DMBT1 polymorphisms

Relationship to malignant glioma tumorigenesis

Hikaru Sasaki, Rebecca Betensky, J. Gregory Cairncross, D. N. Louis

Research output: Contribution to journalArticle

Abstract

The deleted in malignant brain tumors 1 (DMBT1) gene on 10q25-26 is a candidate tumor suppressor gene in malignant gliomas, but its role is controversial, e.g., some DMBT1 homozygous deletions reflect unmasking of constitutional deletion polymorphisms by 10q loss. To clarify the role of DMBT1 in gliomagenesis, we investigated three reported deletion hot spots. Homozygous deletions at DMBT1 repeat 2-4 to 2-7 were found in 10 of 73 gliomas with 10q loss, but all 10 deletions reflected unmasking of constitutional hemizygous deletions. Alleles bearing deletion 2-4/2-7 were not selected significantly for by 10q loss, with retention of only 10 of 16 deleted alleles. No homozygous deletion was detected at locus 74k in the 5′ upstream region of DMBT1, and four tightly linked polymorphisms were found around this region; chromosome 10q loss randomly affected alleles with or without the variant sequences around locus 74k. Moreover, no significant selection pressure was detected for the haplotype with both deletion 2-4/2-7 and 5′ polymorphisms. There was no segregation of deletion 2-4/2-7 in glioma patients compared with unrelated individuals from reference families but a suggestion of a difference in the distribution of the 5′ polymorphisms between the reference individuals and glioma patients. Constitutional polymorphisms at DMBT1 repeat 2-9/2-10 appeared common in patients with both benign brain tumors and gliomas. A homozygote for both the 2-4/2-7 deletion and the 5′ polymorphisms had a glioma arise at a typical age and without an apparent family cancer predisposition. These data suggest that DMBT1 polymorphisms are not likely primary targets of 10q loss in malignant gliomas and do not support a major role for DMBT1 in gliomagenesis.

Original languageEnglish (US)
Pages (from-to)1790-1796
Number of pages7
JournalCancer Research
Volume62
Issue number6
StatePublished - Mar 15 2002

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Brain Neoplasms
Glioma
Carcinogenesis
Alleles
Homozygote
Tumor Suppressor Genes
Haplotypes
Chromosomes
Pressure
Genes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Sasaki, H., Betensky, R., Cairncross, J. G., & Louis, D. N. (2002). DMBT1 polymorphisms: Relationship to malignant glioma tumorigenesis. Cancer Research, 62(6), 1790-1796.

DMBT1 polymorphisms : Relationship to malignant glioma tumorigenesis. / Sasaki, Hikaru; Betensky, Rebecca; Cairncross, J. Gregory; Louis, D. N.

In: Cancer Research, Vol. 62, No. 6, 15.03.2002, p. 1790-1796.

Research output: Contribution to journalArticle

Sasaki, H, Betensky, R, Cairncross, JG & Louis, DN 2002, 'DMBT1 polymorphisms: Relationship to malignant glioma tumorigenesis', Cancer Research, vol. 62, no. 6, pp. 1790-1796.
Sasaki H, Betensky R, Cairncross JG, Louis DN. DMBT1 polymorphisms: Relationship to malignant glioma tumorigenesis. Cancer Research. 2002 Mar 15;62(6):1790-1796.
Sasaki, Hikaru ; Betensky, Rebecca ; Cairncross, J. Gregory ; Louis, D. N. / DMBT1 polymorphisms : Relationship to malignant glioma tumorigenesis. In: Cancer Research. 2002 ; Vol. 62, No. 6. pp. 1790-1796.
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