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Article: Mutation analysis of DMBT1 in glioblastoma, medulloblastoma and oligodendroglial tumors

TitleMutation analysis of DMBT1 in glioblastoma, medulloblastoma and oligodendroglial tumors
Authors
KeywordsDMBT1
Glioblastoma
Homozygous deletion
Medulloblastoma
Mutation
Oligodendroglioma
Issue Date2003
Citation
International Journal of Cancer, 2003, v. 105, n. 1, p. 76-81 How to Cite?
AbstractDMBT1 has been implicated as a candidate tumor suppressor gene on chromosome 10q for brain, gastrointestinal and lung cancer. Homozygous deletion and lack of expression are 2 known mechanisms for inactivating DMBT1. We evaluated whether somatic mutation, which represents a major inactivation mechanism for most tumor suppressor genes, occurs in the DMBT1 gene. A total of 102 primary brain tumors, consisting of 25 glioblastoma multiforme, 24 medulloblastoma and 53 oligodendroglial tumors, were analyzed by conformation-sensitive gel electrophoresis in all 54 coding exons of DMBT1. Twelve different base substitutions were detected in 26 (25%) tumors. Eight base substitutions resulted in amino acid changes and 4 were silent. These base changes were also detected in tumor-matched blood samples, however, indicating that the base variations represent genetic polymorphisms. We also assessed homozygous deletions of the DMBT1 gene in the series and found that 16 of 95 (5 glioblastomas, 5 medulloblastomas, 6 oligodendroglial tumors; total 17%) tumors harbor such alteration. High-quality blood DNA samples were available in 5 tumors carrying homozygous deletion and, using long-range PCR, 3 of these blood samples showed germline hemizygous deletions in a region between introns 10 and 26 of DMBT1. Our results showed that mutation does not play a role in inactivation of DMBT1 in brain tumors. Intragenic homozygous deletion of DMBT1 is common in brain tumors and is likely a result of a germline deletion of I allele followed by loss of the second allele during tumor development. © 2003 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/325066
ISSN
2023 Impact Factor: 5.7
2023 SCImago Journal Rankings: 2.131
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorPang, Jesse Chung sean-
dc.contributor.authorDong, Zhiqian-
dc.contributor.authorZhang, Rong-
dc.contributor.authorLiu, Yanhui-
dc.contributor.authorZhou, Liang fu-
dc.contributor.authorChan, Bik Wan-
dc.contributor.authorPoon, Wai Sang-
dc.contributor.authorNg, Ho keung-
dc.date.accessioned2023-02-27T07:29:26Z-
dc.date.available2023-02-27T07:29:26Z-
dc.date.issued2003-
dc.identifier.citationInternational Journal of Cancer, 2003, v. 105, n. 1, p. 76-81-
dc.identifier.issn0020-7136-
dc.identifier.urihttp://hdl.handle.net/10722/325066-
dc.description.abstractDMBT1 has been implicated as a candidate tumor suppressor gene on chromosome 10q for brain, gastrointestinal and lung cancer. Homozygous deletion and lack of expression are 2 known mechanisms for inactivating DMBT1. We evaluated whether somatic mutation, which represents a major inactivation mechanism for most tumor suppressor genes, occurs in the DMBT1 gene. A total of 102 primary brain tumors, consisting of 25 glioblastoma multiforme, 24 medulloblastoma and 53 oligodendroglial tumors, were analyzed by conformation-sensitive gel electrophoresis in all 54 coding exons of DMBT1. Twelve different base substitutions were detected in 26 (25%) tumors. Eight base substitutions resulted in amino acid changes and 4 were silent. These base changes were also detected in tumor-matched blood samples, however, indicating that the base variations represent genetic polymorphisms. We also assessed homozygous deletions of the DMBT1 gene in the series and found that 16 of 95 (5 glioblastomas, 5 medulloblastomas, 6 oligodendroglial tumors; total 17%) tumors harbor such alteration. High-quality blood DNA samples were available in 5 tumors carrying homozygous deletion and, using long-range PCR, 3 of these blood samples showed germline hemizygous deletions in a region between introns 10 and 26 of DMBT1. Our results showed that mutation does not play a role in inactivation of DMBT1 in brain tumors. Intragenic homozygous deletion of DMBT1 is common in brain tumors and is likely a result of a germline deletion of I allele followed by loss of the second allele during tumor development. © 2003 Wiley-Liss, Inc.-
dc.languageeng-
dc.relation.ispartofInternational Journal of Cancer-
dc.subjectDMBT1-
dc.subjectGlioblastoma-
dc.subjectHomozygous deletion-
dc.subjectMedulloblastoma-
dc.subjectMutation-
dc.subjectOligodendroglioma-
dc.titleMutation analysis of DMBT1 in glioblastoma, medulloblastoma and oligodendroglial tumors-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/ijc.11019-
dc.identifier.pmid12672033-
dc.identifier.scopuseid_2-s2.0-0037457661-
dc.identifier.volume105-
dc.identifier.issue1-
dc.identifier.spage76-
dc.identifier.epage81-
dc.identifier.isiWOS:000182163000012-

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