Clinical significance of phenotypic features of blasts in patients with myelodysplastic syndrome
Knowledge of the blast phenotype in myelodysplastic syndrome (MDS) would be valuable, as in other malignancies, but remains sparse. This is mainly because MDS blasts are a minor population in clinical samples, making analysis difficult. Thus, for this blast phenotype study, we prepared blast-rich sp...
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Veröffentlicht in: | Blood 2002-12, Vol.100 (12), p.3887-3896 |
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creator | Ogata, Kiyoyuki Nakamura, Kyoko Yokose, Norio Tamura, Hideto Tachibana, Mikiko Taniguchi, Osamu Iwakiri, Rika Hayashi, Tatsuyuki Sakamaki, Hisashi Murai, Yoshiro Tohyama, Kaoru Tomoyasu, Shigeru Nonaka, Yasunobu Mori, Mayumi Dan, Kazuo Yoshida, Yataro |
description | Knowledge of the blast phenotype in myelodysplastic syndrome (MDS) would be valuable, as in other malignancies, but remains sparse. This is mainly because MDS blasts are a minor population in clinical samples, making analysis difficult. Thus, for this blast phenotype study, we prepared blast-rich specimens (using a new density centrifugation reagent for harvesting blasts) from blood and marrow samples of 95 patients with various MDS subtypes and 21 patients with acute leukemia transformed from MDS (AL-MDS). Flow cytometry revealed that a high proportion of the enriched blast cells (EBCs) from almost all patients showed an immunophenotype of committed myeloid precursors (CD34+CD38+HLA-DR+CD13+CD33+), regardless of the disease subtype. The cytochemical reaction for myeloperoxidase was negative in 58% of the cases. Thus, the EBC phenotype is more immature in MDS than in de novo acute myeloid leukemia. MDS EBCs often coexpressed stem cell antigens and late-stage myeloid antigens asynchronously, but rarely expressed T- and B-lymphoid cell–specific antigens. Markers for myeloid cell maturation (CD10 and CD15) were more prevalent on EBCs from low-risk MDS (refractory anemia [RA] and RA with ringed sideroblasts), whereas markers for myeloid cell immaturity (CD7 and CD117) were more prevalent on EBCs from high-risk MDS (chronic myelomonocytic leukemia, RA with excess blasts [RAEB], and RAEB in transformation) and AL-MDS. A shift to a more immature phenotype of EBCs, accompanying disease progression, was also documented by sequential phenotyping of the same patients. Further, CD7 positivity of EBCs was an independent variable for a poor prognosis in MDS. These data represent new, valuable information regarding MDS. |
doi_str_mv | 10.1182/blood-2002-01-0222 |
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This is mainly because MDS blasts are a minor population in clinical samples, making analysis difficult. Thus, for this blast phenotype study, we prepared blast-rich specimens (using a new density centrifugation reagent for harvesting blasts) from blood and marrow samples of 95 patients with various MDS subtypes and 21 patients with acute leukemia transformed from MDS (AL-MDS). Flow cytometry revealed that a high proportion of the enriched blast cells (EBCs) from almost all patients showed an immunophenotype of committed myeloid precursors (CD34+CD38+HLA-DR+CD13+CD33+), regardless of the disease subtype. The cytochemical reaction for myeloperoxidase was negative in 58% of the cases. Thus, the EBC phenotype is more immature in MDS than in de novo acute myeloid leukemia. MDS EBCs often coexpressed stem cell antigens and late-stage myeloid antigens asynchronously, but rarely expressed T- and B-lymphoid cell–specific antigens. Markers for myeloid cell maturation (CD10 and CD15) were more prevalent on EBCs from low-risk MDS (refractory anemia [RA] and RA with ringed sideroblasts), whereas markers for myeloid cell immaturity (CD7 and CD117) were more prevalent on EBCs from high-risk MDS (chronic myelomonocytic leukemia, RA with excess blasts [RAEB], and RAEB in transformation) and AL-MDS. A shift to a more immature phenotype of EBCs, accompanying disease progression, was also documented by sequential phenotyping of the same patients. Further, CD7 positivity of EBCs was an independent variable for a poor prognosis in MDS. These data represent new, valuable information regarding MDS.</description><identifier>ISSN: 0006-4971</identifier><identifier>EISSN: 1528-0020</identifier><identifier>DOI: 10.1182/blood-2002-01-0222</identifier><identifier>PMID: 12393641</identifier><language>eng</language><publisher>Washington, DC: Elsevier Inc</publisher><subject>Acute Disease ; Aged ; Antigens, CD - analysis ; Biological and medical sciences ; Case-Control Studies ; Cell Separation - methods ; Centrifugation, Density Gradient - methods ; Disease Progression ; Female ; Flow Cytometry ; Hematologic and hematopoietic diseases ; Humans ; Immunophenotyping ; Leukemia - genetics ; Leukemia - pathology ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Male ; Medical sciences ; Metrizamide ; Middle Aged ; Myelodysplastic Syndromes - genetics ; Myelodysplastic Syndromes - pathology ; Phenotype ; Prognosis ; Survival Analysis</subject><ispartof>Blood, 2002-12, Vol.100 (12), p.3887-3896</ispartof><rights>2002 American Society of Hematology</rights><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c426t-af120852b349fc9ff7e4462fcc932a896af3fd13a1f141bfbacc5ec9cdeaff6d3</citedby></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=14365832$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12393641$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ogata, Kiyoyuki</creatorcontrib><creatorcontrib>Nakamura, Kyoko</creatorcontrib><creatorcontrib>Yokose, Norio</creatorcontrib><creatorcontrib>Tamura, Hideto</creatorcontrib><creatorcontrib>Tachibana, Mikiko</creatorcontrib><creatorcontrib>Taniguchi, Osamu</creatorcontrib><creatorcontrib>Iwakiri, Rika</creatorcontrib><creatorcontrib>Hayashi, Tatsuyuki</creatorcontrib><creatorcontrib>Sakamaki, Hisashi</creatorcontrib><creatorcontrib>Murai, Yoshiro</creatorcontrib><creatorcontrib>Tohyama, Kaoru</creatorcontrib><creatorcontrib>Tomoyasu, Shigeru</creatorcontrib><creatorcontrib>Nonaka, Yasunobu</creatorcontrib><creatorcontrib>Mori, Mayumi</creatorcontrib><creatorcontrib>Dan, Kazuo</creatorcontrib><creatorcontrib>Yoshida, Yataro</creatorcontrib><title>Clinical significance of phenotypic features of blasts in patients with myelodysplastic syndrome</title><title>Blood</title><addtitle>Blood</addtitle><description>Knowledge of the blast phenotype in myelodysplastic syndrome (MDS) would be valuable, as in other malignancies, but remains sparse. This is mainly because MDS blasts are a minor population in clinical samples, making analysis difficult. Thus, for this blast phenotype study, we prepared blast-rich specimens (using a new density centrifugation reagent for harvesting blasts) from blood and marrow samples of 95 patients with various MDS subtypes and 21 patients with acute leukemia transformed from MDS (AL-MDS). Flow cytometry revealed that a high proportion of the enriched blast cells (EBCs) from almost all patients showed an immunophenotype of committed myeloid precursors (CD34+CD38+HLA-DR+CD13+CD33+), regardless of the disease subtype. The cytochemical reaction for myeloperoxidase was negative in 58% of the cases. Thus, the EBC phenotype is more immature in MDS than in de novo acute myeloid leukemia. MDS EBCs often coexpressed stem cell antigens and late-stage myeloid antigens asynchronously, but rarely expressed T- and B-lymphoid cell–specific antigens. Markers for myeloid cell maturation (CD10 and CD15) were more prevalent on EBCs from low-risk MDS (refractory anemia [RA] and RA with ringed sideroblasts), whereas markers for myeloid cell immaturity (CD7 and CD117) were more prevalent on EBCs from high-risk MDS (chronic myelomonocytic leukemia, RA with excess blasts [RAEB], and RAEB in transformation) and AL-MDS. A shift to a more immature phenotype of EBCs, accompanying disease progression, was also documented by sequential phenotyping of the same patients. Further, CD7 positivity of EBCs was an independent variable for a poor prognosis in MDS. These data represent new, valuable information regarding MDS.</description><subject>Acute Disease</subject><subject>Aged</subject><subject>Antigens, CD - analysis</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>Cell Separation - methods</subject><subject>Centrifugation, Density Gradient - methods</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Immunophenotyping</subject><subject>Leukemia - genetics</subject><subject>Leukemia - pathology</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metrizamide</subject><subject>Middle Aged</subject><subject>Myelodysplastic Syndromes - genetics</subject><subject>Myelodysplastic Syndromes - pathology</subject><subject>Phenotype</subject><subject>Prognosis</subject><subject>Survival Analysis</subject><issn>0006-4971</issn><issn>1528-0020</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1r3DAQhkVpaTZp_0APxZfm5lQayV4bcilLviCQS3tWZWmmUbEtR_Im-N9Xzi7k1pOG0fO-DA9jXwS_EKKB710fgiuBcyi5KDkAvGMbUUFT5hV_zzac87pU7VacsNOU_nIulITqIzsRIFtZK7Fhv3e9H701fZH8n9FTHkeLRaBiesQxzMvkbUFo5n3EtK673qQ5FX4sJjN7HPP84ufHYliwD25J0_qfM2kZXQwDfmIfyPQJPx_fM_br-urn7ra8f7i52_24L62Cei4NCeBNBZ1ULdmWaItK1UDWthJM09aGJDkhjSChREedsbZC21qHhqh28oydH3qnGJ72mGY9-GSx782IYZ_0FupmW4HKIBxAG0NKEUlP0Q8mLlpwvXrVr1716lVzoVevOfT12L7vBnRvkaPIDHw7AiZlmxSzRp_eOCXrqpFr0eWBw-zi2WPUyWaLFp2PaGftgv_fHf8A5XuZOQ</recordid><startdate>20021201</startdate><enddate>20021201</enddate><creator>Ogata, Kiyoyuki</creator><creator>Nakamura, Kyoko</creator><creator>Yokose, Norio</creator><creator>Tamura, Hideto</creator><creator>Tachibana, Mikiko</creator><creator>Taniguchi, Osamu</creator><creator>Iwakiri, Rika</creator><creator>Hayashi, Tatsuyuki</creator><creator>Sakamaki, Hisashi</creator><creator>Murai, Yoshiro</creator><creator>Tohyama, Kaoru</creator><creator>Tomoyasu, Shigeru</creator><creator>Nonaka, Yasunobu</creator><creator>Mori, Mayumi</creator><creator>Dan, Kazuo</creator><creator>Yoshida, Yataro</creator><general>Elsevier Inc</general><general>The Americain Society of Hematology</general><scope>6I.</scope><scope>AAFTH</scope><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>20021201</creationdate><title>Clinical significance of phenotypic features of blasts in patients with myelodysplastic syndrome</title><author>Ogata, Kiyoyuki ; Nakamura, Kyoko ; Yokose, Norio ; Tamura, Hideto ; Tachibana, Mikiko ; Taniguchi, Osamu ; Iwakiri, Rika ; Hayashi, Tatsuyuki ; Sakamaki, Hisashi ; Murai, Yoshiro ; Tohyama, Kaoru ; Tomoyasu, Shigeru ; Nonaka, Yasunobu ; Mori, Mayumi ; Dan, Kazuo ; Yoshida, Yataro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c426t-af120852b349fc9ff7e4462fcc932a896af3fd13a1f141bfbacc5ec9cdeaff6d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Acute Disease</topic><topic>Aged</topic><topic>Antigens, CD - analysis</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>Cell Separation - methods</topic><topic>Centrifugation, Density Gradient - methods</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Flow Cytometry</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Immunophenotyping</topic><topic>Leukemia - genetics</topic><topic>Leukemia - pathology</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metrizamide</topic><topic>Middle Aged</topic><topic>Myelodysplastic Syndromes - genetics</topic><topic>Myelodysplastic Syndromes - pathology</topic><topic>Phenotype</topic><topic>Prognosis</topic><topic>Survival Analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ogata, Kiyoyuki</creatorcontrib><creatorcontrib>Nakamura, Kyoko</creatorcontrib><creatorcontrib>Yokose, Norio</creatorcontrib><creatorcontrib>Tamura, Hideto</creatorcontrib><creatorcontrib>Tachibana, Mikiko</creatorcontrib><creatorcontrib>Taniguchi, Osamu</creatorcontrib><creatorcontrib>Iwakiri, Rika</creatorcontrib><creatorcontrib>Hayashi, Tatsuyuki</creatorcontrib><creatorcontrib>Sakamaki, Hisashi</creatorcontrib><creatorcontrib>Murai, Yoshiro</creatorcontrib><creatorcontrib>Tohyama, Kaoru</creatorcontrib><creatorcontrib>Tomoyasu, Shigeru</creatorcontrib><creatorcontrib>Nonaka, Yasunobu</creatorcontrib><creatorcontrib>Mori, Mayumi</creatorcontrib><creatorcontrib>Dan, Kazuo</creatorcontrib><creatorcontrib>Yoshida, Yataro</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>Blood</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ogata, Kiyoyuki</au><au>Nakamura, Kyoko</au><au>Yokose, Norio</au><au>Tamura, Hideto</au><au>Tachibana, Mikiko</au><au>Taniguchi, Osamu</au><au>Iwakiri, Rika</au><au>Hayashi, Tatsuyuki</au><au>Sakamaki, Hisashi</au><au>Murai, Yoshiro</au><au>Tohyama, Kaoru</au><au>Tomoyasu, Shigeru</au><au>Nonaka, Yasunobu</au><au>Mori, Mayumi</au><au>Dan, Kazuo</au><au>Yoshida, Yataro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Clinical significance of phenotypic features of blasts in patients with myelodysplastic syndrome</atitle><jtitle>Blood</jtitle><addtitle>Blood</addtitle><date>2002-12-01</date><risdate>2002</risdate><volume>100</volume><issue>12</issue><spage>3887</spage><epage>3896</epage><pages>3887-3896</pages><issn>0006-4971</issn><eissn>1528-0020</eissn><abstract>Knowledge of the blast phenotype in myelodysplastic syndrome (MDS) would be valuable, as in other malignancies, but remains sparse. This is mainly because MDS blasts are a minor population in clinical samples, making analysis difficult. Thus, for this blast phenotype study, we prepared blast-rich specimens (using a new density centrifugation reagent for harvesting blasts) from blood and marrow samples of 95 patients with various MDS subtypes and 21 patients with acute leukemia transformed from MDS (AL-MDS). Flow cytometry revealed that a high proportion of the enriched blast cells (EBCs) from almost all patients showed an immunophenotype of committed myeloid precursors (CD34+CD38+HLA-DR+CD13+CD33+), regardless of the disease subtype. The cytochemical reaction for myeloperoxidase was negative in 58% of the cases. Thus, the EBC phenotype is more immature in MDS than in de novo acute myeloid leukemia. MDS EBCs often coexpressed stem cell antigens and late-stage myeloid antigens asynchronously, but rarely expressed T- and B-lymphoid cell–specific antigens. Markers for myeloid cell maturation (CD10 and CD15) were more prevalent on EBCs from low-risk MDS (refractory anemia [RA] and RA with ringed sideroblasts), whereas markers for myeloid cell immaturity (CD7 and CD117) were more prevalent on EBCs from high-risk MDS (chronic myelomonocytic leukemia, RA with excess blasts [RAEB], and RAEB in transformation) and AL-MDS. A shift to a more immature phenotype of EBCs, accompanying disease progression, was also documented by sequential phenotyping of the same patients. Further, CD7 positivity of EBCs was an independent variable for a poor prognosis in MDS. These data represent new, valuable information regarding MDS.</abstract><cop>Washington, DC</cop><pub>Elsevier Inc</pub><pmid>12393641</pmid><doi>10.1182/blood-2002-01-0222</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acute Disease Aged Antigens, CD - analysis Biological and medical sciences Case-Control Studies Cell Separation - methods Centrifugation, Density Gradient - methods Disease Progression Female Flow Cytometry Hematologic and hematopoietic diseases Humans Immunophenotyping Leukemia - genetics Leukemia - pathology Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Male Medical sciences Metrizamide Middle Aged Myelodysplastic Syndromes - genetics Myelodysplastic Syndromes - pathology Phenotype Prognosis Survival Analysis |
title | Clinical significance of phenotypic features of blasts in patients with myelodysplastic syndrome |
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