Somatic mutations of PTEN in glioblastoma multiforme

Steven I. Wang; Janusz Puc; Jing Li; Jeffrey N. Bruce; Paul Cairns; David Sidransky; Ramon Parsons

Somatic mutations of PTEN in glioblastoma multiforme

Steven I. Wang, Janusz Puc, Jing Li, Jeffrey N. Bruce, Paul Cairns, David Sidransky, Ramon Parsons

School of Medicine

Research output: Contribution to journal › Article › peer-review

460 Scopus citations

Abstract

Alterations of the PTEN gene occur in glioblastoma multiforme. To determine the frequency of PTEN alteration, 34 consecutive glioblastomas were studied in detail. Sequencing each of the nine exons amplified from tumor DNA revealed 11 mutations. Analysis of polymorphic markers within and surrounding the PTEN gene identified an additional four homozygous deletion mutations. Loss of heterozygosity (LOH) was observed in 25 of 34 (74%) cases. All mutations occurred in the presence of LOH. PTEN was mutated in 44% (15 of 34) of all glioblastomas studied and 60% (15 of 25) of tumors with LOH on 10q. Thus, PTEN appears to be the major target of inactivation on chromosome 10q in glioblastoma multiforme.

Original language	English (US)
Pages (from-to)	4183-4186
Number of pages	4
Journal	Cancer Research
Volume	57
Issue number	19
State	Published - Oct 1 1997

ASJC Scopus subject areas

Oncology
Cancer Research

Cite this

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title = "Somatic mutations of PTEN in glioblastoma multiforme",

abstract = "Alterations of the PTEN gene occur in glioblastoma multiforme. To determine the frequency of PTEN alteration, 34 consecutive glioblastomas were studied in detail. Sequencing each of the nine exons amplified from tumor DNA revealed 11 mutations. Analysis of polymorphic markers within and surrounding the PTEN gene identified an additional four homozygous deletion mutations. Loss of heterozygosity (LOH) was observed in 25 of 34 (74%) cases. All mutations occurred in the presence of LOH. PTEN was mutated in 44% (15 of 34) of all glioblastomas studied and 60% (15 of 25) of tumors with LOH on 10q. Thus, PTEN appears to be the major target of inactivation on chromosome 10q in glioblastoma multiforme.",

author = "Wang, {Steven I.} and Janusz Puc and Jing Li and Bruce, {Jeffrey N.} and Paul Cairns and David Sidransky and Ramon Parsons",

year = "1997",

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T1 - Somatic mutations of PTEN in glioblastoma multiforme

AU - Wang, Steven I.

AU - Puc, Janusz

AU - Li, Jing

AU - Bruce, Jeffrey N.

AU - Cairns, Paul

AU - Sidransky, David

AU - Parsons, Ramon

PY - 1997/10/1

Y1 - 1997/10/1

N2 - Alterations of the PTEN gene occur in glioblastoma multiforme. To determine the frequency of PTEN alteration, 34 consecutive glioblastomas were studied in detail. Sequencing each of the nine exons amplified from tumor DNA revealed 11 mutations. Analysis of polymorphic markers within and surrounding the PTEN gene identified an additional four homozygous deletion mutations. Loss of heterozygosity (LOH) was observed in 25 of 34 (74%) cases. All mutations occurred in the presence of LOH. PTEN was mutated in 44% (15 of 34) of all glioblastomas studied and 60% (15 of 25) of tumors with LOH on 10q. Thus, PTEN appears to be the major target of inactivation on chromosome 10q in glioblastoma multiforme.

AB - Alterations of the PTEN gene occur in glioblastoma multiforme. To determine the frequency of PTEN alteration, 34 consecutive glioblastomas were studied in detail. Sequencing each of the nine exons amplified from tumor DNA revealed 11 mutations. Analysis of polymorphic markers within and surrounding the PTEN gene identified an additional four homozygous deletion mutations. Loss of heterozygosity (LOH) was observed in 25 of 34 (74%) cases. All mutations occurred in the presence of LOH. PTEN was mutated in 44% (15 of 34) of all glioblastomas studied and 60% (15 of 25) of tumors with LOH on 10q. Thus, PTEN appears to be the major target of inactivation on chromosome 10q in glioblastoma multiforme.

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C2 - 9331071

AN - SCOPUS:0030799909

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JF - Cancer Research

IS - 19

ER -

Somatic mutations of PTEN in glioblastoma multiforme

Abstract

ASJC Scopus subject areas

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