Biologic Characteristics of Acute Leukemia After Myelodysplastic Syndrome
Ten patients with acute leukemia after primary myelodysplastic syndrome (MDS-AL) were examined to clarify the biologic nature of the leukemic cells in comparison with that of de novo acute myelocytic leukemia (AML). The morphologic and cytochemical features of the leukemic cells from all these patie...
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Veröffentlicht in: | Blood 1993-06, Vol.81 (12), p.3388-3394 |
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description | Ten patients with acute leukemia after primary myelodysplastic syndrome (MDS-AL) were examined to clarify the biologic nature of the leukemic cells in comparison with that of de novo acute myelocytic leukemia (AML). The morphologic and cytochemical features of the leukemic cells from all these patients corresponded well to those of de novo AML, and they were diagnosed with MDS-AML. Phenotypically, the frequent expression of the lymphocyte activation antigens, CD25 and CD30, was characteristic in MDS-AML. The in vitro response of MDS-AML cells to various growth factors was similar to that of de novo AML cells. Transforming growth factor β1 (TGFβ1) suppressed growth factor-dependent colony formation by normal bone marrow cells, MDS bone marrow cells, and de novo AML cells, but did not inhibit colony formation by MDS-AML cells. The number of TGFβ 1 high-affinity binding sites of MDS-AML samples (< 5 to 47 sites/cell) was markedly lower than that in de novo AML samples (120 to 221 sites/cell). Our results indicate that the reduced TGFβ1 may represent disregulation of the proliferation system in MDS-AML cells. This is thought to occur during the MDS phase, and may be related to the poorer response shown to conventional chemotherapy of AML. |
doi_str_mv | 10.1182/blood.V81.12.3388.3388 |
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The morphologic and cytochemical features of the leukemic cells from all these patients corresponded well to those of de novo AML, and they were diagnosed with MDS-AML. Phenotypically, the frequent expression of the lymphocyte activation antigens, CD25 and CD30, was characteristic in MDS-AML. The in vitro response of MDS-AML cells to various growth factors was similar to that of de novo AML cells. Transforming growth factor β1 (TGFβ1) suppressed growth factor-dependent colony formation by normal bone marrow cells, MDS bone marrow cells, and de novo AML cells, but did not inhibit colony formation by MDS-AML cells. The number of TGFβ 1 high-affinity binding sites of MDS-AML samples (< 5 to 47 sites/cell) was markedly lower than that in de novo AML samples (120 to 221 sites/cell). Our results indicate that the reduced TGFβ1 may represent disregulation of the proliferation system in MDS-AML cells. This is thought to occur during the MDS phase, and may be related to the poorer response shown to conventional chemotherapy of AML.</description><identifier>ISSN: 0006-4971</identifier><identifier>EISSN: 1528-0020</identifier><identifier>DOI: 10.1182/blood.V81.12.3388.3388</identifier><identifier>PMID: 7685204</identifier><language>eng</language><publisher>Washington, DC: Elsevier Inc</publisher><subject>Adult ; Aged ; Antigens, CD - analysis ; Antigens, Neoplasm - analysis ; Biological and medical sciences ; Female ; Genotype ; Granulocyte Colony-Stimulating Factor - pharmacology ; Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology ; Hematologic and hematopoietic diseases ; Humans ; Interleukin-3 - pharmacology ; Ki-1 Antigen ; Leukemia, Myeloid, Acute - immunology ; Leukemia, Myeloid, Acute - pathology ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Male ; Medical sciences ; Middle Aged ; Myelodysplastic Syndromes - immunology ; Myelodysplastic Syndromes - pathology ; Phenotype ; Receptors, Cell Surface - metabolism ; Receptors, Interleukin-2 - analysis ; Receptors, Transforming Growth Factor beta ; Transforming Growth Factor beta - metabolism ; Transforming Growth Factor beta - pharmacology</subject><ispartof>Blood, 1993-06, Vol.81 (12), p.3388-3394</ispartof><rights>1993 American Society of Hematology</rights><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c440t-85d06cbf594176d36744ae1c34ea30007f843414bec7de3ef9bcd25d6bfe8563</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=4821340$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7685204$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Masuya, Masahiro</creatorcontrib><creatorcontrib>Kita, Kenkichi</creatorcontrib><creatorcontrib>Shimizu, Noriko</creatorcontrib><creatorcontrib>Ohishi, Kohshi</creatorcontrib><creatorcontrib>Katayama, Naoyuki</creatorcontrib><creatorcontrib>Sekine, Takao</creatorcontrib><creatorcontrib>Otsuji, Akira</creatorcontrib><creatorcontrib>Miwa, Hiroshi</creatorcontrib><creatorcontrib>Shirakawa, Shigeru</creatorcontrib><title>Biologic Characteristics of Acute Leukemia After Myelodysplastic Syndrome</title><title>Blood</title><addtitle>Blood</addtitle><description>Ten patients with acute leukemia after primary myelodysplastic syndrome (MDS-AL) were examined to clarify the biologic nature of the leukemic cells in comparison with that of de novo acute myelocytic leukemia (AML). The morphologic and cytochemical features of the leukemic cells from all these patients corresponded well to those of de novo AML, and they were diagnosed with MDS-AML. Phenotypically, the frequent expression of the lymphocyte activation antigens, CD25 and CD30, was characteristic in MDS-AML. The in vitro response of MDS-AML cells to various growth factors was similar to that of de novo AML cells. Transforming growth factor β1 (TGFβ1) suppressed growth factor-dependent colony formation by normal bone marrow cells, MDS bone marrow cells, and de novo AML cells, but did not inhibit colony formation by MDS-AML cells. The number of TGFβ 1 high-affinity binding sites of MDS-AML samples (< 5 to 47 sites/cell) was markedly lower than that in de novo AML samples (120 to 221 sites/cell). Our results indicate that the reduced TGFβ1 may represent disregulation of the proliferation system in MDS-AML cells. This is thought to occur during the MDS phase, and may be related to the poorer response shown to conventional chemotherapy of AML.</description><subject>Adult</subject><subject>Aged</subject><subject>Antigens, CD - analysis</subject><subject>Antigens, Neoplasm - analysis</subject><subject>Biological and medical sciences</subject><subject>Female</subject><subject>Genotype</subject><subject>Granulocyte Colony-Stimulating Factor - pharmacology</subject><subject>Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Interleukin-3 - pharmacology</subject><subject>Ki-1 Antigen</subject><subject>Leukemia, Myeloid, Acute - immunology</subject><subject>Leukemia, Myeloid, Acute - pathology</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myelodysplastic Syndromes - immunology</subject><subject>Myelodysplastic Syndromes - pathology</subject><subject>Phenotype</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Receptors, Interleukin-2 - analysis</subject><subject>Receptors, Transforming Growth Factor beta</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>Transforming Growth Factor beta - pharmacology</subject><issn>0006-4971</issn><issn>1528-0020</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMlOwzAQhi0EKmV5BFAOiFuKtzjujVKxVCriAOJqOfYYDEld7ASpb0-6qFcuM4f_m0UfQpcEjwiR9KaqQ7Cjd0lGhI4Yk3JTDtCQFFTmGFN8iIYYY5HzcUmO0UlKXxgTzmgxQINSyIJiPkSzOx_q8OFNNv3UUZsWok-tNykLLpuYroVsDt03NF5nE9en2fMK6mBXaVnrNZi9rhY2hgbO0JHTdYLzXT9Fbw_3b9OnfP7yOJtO5rnhHLe5LCwWpnLFmJNSWCZKzjUQwzho1v9bOskZJ7wCU1pg4MaVsbSwonIgC8FO0fV27TKGnw5SqxqfDNS1XkDokiqLUoyZWINiC5oYUorg1DL6RseVIlitFaqNQtUrVISqtb1N6Qcvdhe6qgG7H9s56_OrXa6T0bWLemF82mNcUsI47rHbLQa9jF8PUSXjYWHA-gimVTb4_z75A4GBkRs</recordid><startdate>19930615</startdate><enddate>19930615</enddate><creator>Masuya, Masahiro</creator><creator>Kita, Kenkichi</creator><creator>Shimizu, Noriko</creator><creator>Ohishi, Kohshi</creator><creator>Katayama, Naoyuki</creator><creator>Sekine, Takao</creator><creator>Otsuji, Akira</creator><creator>Miwa, Hiroshi</creator><creator>Shirakawa, Shigeru</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>19930615</creationdate><title>Biologic Characteristics of Acute Leukemia After Myelodysplastic Syndrome</title><author>Masuya, Masahiro ; Kita, Kenkichi ; Shimizu, Noriko ; Ohishi, Kohshi ; Katayama, Naoyuki ; Sekine, Takao ; Otsuji, Akira ; Miwa, Hiroshi ; Shirakawa, Shigeru</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c440t-85d06cbf594176d36744ae1c34ea30007f843414bec7de3ef9bcd25d6bfe8563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Antigens, CD - analysis</topic><topic>Antigens, Neoplasm - analysis</topic><topic>Biological and medical sciences</topic><topic>Female</topic><topic>Genotype</topic><topic>Granulocyte Colony-Stimulating Factor - pharmacology</topic><topic>Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Interleukin-3 - pharmacology</topic><topic>Ki-1 Antigen</topic><topic>Leukemia, Myeloid, Acute - immunology</topic><topic>Leukemia, Myeloid, Acute - pathology</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Myelodysplastic Syndromes - immunology</topic><topic>Myelodysplastic Syndromes - pathology</topic><topic>Phenotype</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>Receptors, Interleukin-2 - analysis</topic><topic>Receptors, Transforming Growth Factor beta</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>Transforming Growth Factor beta - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Masuya, Masahiro</creatorcontrib><creatorcontrib>Kita, Kenkichi</creatorcontrib><creatorcontrib>Shimizu, Noriko</creatorcontrib><creatorcontrib>Ohishi, Kohshi</creatorcontrib><creatorcontrib>Katayama, Naoyuki</creatorcontrib><creatorcontrib>Sekine, Takao</creatorcontrib><creatorcontrib>Otsuji, Akira</creatorcontrib><creatorcontrib>Miwa, Hiroshi</creatorcontrib><creatorcontrib>Shirakawa, Shigeru</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>Masuya, Masahiro</au><au>Kita, Kenkichi</au><au>Shimizu, Noriko</au><au>Ohishi, Kohshi</au><au>Katayama, Naoyuki</au><au>Sekine, Takao</au><au>Otsuji, Akira</au><au>Miwa, Hiroshi</au><au>Shirakawa, Shigeru</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Biologic Characteristics of Acute Leukemia After Myelodysplastic Syndrome</atitle><jtitle>Blood</jtitle><addtitle>Blood</addtitle><date>1993-06-15</date><risdate>1993</risdate><volume>81</volume><issue>12</issue><spage>3388</spage><epage>3394</epage><pages>3388-3394</pages><issn>0006-4971</issn><eissn>1528-0020</eissn><abstract>Ten patients with acute leukemia after primary myelodysplastic syndrome (MDS-AL) were examined to clarify the biologic nature of the leukemic cells in comparison with that of de novo acute myelocytic leukemia (AML). The morphologic and cytochemical features of the leukemic cells from all these patients corresponded well to those of de novo AML, and they were diagnosed with MDS-AML. Phenotypically, the frequent expression of the lymphocyte activation antigens, CD25 and CD30, was characteristic in MDS-AML. The in vitro response of MDS-AML cells to various growth factors was similar to that of de novo AML cells. Transforming growth factor β1 (TGFβ1) suppressed growth factor-dependent colony formation by normal bone marrow cells, MDS bone marrow cells, and de novo AML cells, but did not inhibit colony formation by MDS-AML cells. The number of TGFβ 1 high-affinity binding sites of MDS-AML samples (< 5 to 47 sites/cell) was markedly lower than that in de novo AML samples (120 to 221 sites/cell). Our results indicate that the reduced TGFβ1 may represent disregulation of the proliferation system in MDS-AML cells. This is thought to occur during the MDS phase, and may be related to the poorer response shown to conventional chemotherapy of AML.</abstract><cop>Washington, DC</cop><pub>Elsevier Inc</pub><pmid>7685204</pmid><doi>10.1182/blood.V81.12.3388.3388</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Aged Antigens, CD - analysis Antigens, Neoplasm - analysis Biological and medical sciences Female Genotype Granulocyte Colony-Stimulating Factor - pharmacology Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology Hematologic and hematopoietic diseases Humans Interleukin-3 - pharmacology Ki-1 Antigen Leukemia, Myeloid, Acute - immunology Leukemia, Myeloid, Acute - pathology Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Male Medical sciences Middle Aged Myelodysplastic Syndromes - immunology Myelodysplastic Syndromes - pathology Phenotype Receptors, Cell Surface - metabolism Receptors, Interleukin-2 - analysis Receptors, Transforming Growth Factor beta Transforming Growth Factor beta - metabolism Transforming Growth Factor beta - pharmacology |
title | Biologic Characteristics of Acute Leukemia After Myelodysplastic Syndrome |
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