Relationship of T leukaemias with cerebriform nuclei to T‐prolymphocytic leukaemia: a cytogenetic analysis with in situ hybridization
Sezary cell leukaemia (SCL) is a mature T‐cell leukaemia with characteristic cerebriform nuclei, whereas Sezary syndrome (SS) involves a mature T‐cell lymphoma with a similar nuclear morphology. We have examined these diseases by cytogenetics, chromosome painting and fluorescence in situ hybridizati...
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| Veröffentlicht in: | British journal of haematology 1997-03, Vol.96 (4), p.724-732 |
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| container_title | British journal of haematology |
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| creator | BRITO‐BABAPULLE, VASANTHA HODA MALJAIE, S. MATUTES, ESTELLA HEDGES, MICHAEL YUILLE, MARTIN CATOVSKY, DANIEL |
| description | Sezary cell leukaemia (SCL) is a mature T‐cell leukaemia with characteristic cerebriform nuclei, whereas Sezary syndrome (SS) involves a mature T‐cell lymphoma with a similar nuclear morphology. We have examined these diseases by cytogenetics, chromosome painting and fluorescence in situ hybridization (FISH). Both diseases had complex cytogenetic abnormalities. All three cases of SCL investigated had inv(14)(q11;q32) and two had iso(8q). No case of SS had these abnormalities but, instead, iso(17q) or 17p+ was present in the three cases of SS investigated and FISH indicated loss of heterozygosity due to deletion of a region at 17p13 that included the tumour suppressor gene P53, implicating it in this malignancy. One case of SCL had iso(17q). The abnormalities of chromosomes 8 and 14 in SCL are commonly observed in T‐prolymphocytic leukaemia (T‐PLL) and suggest that SCL may be a variant of T‐PLL rather than of SS. |
| doi_str_mv | 10.1046/j.1365-2141.1997.9702605.x |
| format | Article |
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We have examined these diseases by cytogenetics, chromosome painting and fluorescence in situ hybridization (FISH). Both diseases had complex cytogenetic abnormalities. All three cases of SCL investigated had inv(14)(q11;q32) and two had iso(8q). No case of SS had these abnormalities but, instead, iso(17q) or 17p+ was present in the three cases of SS investigated and FISH indicated loss of heterozygosity due to deletion of a region at 17p13 that included the tumour suppressor gene P53, implicating it in this malignancy. One case of SCL had iso(17q). The abnormalities of chromosomes 8 and 14 in SCL are commonly observed in T‐prolymphocytic leukaemia (T‐PLL) and suggest that SCL may be a variant of T‐PLL rather than of SS.</description><identifier>ISSN: 0007-1048</identifier><identifier>EISSN: 1365-2141</identifier><identifier>DOI: 10.1046/j.1365-2141.1997.9702605.x</identifier><identifier>PMID: 9074412</identifier><identifier>CODEN: BJHEAL</identifier><language>eng</language><publisher>Oxford, U.K. and Cambridge, USA: Blackwell Science Ltd</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Biological and medical sciences ; cerebriform cells ; Chromosome Aberrations ; Chromosomes, Human, Pair 14 ; Chromosomes, Human, Pair 18 ; Chromosomes, Human, Pair 8 ; Female ; FISH ; Hematologic and hematopoietic diseases ; Humans ; In Situ Hybridization, Fluorescence ; Karyotyping ; Leukemia, Prolymphocytic - genetics ; Leukemia, Prolymphocytic - pathology ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Male ; Medical sciences ; Middle Aged ; paints ; Sezary Syndrome - genetics ; Sezary Syndrome - pathology ; Skin Neoplasms - genetics ; Skin Neoplasms - pathology ; Translocation, Genetic ; tumour suppressor genes ; T‐PLL</subject><ispartof>British journal of haematology, 1997-03, Vol.96 (4), p.724-732</ispartof><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4790-d32fb7e6cf6cca5a93f6d5d37bfee411345ac3692a8dba88378ac8f0776b1ebf3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1365-2141.1997.9702605.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1365-2141.1997.9702605.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27903,27904,45553,45554,46388,46812</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2590796$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9074412$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>BRITO‐BABAPULLE, VASANTHA</creatorcontrib><creatorcontrib>HODA MALJAIE, S.</creatorcontrib><creatorcontrib>MATUTES, ESTELLA</creatorcontrib><creatorcontrib>HEDGES, MICHAEL</creatorcontrib><creatorcontrib>YUILLE, MARTIN</creatorcontrib><creatorcontrib>CATOVSKY, DANIEL</creatorcontrib><title>Relationship of T leukaemias with cerebriform nuclei to T‐prolymphocytic leukaemia: a cytogenetic analysis with in situ hybridization</title><title>British journal of haematology</title><addtitle>Br J Haematol</addtitle><description>Sezary cell leukaemia (SCL) is a mature T‐cell leukaemia with characteristic cerebriform nuclei, whereas Sezary syndrome (SS) involves a mature T‐cell lymphoma with a similar nuclear morphology. We have examined these diseases by cytogenetics, chromosome painting and fluorescence in situ hybridization (FISH). Both diseases had complex cytogenetic abnormalities. All three cases of SCL investigated had inv(14)(q11;q32) and two had iso(8q). No case of SS had these abnormalities but, instead, iso(17q) or 17p+ was present in the three cases of SS investigated and FISH indicated loss of heterozygosity due to deletion of a region at 17p13 that included the tumour suppressor gene P53, implicating it in this malignancy. One case of SCL had iso(17q). The abnormalities of chromosomes 8 and 14 in SCL are commonly observed in T‐prolymphocytic leukaemia (T‐PLL) and suggest that SCL may be a variant of T‐PLL rather than of SS.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>cerebriform cells</subject><subject>Chromosome Aberrations</subject><subject>Chromosomes, Human, Pair 14</subject><subject>Chromosomes, Human, Pair 18</subject><subject>Chromosomes, Human, Pair 8</subject><subject>Female</subject><subject>FISH</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>In Situ Hybridization, Fluorescence</subject><subject>Karyotyping</subject><subject>Leukemia, Prolymphocytic - genetics</subject><subject>Leukemia, Prolymphocytic - pathology</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>paints</subject><subject>Sezary Syndrome - genetics</subject><subject>Sezary Syndrome - pathology</subject><subject>Skin Neoplasms - genetics</subject><subject>Skin Neoplasms - pathology</subject><subject>Translocation, Genetic</subject><subject>tumour suppressor genes</subject><subject>T‐PLL</subject><issn>0007-1048</issn><issn>1365-2141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVUU2L1TAUDaKMz9GfIAQRd61J0zbpLIRxUEcZEOS5Dml648szbZ5Jy0xduXPrb_SXmPrKc-0q3JyPezkHoWeU5JSU9ct9TlldZQUtaU6bhucNJ0VNqvzuHtqcoPtoQwjhWZKIh-hRjHtCKCMVPUNnDeFlSYsN-vkJnBqtH-LOHrA3eIsdTF8V9FZFfGvHHdYQoA3W-NDjYdIOLB493v7-8esQvJv7w87rebT6n_ACK5y-_BcYYAHUoNwc7epnBxztOOHdnFw7-_3v-sfogVEuwpP1PUef377ZXl1nNx_fvb-6vMl0yRuSdawwLYdam1prVamGmbqrOsZbA1BSyspKaVY3hRJdq4RgXCgtDOG8bim0hp2jF0ffdPu3CeIoexs1OKcG8FOUXAhREc4S8eJI1MHHGMDIQ7C9CrOkRC4tyL1copZL1HJpQa4tyLskfrpumdoeupN0jT3hz1dcRa2cCWrQNp5oRZWITZ1or460W-tg_o8D5OsP12lgfwBBg6hH</recordid><startdate>199703</startdate><enddate>199703</enddate><creator>BRITO‐BABAPULLE, VASANTHA</creator><creator>HODA MALJAIE, S.</creator><creator>MATUTES, ESTELLA</creator><creator>HEDGES, MICHAEL</creator><creator>YUILLE, MARTIN</creator><creator>CATOVSKY, DANIEL</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>199703</creationdate><title>Relationship of T leukaemias with cerebriform nuclei to T‐prolymphocytic leukaemia: a cytogenetic analysis with in situ hybridization</title><author>BRITO‐BABAPULLE, VASANTHA ; HODA MALJAIE, S. ; MATUTES, ESTELLA ; HEDGES, MICHAEL ; YUILLE, MARTIN ; CATOVSKY, DANIEL</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4790-d32fb7e6cf6cca5a93f6d5d37bfee411345ac3692a8dba88378ac8f0776b1ebf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biological and medical sciences</topic><topic>cerebriform cells</topic><topic>Chromosome Aberrations</topic><topic>Chromosomes, Human, Pair 14</topic><topic>Chromosomes, Human, Pair 18</topic><topic>Chromosomes, Human, Pair 8</topic><topic>Female</topic><topic>FISH</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>In Situ Hybridization, Fluorescence</topic><topic>Karyotyping</topic><topic>Leukemia, Prolymphocytic - genetics</topic><topic>Leukemia, Prolymphocytic - pathology</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>paints</topic><topic>Sezary Syndrome - genetics</topic><topic>Sezary Syndrome - pathology</topic><topic>Skin Neoplasms - genetics</topic><topic>Skin Neoplasms - pathology</topic><topic>Translocation, Genetic</topic><topic>tumour suppressor genes</topic><topic>T‐PLL</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>BRITO‐BABAPULLE, VASANTHA</creatorcontrib><creatorcontrib>HODA MALJAIE, S.</creatorcontrib><creatorcontrib>MATUTES, ESTELLA</creatorcontrib><creatorcontrib>HEDGES, MICHAEL</creatorcontrib><creatorcontrib>YUILLE, MARTIN</creatorcontrib><creatorcontrib>CATOVSKY, DANIEL</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>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>British journal of haematology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>BRITO‐BABAPULLE, VASANTHA</au><au>HODA MALJAIE, S.</au><au>MATUTES, ESTELLA</au><au>HEDGES, MICHAEL</au><au>YUILLE, MARTIN</au><au>CATOVSKY, DANIEL</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Relationship of T leukaemias with cerebriform nuclei to T‐prolymphocytic leukaemia: a cytogenetic analysis with in situ hybridization</atitle><jtitle>British journal of haematology</jtitle><addtitle>Br J Haematol</addtitle><date>1997-03</date><risdate>1997</risdate><volume>96</volume><issue>4</issue><spage>724</spage><epage>732</epage><pages>724-732</pages><issn>0007-1048</issn><eissn>1365-2141</eissn><coden>BJHEAL</coden><abstract>Sezary cell leukaemia (SCL) is a mature T‐cell leukaemia with characteristic cerebriform nuclei, whereas Sezary syndrome (SS) involves a mature T‐cell lymphoma with a similar nuclear morphology. We have examined these diseases by cytogenetics, chromosome painting and fluorescence in situ hybridization (FISH). Both diseases had complex cytogenetic abnormalities. All three cases of SCL investigated had inv(14)(q11;q32) and two had iso(8q). No case of SS had these abnormalities but, instead, iso(17q) or 17p+ was present in the three cases of SS investigated and FISH indicated loss of heterozygosity due to deletion of a region at 17p13 that included the tumour suppressor gene P53, implicating it in this malignancy. One case of SCL had iso(17q). The abnormalities of chromosomes 8 and 14 in SCL are commonly observed in T‐prolymphocytic leukaemia (T‐PLL) and suggest that SCL may be a variant of T‐PLL rather than of SS.</abstract><cop>Oxford, U.K. and Cambridge, USA</cop><pub>Blackwell Science Ltd</pub><pmid>9074412</pmid><doi>10.1046/j.1365-2141.1997.9702605.x</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Aged, 80 and over Biological and medical sciences cerebriform cells Chromosome Aberrations Chromosomes, Human, Pair 14 Chromosomes, Human, Pair 18 Chromosomes, Human, Pair 8 Female FISH Hematologic and hematopoietic diseases Humans In Situ Hybridization, Fluorescence Karyotyping Leukemia, Prolymphocytic - genetics Leukemia, Prolymphocytic - pathology Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Male Medical sciences Middle Aged paints Sezary Syndrome - genetics Sezary Syndrome - pathology Skin Neoplasms - genetics Skin Neoplasms - pathology Translocation, Genetic tumour suppressor genes T‐PLL |
| title | Relationship of T leukaemias with cerebriform nuclei to T‐prolymphocytic leukaemia: a cytogenetic analysis with in situ hybridization |
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