DMBT1, a new member of the SRCR superfamily, on chromosome 10q25.3-26.1 is deleted in malignant brain tumours

被引:405
作者
Mollenhauer, J
Wiemann, S
Scheurlen, W
Korn, B
Hayashi, Y
Wilgenbus, KK
vonDeimling, A
Poustka, A
机构
[1] DEUTSCH KREBSFORSCHUNGSZENTRUM, DIV MOL GENOME ANAL, D-69120 HEIDELBERG, GERMANY
[2] CHILDRENS HOSP, D-68167 MANNHEIM, GERMANY
[3] UNIV BONN, MED CTR, DEPT NEUROPATHOL, D-53105 BONN, GERMANY
关键词
PRIMITIVE NEUROECTODERMAL TUMORS; CENTRAL-NERVOUS-SYSTEM; LONG ARM; RECEPTOR; HETEROZYGOSITY; SEQUENCES; DOMAIN; HYBRIDIZATION; PROGRESSION; MELANOMA;
D O I
10.1038/ng0997-32
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Loss of sequences from human chromosome 10q has been associated with the progression of human cancer. Medulloblastoma and glioblastoma multiforme ave the most common malignant brain tumours in children and adults, respectively. In glioblastoma multiforme, the most aggressive form, 80% of the tumours show loss of 10q. We have used representational difference analysis to identify a homozygous deletion at 10q25.3-26.1 in a medulloblastoma cell line and have cloned a novel gene, DMBT1, spanning this deletion. DMBT1 shows homology to the scavenger receptor cysteine-rich (SRCR) superfamily. Intragenic homozygous deletions have been detected in 2/20 medulloblastomas and in 9/39 glioblastomas mutliformes. Lack of DMBT1 expression has been demonstrated in 4/5 brain-tumour cell lines. We suggest that DMBT1 is a putative tumour-suppressor gene implicated in the carcinogenesis of medulloblastoma and glioblastoma multiforme.
引用
收藏
页码:32 / 39
页数:8
相关论文
共 43 条
  • [1] Plasticity in epithelial polarity of renal intercalated cells: Targeting of the H+-ATPase and band 3
    AlAwqati, Q
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 1996, 270 (06): : C1571 - C1580
  • [2] Albarosa R, 1996, AM J HUM GENET, V58, P1260
  • [3] MICROSATELLITE ANALYSIS OF LOSS OF HETEROZYGOSITY ON CHROMOSOMES 9Q, 11P AND 17P IN MEDULLOBLASTOMAS
    ALBRECHT, S
    VONDEIMLING, A
    PIETSCH, T
    GIANGASPERO, F
    BRANDNER, S
    KLEIHUES, P
    WIESTLER, OD
    [J]. NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, 1994, 20 (01) : 74 - 81
  • [4] AZIZI E, 1995, CANCER, V76, P1571, DOI 10.1002/1097-0142(19951101)76:9<1571::AID-CNCR2820760912>3.0.CO
  • [5] 2-6
  • [6] ISOCHROMOSOME 17Q DEMONSTRATED BY INTERPHASE FLUORESCENCE IN-SITU HYBRIDIZATION IN PRIMITIVE NEUROECTODERMAL TUMORS OF THE CENTRAL-NERVOUS-SYSTEM
    BIEGEL, JA
    RORKE, LB
    JANSS, AJ
    SUTTON, LN
    PARMITER, AH
    [J]. GENES CHROMOSOMES & CANCER, 1995, 14 (02) : 85 - 96
  • [7] ISOCHROMOSOME-17Q IN PRIMITIVE NEUROECTODERMAL TUMORS OF THE CENTRAL-NERVOUS-SYSTEM
    BIEGEL, JA
    RORKE, LB
    PACKER, RJ
    SUTTON, LN
    SCHUT, L
    BONNER, K
    EMANUEL, BS
    [J]. GENES CHROMOSOMES & CANCER, 1989, 1 (02) : 139 - 147
  • [8] A LARGE DOMAIN COMMON TO SPERM RECEPTORS (ZP2 AND ZP3) AND TGF-BETA TYPE-III RECEPTOR
    BORK, P
    SANDER, C
    [J]. FEBS LETTERS, 1992, 300 (03): : 237 - 240
  • [9] THE CUB DOMAIN - A WIDESPREAD MODULE IN DEVELOPMENTALLY-REGULATED PROTEINS
    BORK, P
    BECKMANN, G
    [J]. JOURNAL OF MOLECULAR BIOLOGY, 1993, 231 (02) : 539 - 545
  • [10] Cheng H, 1996, ANAT REC, V244, P327