grade astrocytoma through anaplastic astrocytoma to secondary GBM, or else it may arise "de novo" as primary GBM. Both types of glioblastoma are usually histologically indistinguishable. However, distinct molecular alterations have been described between them that potentially allow differentiation between the two mechanisms of origin. Since malignant transformation is a multistep process, we summarize in this review the earliest genetic changes that seem to be involved in the appearance and development of low-grade astrocytic tumors, where early detection and treatment could be possible.
引用
收藏
页码:645 / 650
页数:6
相关论文
共 80 条
[61]   Analysis of p53 mutation and epidermal growth factor receptor amplification in recurrent gliomas with malignant progression [J].
Reifenberger, J ;
Ring, GU ;
Gies, U ;
Cobbers, JMJL ;
Oberstrass, J ;
An, HX ;
Niederacher, D ;
Wechsler, W ;
Reifenberger, G .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1996, 55 (07) :822-831
[62]   Refined mapping of 1q32 amplicons in malignant gliomas confirms MDM4 as the main amplification target [J].
Riemenschneider, MJ ;
Knobbe, CB ;
Reifenberger, G .
INTERNATIONAL JOURNAL OF CANCER, 2003, 104 (06) :752-757
[63]  
Riemenschneider MJ, 1999, CANCER RES, V59, P6091
[64]   Amplification of the cyclin-dependent kinase 4 (CDK4) gene is associated with high cdk4 protein levels in glioblastoma multiforme [J].
Rollbrocker, B ;
Waha, A ;
Louis, DN ;
Wiestler, OD ;
vonDeimling, A .
ACTA NEUROPATHOLOGICA, 1996, 92 (01) :70-74
[65]   Infrequent methylation of CDKN2A(MTS1/p16) and rare mutation of both CDKN2A and CDKN2B(MTS2/p15) in primary astrocytic tumours [J].
Schmidt, EE ;
Ichimura, K ;
Messerle, KR ;
Goike, HM ;
Collins, VP .
BRITISH JOURNAL OF CANCER, 1997, 75 (01) :2-8
[66]   Impact of genotype and morphology on the prognosis of glioblastoma [J].
Schmidt, MC ;
Antweiler, S ;
Urban, N ;
Mueller, W ;
Kuklik, A ;
Meyer-Puttlitz, B ;
Wiestler, OD ;
Louis, DN ;
Fimmers, R ;
von Deimling, A .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 2002, 61 (04) :321-328
[67]  
Sherr CJ, 2000, CANCER RES, V60, P3689
[68]   Cancer cell cycles [J].
Sherr, CJ .
SCIENCE, 1996, 274 (5293) :1672-1677
[69]   MDMX: A novel p53-binding protein with some functional properties of MDM2 [J].
Shvarts, A ;
Steegenga, WT ;
Riteco, N ;
vanLaar, T ;
Dekker, P ;
Bazuine, M ;
vanHam, RCA ;
vanOordt, WV ;
Hateboer, G ;
vanderEb, AJ ;
Jochemsen, AG .
EMBO JOURNAL, 1996, 15 (19) :5349-5357
[70]  
Simpson DJ, 2000, CANCER RES, V60, P1211