Disruption of the MMAC1/PTEN gene by deletion or mutation is a frequent event in malignant melanoma
The MMAC1/PTEN gene, located at 10q23.3, is a candidate tumor suppressor commonly mutated in glioma. We have studied the pattern of deletion, mutation, and expression of MMAC1/PTEN in 35 unrelated melanoma cell lines. Nine (26%) of the cell lines showed partial or complete homozygous deletion of the...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 1997-09, Vol.57 (17), p.3660-3663 |
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| container_title | Cancer research (Chicago, Ill.) |
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| creator | GULDBERG, P THOR STRATEN, P BIRCK, A AHRENKIEL, V KIRKIN, A. F ZEUTHEN, J |
| description | The MMAC1/PTEN gene, located at 10q23.3, is a candidate tumor suppressor commonly mutated in glioma. We have studied the pattern of deletion, mutation, and expression of MMAC1/PTEN in 35 unrelated melanoma cell lines. Nine (26%) of the cell lines showed partial or complete homozygous deletion of the MMAC1/PTEN gene, and another six (17%) harbored a mutation in combination with loss of the second allele. Mutations could also be demonstrated in uncultured tumor specimens from which the cell lines had been established, and cell lines derived from two different metastases from one individual carried the same missense mutation. Collectively, these findings suggest that disruption of MMAC1/PTEN by allelic loss or mutation may contribute to the pathogenesis or neoplastic evolution in a large proportion of malignant melanomas. |
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F ; ZEUTHEN, J</creator><creatorcontrib>GULDBERG, P ; THOR STRATEN, P ; BIRCK, A ; AHRENKIEL, V ; KIRKIN, A. F ; ZEUTHEN, J</creatorcontrib><description>The MMAC1/PTEN gene, located at 10q23.3, is a candidate tumor suppressor commonly mutated in glioma. We have studied the pattern of deletion, mutation, and expression of MMAC1/PTEN in 35 unrelated melanoma cell lines. Nine (26%) of the cell lines showed partial or complete homozygous deletion of the MMAC1/PTEN gene, and another six (17%) harbored a mutation in combination with loss of the second allele. Mutations could also be demonstrated in uncultured tumor specimens from which the cell lines had been established, and cell lines derived from two different metastases from one individual carried the same missense mutation. Collectively, these findings suggest that disruption of MMAC1/PTEN by allelic loss or mutation may contribute to the pathogenesis or neoplastic evolution in a large proportion of malignant melanomas.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>PMID: 9288767</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Base Sequence ; Biological and medical sciences ; Chromosomes, Human, Pair 10 - genetics ; Dermatology ; Exons - genetics ; Gene Deletion ; Genes, Tumor Suppressor - genetics ; Humans ; Medical sciences ; Melanoma - genetics ; Molecular Sequence Data ; Mutation ; Phosphoric Monoester Hydrolases ; Polymerase Chain Reaction ; Protein Tyrosine Phosphatases - genetics ; PTEN Phosphohydrolase ; Skin Neoplasms - genetics ; Tumor Cells, Cultured ; Tumor Suppressor Proteins ; Tumors of the skin and soft tissue. 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F</creatorcontrib><creatorcontrib>ZEUTHEN, J</creatorcontrib><title>Disruption of the MMAC1/PTEN gene by deletion or mutation is a frequent event in malignant melanoma</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>The MMAC1/PTEN gene, located at 10q23.3, is a candidate tumor suppressor commonly mutated in glioma. We have studied the pattern of deletion, mutation, and expression of MMAC1/PTEN in 35 unrelated melanoma cell lines. Nine (26%) of the cell lines showed partial or complete homozygous deletion of the MMAC1/PTEN gene, and another six (17%) harbored a mutation in combination with loss of the second allele. Mutations could also be demonstrated in uncultured tumor specimens from which the cell lines had been established, and cell lines derived from two different metastases from one individual carried the same missense mutation. Collectively, these findings suggest that disruption of MMAC1/PTEN by allelic loss or mutation may contribute to the pathogenesis or neoplastic evolution in a large proportion of malignant melanomas.</description><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Chromosomes, Human, Pair 10 - genetics</subject><subject>Dermatology</subject><subject>Exons - genetics</subject><subject>Gene Deletion</subject><subject>Genes, Tumor Suppressor - genetics</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Melanoma - genetics</subject><subject>Molecular Sequence Data</subject><subject>Mutation</subject><subject>Phosphoric Monoester Hydrolases</subject><subject>Polymerase Chain Reaction</subject><subject>Protein Tyrosine Phosphatases - genetics</subject><subject>PTEN Phosphohydrolase</subject><subject>Skin Neoplasms - genetics</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Suppressor Proteins</subject><subject>Tumors of the skin and soft tissue. Premalignant lesions</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtPwzAQhC0EKqXwE5B8QNwibMeO7WNVykNqgUM5R5t40xrlUeIEqf-eQCOuXHZ3NJ9WozkhU65iE2kp1SmZMsZMpKQW5-QihI9BKs7UhEysMEYnekryex_aft_5pqZNQbsd0vV6vuB3b5vlC91ijTQ7UIclHpGWVn0Hv7cPFGjR4mePdUfx62f6mlZQ-m0Ng6iwhLqp4JKcFVAGvBr3jLw_LDeLp2j1-vi8mK-iXcxYFwFHya0FlUvugLmCgwQrMgNJLhQ6DpljmVYMuDZZrFmRO2ttIVwsdKZMPCO3x7_7thlChS6tfMixHFJg04dUW5EkNv4f5AnTQgo7gNcj2GcVunTf-graQzrWN_g3ow8hh7Jooc59-MOEYUoaHX8DUnV5Gw</recordid><startdate>19970901</startdate><enddate>19970901</enddate><creator>GULDBERG, P</creator><creator>THOR STRATEN, P</creator><creator>BIRCK, A</creator><creator>AHRENKIEL, V</creator><creator>KIRKIN, A. 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F ; ZEUTHEN, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h300t-a1e4199a5c41da0df1a4a92b8a6c25ed1abd0b750a178b370fcd999f2d327b583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Chromosomes, Human, Pair 10 - genetics</topic><topic>Dermatology</topic><topic>Exons - genetics</topic><topic>Gene Deletion</topic><topic>Genes, Tumor Suppressor - genetics</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Melanoma - genetics</topic><topic>Molecular Sequence Data</topic><topic>Mutation</topic><topic>Phosphoric Monoester Hydrolases</topic><topic>Polymerase Chain Reaction</topic><topic>Protein Tyrosine Phosphatases - genetics</topic><topic>PTEN Phosphohydrolase</topic><topic>Skin Neoplasms - genetics</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Suppressor Proteins</topic><topic>Tumors of the skin and soft tissue. Premalignant lesions</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GULDBERG, P</creatorcontrib><creatorcontrib>THOR STRATEN, P</creatorcontrib><creatorcontrib>BIRCK, A</creatorcontrib><creatorcontrib>AHRENKIEL, V</creatorcontrib><creatorcontrib>KIRKIN, A. F</creatorcontrib><creatorcontrib>ZEUTHEN, J</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GULDBERG, P</au><au>THOR STRATEN, P</au><au>BIRCK, A</au><au>AHRENKIEL, V</au><au>KIRKIN, A. F</au><au>ZEUTHEN, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Disruption of the MMAC1/PTEN gene by deletion or mutation is a frequent event in malignant melanoma</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>1997-09-01</date><risdate>1997</risdate><volume>57</volume><issue>17</issue><spage>3660</spage><epage>3663</epage><pages>3660-3663</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>The MMAC1/PTEN gene, located at 10q23.3, is a candidate tumor suppressor commonly mutated in glioma. We have studied the pattern of deletion, mutation, and expression of MMAC1/PTEN in 35 unrelated melanoma cell lines. Nine (26%) of the cell lines showed partial or complete homozygous deletion of the MMAC1/PTEN gene, and another six (17%) harbored a mutation in combination with loss of the second allele. Mutations could also be demonstrated in uncultured tumor specimens from which the cell lines had been established, and cell lines derived from two different metastases from one individual carried the same missense mutation. Collectively, these findings suggest that disruption of MMAC1/PTEN by allelic loss or mutation may contribute to the pathogenesis or neoplastic evolution in a large proportion of malignant melanomas.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>9288767</pmid><tpages>4</tpages></addata></record> |
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| ispartof | Cancer research (Chicago, Ill.), 1997-09, Vol.57 (17), p.3660-3663 |
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| source | MEDLINE; American Association for Cancer Research; EZB-FREE-00999 freely available EZB journals |
| subjects | Base Sequence Biological and medical sciences Chromosomes, Human, Pair 10 - genetics Dermatology Exons - genetics Gene Deletion Genes, Tumor Suppressor - genetics Humans Medical sciences Melanoma - genetics Molecular Sequence Data Mutation Phosphoric Monoester Hydrolases Polymerase Chain Reaction Protein Tyrosine Phosphatases - genetics PTEN Phosphohydrolase Skin Neoplasms - genetics Tumor Cells, Cultured Tumor Suppressor Proteins Tumors of the skin and soft tissue. Premalignant lesions |
| title | Disruption of the MMAC1/PTEN gene by deletion or mutation is a frequent event in malignant melanoma |
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