Correlations between the clinical course, characteristics of blast cells, and karyotype patterns in chronic myeloid leukemia
Results of chromosome studies of blood and bone marrow cells from 101 patients with Ph1 positive chronic myeloid leukemia (CML) confirm the assumptions that clinical and morphologic manifestations of the disease correlate with karyotype peculiarities of leukemia cells. Several variants of the clinic...
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Veröffentlicht in: | Human genetics 1981-01, Vol.58 (3), p.285-293 |
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creator | Fleischman, E W Prigogina, E L Volkova, M A Frenkel, M A Zakhartchenko, N A Konstantinova, L N Puchkova, G P Balakirev, S A |
description | Results of chromosome studies of blood and bone marrow cells from 101 patients with Ph1 positive chronic myeloid leukemia (CML) confirm the assumptions that clinical and morphologic manifestations of the disease correlate with karyotype peculiarities of leukemia cells. Several variants of the clinical course of CML may be distinguished. One is the variant with a short chronic phase and a comparatively long terminal phase. In blastic crisis the blast cells are peroxidase negative and do not possess cytoplasmic inclusions. Acute transformation occurs without any additional chromosome damage. The second, more common form is less severe because of longer chronic phase but it has a short and grave acute stage. The blast cells present definite signs of myeloid differentiation, they have basophilic or neutrophilic cytoplasmic granules and are peroxidase positive. Marker i(17q) often combined with trisomy 8 is a characteristic chromosome abnormality in the terminal stage of this variant. The third type has an extremely long chronic phase but ends in a rapidly progressing severe and resistant to therapy "lymphoid" blastic crisis. Blast cells have typical "lymphoid" morphology, they are peroxidase negative and contain granular PAS positive substance. Various additional chromosome changes appear in the terminal stage. Future studies of a larger series of patients may possibly reveal more CML variants. |
doi_str_mv | 10.1007/BF00294925 |
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Several variants of the clinical course of CML may be distinguished. One is the variant with a short chronic phase and a comparatively long terminal phase. In blastic crisis the blast cells are peroxidase negative and do not possess cytoplasmic inclusions. Acute transformation occurs without any additional chromosome damage. The second, more common form is less severe because of longer chronic phase but it has a short and grave acute stage. The blast cells present definite signs of myeloid differentiation, they have basophilic or neutrophilic cytoplasmic granules and are peroxidase positive. Marker i(17q) often combined with trisomy 8 is a characteristic chromosome abnormality in the terminal stage of this variant. The third type has an extremely long chronic phase but ends in a rapidly progressing severe and resistant to therapy "lymphoid" blastic crisis. Blast cells have typical "lymphoid" morphology, they are peroxidase negative and contain granular PAS positive substance. Various additional chromosome changes appear in the terminal stage. 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Several variants of the clinical course of CML may be distinguished. One is the variant with a short chronic phase and a comparatively long terminal phase. In blastic crisis the blast cells are peroxidase negative and do not possess cytoplasmic inclusions. Acute transformation occurs without any additional chromosome damage. The second, more common form is less severe because of longer chronic phase but it has a short and grave acute stage. The blast cells present definite signs of myeloid differentiation, they have basophilic or neutrophilic cytoplasmic granules and are peroxidase positive. Marker i(17q) often combined with trisomy 8 is a characteristic chromosome abnormality in the terminal stage of this variant. The third type has an extremely long chronic phase but ends in a rapidly progressing severe and resistant to therapy "lymphoid" blastic crisis. Blast cells have typical "lymphoid" morphology, they are peroxidase negative and contain granular PAS positive substance. Various additional chromosome changes appear in the terminal stage. Future studies of a larger series of patients may possibly reveal more CML variants.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Bone Marrow - ultrastructure</subject><subject>Cells, Cultured</subject><subject>Child</subject><subject>Chromosomes, Human - ultrastructure</subject><subject>Chromosomes, Human, 21-22 and Y - ultrastructure</subject><subject>Genetic Variation</subject><subject>Humans</subject><subject>Karyotyping</subject><subject>Leukemia, Myeloid - genetics</subject><subject>Lymphocytes - ultrastructure</subject><subject>Phenotype</subject><subject>Time Factors</subject><issn>0340-6717</issn><issn>1432-1203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1981</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE1LAzEQhoMotVYv3oWcPIir-ehuNkctfkHBi56XbDJLY7ObmmSRgj_eSIueBobnfZh5ETqn5IYSIm7vHwlhci5ZeYCmdM5ZQRnhh2hK-JwUlaDiGJ3E-EEILTM0QZNKzmtRlVP0vfAhgFPJ-iHiFtIXwIDTCrB2drBaOaz9GCJcY71SQekEwcZkdcS-w61TMWENzsVrrAaD1ypsfdpuAG9Uymh22iEng88u3G_BeWuwg3ENvVWn6KhTLsLZfs7Q--PD2-K5WL4-vSzuloVmNUuFbrmRpWjbSkjT8croDqgxZcekEiXnrWSVpAyM4nkDulS6y6iuask0pZrP0OXOuwn-c4SYmt7G36vVAH6MjeB1XQnOMni1A3XwMQbomk2wff6poaT5rbr5rzrDF3vr2PZg_tB9t_wHyzd75w</recordid><startdate>19810101</startdate><enddate>19810101</enddate><creator>Fleischman, E W</creator><creator>Prigogina, E L</creator><creator>Volkova, M A</creator><creator>Frenkel, M A</creator><creator>Zakhartchenko, N A</creator><creator>Konstantinova, L N</creator><creator>Puchkova, G P</creator><creator>Balakirev, S A</creator><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>19810101</creationdate><title>Correlations between the clinical course, characteristics of blast cells, and karyotype patterns in chronic myeloid leukemia</title><author>Fleischman, E W ; Prigogina, E L ; Volkova, M A ; Frenkel, M A ; Zakhartchenko, N A ; Konstantinova, L N ; Puchkova, G P ; Balakirev, S A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c282t-cb3d957bb679df36dcfe1dd5f29a7533b926912eda329aec5acf679c6892c11c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1981</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Bone Marrow - ultrastructure</topic><topic>Cells, Cultured</topic><topic>Child</topic><topic>Chromosomes, Human - ultrastructure</topic><topic>Chromosomes, Human, 21-22 and Y - ultrastructure</topic><topic>Genetic Variation</topic><topic>Humans</topic><topic>Karyotyping</topic><topic>Leukemia, Myeloid - genetics</topic><topic>Lymphocytes - ultrastructure</topic><topic>Phenotype</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fleischman, E W</creatorcontrib><creatorcontrib>Prigogina, E L</creatorcontrib><creatorcontrib>Volkova, M A</creatorcontrib><creatorcontrib>Frenkel, M A</creatorcontrib><creatorcontrib>Zakhartchenko, N A</creatorcontrib><creatorcontrib>Konstantinova, L N</creatorcontrib><creatorcontrib>Puchkova, G P</creatorcontrib><creatorcontrib>Balakirev, S A</creatorcontrib><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>Human genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fleischman, E W</au><au>Prigogina, E L</au><au>Volkova, M A</au><au>Frenkel, M A</au><au>Zakhartchenko, N A</au><au>Konstantinova, L N</au><au>Puchkova, G P</au><au>Balakirev, S A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Correlations between the clinical course, characteristics of blast cells, and karyotype patterns in chronic myeloid leukemia</atitle><jtitle>Human genetics</jtitle><addtitle>Hum Genet</addtitle><date>1981-01-01</date><risdate>1981</risdate><volume>58</volume><issue>3</issue><spage>285</spage><epage>293</epage><pages>285-293</pages><issn>0340-6717</issn><eissn>1432-1203</eissn><abstract>Results of chromosome studies of blood and bone marrow cells from 101 patients with Ph1 positive chronic myeloid leukemia (CML) confirm the assumptions that clinical and morphologic manifestations of the disease correlate with karyotype peculiarities of leukemia cells. Several variants of the clinical course of CML may be distinguished. One is the variant with a short chronic phase and a comparatively long terminal phase. In blastic crisis the blast cells are peroxidase negative and do not possess cytoplasmic inclusions. Acute transformation occurs without any additional chromosome damage. The second, more common form is less severe because of longer chronic phase but it has a short and grave acute stage. The blast cells present definite signs of myeloid differentiation, they have basophilic or neutrophilic cytoplasmic granules and are peroxidase positive. Marker i(17q) often combined with trisomy 8 is a characteristic chromosome abnormality in the terminal stage of this variant. The third type has an extremely long chronic phase but ends in a rapidly progressing severe and resistant to therapy "lymphoid" blastic crisis. Blast cells have typical "lymphoid" morphology, they are peroxidase negative and contain granular PAS positive substance. Various additional chromosome changes appear in the terminal stage. Future studies of a larger series of patients may possibly reveal more CML variants.</abstract><cop>Germany</cop><pmid>6948765</pmid><doi>10.1007/BF00294925</doi><tpages>9</tpages></addata></record> |
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subjects | Adolescent Adult Bone Marrow - ultrastructure Cells, Cultured Child Chromosomes, Human - ultrastructure Chromosomes, Human, 21-22 and Y - ultrastructure Genetic Variation Humans Karyotyping Leukemia, Myeloid - genetics Lymphocytes - ultrastructure Phenotype Time Factors |
title | Correlations between the clinical course, characteristics of blast cells, and karyotype patterns in chronic myeloid leukemia |
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