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A New Translocation, t(2;4;12)(p21;q12;p13), in CD7-Positive Acute Myeloid Leukemia: A Variant Form of t(4;12)
We describe a 41-year-old man with CD7-positive acute myeloid leukemia (AML-M0) with trilineage-myelodysplasia. Chromosome analysis of the bone marrow cells showed 46,XY,t(2;4;12)(p21;q12;p13). Cytological and clinical features of our case were quite similar to those of AML with t(4;12)(q11∼12;p13)....
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Published in: | Cancer genetics and cytogenetics 1999-10, Vol.114 (2), p.96-99 |
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creator | Hamaguchi, Hiroyuki Nagata, Kaoru Yamamoto, Katsuya Kobayashi, Masaru Takashima, Teruyuki Taniwaki, Masafumi |
description | We describe a 41-year-old man with CD7-positive acute myeloid leukemia (AML-M0) with trilineage-myelodysplasia. Chromosome analysis of the bone marrow cells showed 46,XY,t(2;4;12)(p21;q12;p13). Cytological and clinical features of our case were quite similar to those of AML with t(4;12)(q11∼12;p13). The karyotypic interpretation was confirmed by fluorescence in situ hybridization (FISH) by using the whole-chromosome painting probes specific for chromosomes 2, 4, and 12. FISH analysis with the use of the YAC 936e2 probe, which covers the
TEL gene, did not show the split signal, suggesting that a gene other than
TEL was involved in the leukemogenesis of the present case. Our case with AML with t(2;4;12)(p21;q12;p13) appears to be the first case of a variant type of AML with t(4;12)(q11∼12;p13). |
doi_str_mv | 10.1016/S0165-4608(99)00060-6 |
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TEL gene, did not show the split signal, suggesting that a gene other than
TEL was involved in the leukemogenesis of the present case. Our case with AML with t(2;4;12)(p21;q12;p13) appears to be the first case of a variant type of AML with t(4;12)(q11∼12;p13).</description><identifier>ISSN: 0165-4608</identifier><identifier>EISSN: 1873-4456</identifier><identifier>DOI: 10.1016/S0165-4608(99)00060-6</identifier><identifier>PMID: 10549263</identifier><identifier>CODEN: CGCYDF</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Acute Disease ; Adult ; Antigens, CD7 - analysis ; Biological and medical sciences ; Chromosomes, Human, Pair 12 - genetics ; Chromosomes, Human, Pair 2 - genetics ; Chromosomes, Human, Pair 4 - genetics ; DNA-Binding Proteins - genetics ; ETS Translocation Variant 6 Protein ; Genetic Variation - genetics ; Hematologic and hematopoietic diseases ; Humans ; In Situ Hybridization, Fluorescence ; Karyotyping ; Leukemia, Myeloid - genetics ; Leukemia, Myeloid - immunology ; Leukemia, Myeloid - pathology ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Male ; Medical sciences ; Proto-Oncogene Proteins c-ets ; Repressor Proteins ; Transcription Factors - genetics ; Translocation, Genetic - genetics</subject><ispartof>Cancer genetics and cytogenetics, 1999-10, Vol.114 (2), p.96-99</ispartof><rights>1999 Elsevier Science Inc.</rights><rights>1999 INIST-CNRS</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1994873$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10549263$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hamaguchi, Hiroyuki</creatorcontrib><creatorcontrib>Nagata, Kaoru</creatorcontrib><creatorcontrib>Yamamoto, Katsuya</creatorcontrib><creatorcontrib>Kobayashi, Masaru</creatorcontrib><creatorcontrib>Takashima, Teruyuki</creatorcontrib><creatorcontrib>Taniwaki, Masafumi</creatorcontrib><title>A New Translocation, t(2;4;12)(p21;q12;p13), in CD7-Positive Acute Myeloid Leukemia: A Variant Form of t(4;12)</title><title>Cancer genetics and cytogenetics</title><addtitle>Cancer Genet Cytogenet</addtitle><description>We describe a 41-year-old man with CD7-positive acute myeloid leukemia (AML-M0) with trilineage-myelodysplasia. Chromosome analysis of the bone marrow cells showed 46,XY,t(2;4;12)(p21;q12;p13). Cytological and clinical features of our case were quite similar to those of AML with t(4;12)(q11∼12;p13). The karyotypic interpretation was confirmed by fluorescence in situ hybridization (FISH) by using the whole-chromosome painting probes specific for chromosomes 2, 4, and 12. FISH analysis with the use of the YAC 936e2 probe, which covers the
TEL gene, did not show the split signal, suggesting that a gene other than
TEL was involved in the leukemogenesis of the present case. Our case with AML with t(2;4;12)(p21;q12;p13) appears to be the first case of a variant type of AML with t(4;12)(q11∼12;p13).</description><subject>Acute Disease</subject><subject>Adult</subject><subject>Antigens, CD7 - analysis</subject><subject>Biological and medical sciences</subject><subject>Chromosomes, Human, Pair 12 - genetics</subject><subject>Chromosomes, Human, Pair 2 - genetics</subject><subject>Chromosomes, Human, Pair 4 - genetics</subject><subject>DNA-Binding Proteins - genetics</subject><subject>ETS Translocation Variant 6 Protein</subject><subject>Genetic Variation - genetics</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>In Situ Hybridization, Fluorescence</subject><subject>Karyotyping</subject><subject>Leukemia, Myeloid - genetics</subject><subject>Leukemia, Myeloid - immunology</subject><subject>Leukemia, Myeloid - pathology</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Proto-Oncogene Proteins c-ets</subject><subject>Repressor Proteins</subject><subject>Transcription Factors - genetics</subject><subject>Translocation, Genetic - genetics</subject><issn>0165-4608</issn><issn>1873-4456</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><recordid>eNpFkctOwzAQRS0EoqXwCSAvWLRSA7aTODFZoKhQQCoPicLWcpyJZMiLJC3q3-M-gM3M5uho7lyETim5oITyy1c7fMfjJBwKMSKEcOLwPdSnYeA6nufzfdT_Q3roqG0_LBQwwQ9RjxLfE4y7fVTG-Am-8bxRZZtXWnWmKse4G7LIiygbDWtGoy_Kopq6ozE2JZ7cBM5L1ZrOLAHHetEBflxBXpkUz2DxCYVRVzjG76oxquzwtGoKXGXWuPEdo4NM5S2c7PYAvU1v55N7Z_Z89zCJZw4wwTrH1TwMOQiRsIDqJEggoVz7KlVCp0kIhFHKPSJCn_CQK-KRTCnXV1kW6DDQwh2gs623XiQFpLJuTKGalfwNboHzHaBarfLM5tem_eeE8OwjLXa9xcAeuzTQyFYbKDWkpgHdybQy1inXjchNI3L9bimE3DQiufsDi5t3Pw</recordid><startdate>19991015</startdate><enddate>19991015</enddate><creator>Hamaguchi, Hiroyuki</creator><creator>Nagata, Kaoru</creator><creator>Yamamoto, Katsuya</creator><creator>Kobayashi, Masaru</creator><creator>Takashima, Teruyuki</creator><creator>Taniwaki, Masafumi</creator><general>Elsevier Inc</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>19991015</creationdate><title>A New Translocation, t(2;4;12)(p21;q12;p13), in CD7-Positive Acute Myeloid Leukemia: A Variant Form of t(4;12)</title><author>Hamaguchi, Hiroyuki ; Nagata, Kaoru ; Yamamoto, Katsuya ; Kobayashi, Masaru ; Takashima, Teruyuki ; Taniwaki, Masafumi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-e292t-3c6886e99b271cb7beb16c5ada9cdb8e02116409850686a040faa35aff7c87c93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Acute Disease</topic><topic>Adult</topic><topic>Antigens, CD7 - analysis</topic><topic>Biological and medical sciences</topic><topic>Chromosomes, Human, Pair 12 - genetics</topic><topic>Chromosomes, Human, Pair 2 - genetics</topic><topic>Chromosomes, Human, Pair 4 - genetics</topic><topic>DNA-Binding Proteins - genetics</topic><topic>ETS Translocation Variant 6 Protein</topic><topic>Genetic Variation - genetics</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>In Situ Hybridization, Fluorescence</topic><topic>Karyotyping</topic><topic>Leukemia, Myeloid - genetics</topic><topic>Leukemia, Myeloid - immunology</topic><topic>Leukemia, Myeloid - pathology</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Proto-Oncogene Proteins c-ets</topic><topic>Repressor Proteins</topic><topic>Transcription Factors - genetics</topic><topic>Translocation, Genetic - genetics</topic><toplevel>online_resources</toplevel><creatorcontrib>Hamaguchi, Hiroyuki</creatorcontrib><creatorcontrib>Nagata, Kaoru</creatorcontrib><creatorcontrib>Yamamoto, Katsuya</creatorcontrib><creatorcontrib>Kobayashi, Masaru</creatorcontrib><creatorcontrib>Takashima, Teruyuki</creatorcontrib><creatorcontrib>Taniwaki, Masafumi</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Cancer genetics and cytogenetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hamaguchi, Hiroyuki</au><au>Nagata, Kaoru</au><au>Yamamoto, Katsuya</au><au>Kobayashi, Masaru</au><au>Takashima, Teruyuki</au><au>Taniwaki, Masafumi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A New Translocation, t(2;4;12)(p21;q12;p13), in CD7-Positive Acute Myeloid Leukemia: A Variant Form of t(4;12)</atitle><jtitle>Cancer genetics and cytogenetics</jtitle><addtitle>Cancer Genet Cytogenet</addtitle><date>1999-10-15</date><risdate>1999</risdate><volume>114</volume><issue>2</issue><spage>96</spage><epage>99</epage><pages>96-99</pages><issn>0165-4608</issn><eissn>1873-4456</eissn><coden>CGCYDF</coden><abstract>We describe a 41-year-old man with CD7-positive acute myeloid leukemia (AML-M0) with trilineage-myelodysplasia. Chromosome analysis of the bone marrow cells showed 46,XY,t(2;4;12)(p21;q12;p13). Cytological and clinical features of our case were quite similar to those of AML with t(4;12)(q11∼12;p13). The karyotypic interpretation was confirmed by fluorescence in situ hybridization (FISH) by using the whole-chromosome painting probes specific for chromosomes 2, 4, and 12. FISH analysis with the use of the YAC 936e2 probe, which covers the
TEL gene, did not show the split signal, suggesting that a gene other than
TEL was involved in the leukemogenesis of the present case. Our case with AML with t(2;4;12)(p21;q12;p13) appears to be the first case of a variant type of AML with t(4;12)(q11∼12;p13).</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>10549263</pmid><doi>10.1016/S0165-4608(99)00060-6</doi><tpages>4</tpages></addata></record> |
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subjects | Acute Disease Adult Antigens, CD7 - analysis Biological and medical sciences Chromosomes, Human, Pair 12 - genetics Chromosomes, Human, Pair 2 - genetics Chromosomes, Human, Pair 4 - genetics DNA-Binding Proteins - genetics ETS Translocation Variant 6 Protein Genetic Variation - genetics Hematologic and hematopoietic diseases Humans In Situ Hybridization, Fluorescence Karyotyping Leukemia, Myeloid - genetics Leukemia, Myeloid - immunology Leukemia, Myeloid - pathology Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Male Medical sciences Proto-Oncogene Proteins c-ets Repressor Proteins Transcription Factors - genetics Translocation, Genetic - genetics |
title | A New Translocation, t(2;4;12)(p21;q12;p13), in CD7-Positive Acute Myeloid Leukemia: A Variant Form of t(4;12) |
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