PTEN mutation analysis in two genetic subtypes of high-grade oligodendroglial tumors:: PTEN is only occasionally mutated in one of the two genetic subtypes

被引：16

作者：

Jeuken, JWM

Nelen, MR

Vermeer, H

van Staveren, WCG

Kremer, H

van Overbeeke, JJ

Boerman, RH

机构：

[1] Univ Nijmegen Hosp, Dept Neurosurg 309, NL-6525 GC Nijmegen, Netherlands

[2] Univ Nijmegen Hosp, Dept Neurol, NL-6525 GC Nijmegen, Netherlands

[3] Univ Nijmegen Hosp, Dept Human Genet, NL-6525 GC Nijmegen, Netherlands

[4] Wilhelmina Childrens Hosp, Dept Endocrinol, Utrecht, Netherlands

来源：

CANCER GENETICS AND CYTOGENETICS | 2000年 / 119卷 / 01期

关键词：

D O I：

10.1016/S0165-4608(99)00210-1

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

We recently identified two genetic subtypes of high-grade oligodendroglial tumors (HG-OT): 1p-/19q- HG-OT are characterized by a loss of chromosome 1p32-36 (del(1)(p32-p36) and/or a del(19)(q13.3); whereas +7/-10 HG-OT harbor a gain of chromosome 7 (+ 7) and/or a -10 without a loss of 1p32-36 and 19q13.3. Because a -10 and a +7 are most frequently defected in glioblastomas (GBM), the genotype of +7/-10 HG-OT suggests that these tumors are GEM with a prominent oligodendroglial phenotype rather than anaplastic oligodendrogliomas. PTEN is a tumor suppressor gene, located at 10q23.3, which is involved in tumor progression of GEM and other neoplasms. In this study, we screened for PTEN mutations in six low-grade oligodendroglial tumors (LG-OT), five 1p-/19q- HG-seven +7/-10 HG-OT, and nine xenografted GEM. PTEN mutations were detected in none of the LG-OT and 1p-/19q- HG-OT, once in +7/-10 HG-OT, and frequently in GEM. As one of the + 7/-10 HG-OT harbored a PTEN mutation, this demonstrates that PTEN can be involved in the oncogencsis of this genetic subtype of HG-OT. The lower frequency of PTEN mutations in +7/-10 HG-OT compared to GEM suggests that these tumors are of a distinct tumor type rather than GEM. Published by Elsevier Science Inc.

引用

页码：42 / 47

页数：6

共 47 条

[31] Novel PTEN mutations in patients with Cowden disease:: absence of clear genotype-phenotype correlations [J].

Nelen, MR ;

Kremer, H ;

Konings, IBM ;

Schoute, F ;

van Essen, AJ ;

Koch, R ;

Woods, CG ;

Fryns, JP ;

Hamel, B ;

Hoefsloot, LH ;

Peeters, EAJ ;

Padberg, GW .

EUROPEAN JOURNAL OF HUMAN GENETICS, 1999, 7 (03) :267-273

[32] Germline mutations in the PTEN/MMAC1 gene in patients with Cowden disease [J].

Nelen, MR ;

vanStaveren, WCG ;

Peeters, EAJ ;

BenHassel, M ;

Gorlin, RJ ;

Hamm, H ;

Lindboe, CF ;

Fryns, JP ;

Sijmons, RH ;

Woods, DG ;

Mariman, ECM ;

Padberg, GW ;

Kremer, H .

HUMAN MOLECULAR GENETICS, 1997, 6 (08) :1383-1387

[33] PTEN germ-line mutations in juvenile polyposis coli [J].

Olschwang, S ;

Serova-Sinilnikova, OM ;

Lenoir, GM ;

Thomas, G .

NATURE GENETICS, 1998, 18 (01) :12-14

[34] RAPID AND SENSITIVE DETECTION OF POINT MUTATIONS AND DNA POLYMORPHISMS USING THE POLYMERASE CHAIN-REACTION [J].

ORITA, M ;

SUZUKI, Y ;

SEKIYA, T ;

HAYASHI, K .

GENOMICS, 1989, 5 (04) :874-879

[35]

Rasheed BKA, 1997, CANCER RES, V57, P4187

[36]

REIFENBERGER J, 1994, AM J PATHOL, V145, P1175

[37] Negative regulation of PKB/Akt-dependent cell survival by the tumor suppressor PTEN [J].

Stambolic, V ;

Suzuki, A ;

de la Pompa, JL ;

Brothers, GM ;

Mirtsos, C ;

Sasaki, T ;

Ruland, J ;

Penninger, JM ;

Siderovski, DP ;

Mak, TW .

CELL, 1998, 95 (01) :29-39

[38] Identification of a candidate tumour suppressor gene, MMAC1, at chromosome 10q23.3 that is mutated in multiple advanced cancers [J].

Steck, PA ;

Pershouse, MA ;

Jasser, SA ;

Yung, WKA ;

Lin, H ;

Ligon, AH ;

Langford, LA ;

Baumgard, ML ;

Hattier, T ;

Davis, T ;

Frye, C ;

Hu, R ;

Swedlund, B ;

Teng, DHF ;

Tavtigian, SV .

NATURE GENETICS, 1997, 15 (04) :356-362

[39]

STECK PA, 1995, GENE CHROMOSOME CANC, V12, P255

[40]

Suzuki H, 1998, CANCER RES, V58, P204

← 1 2 3 4 5 →