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
Hauptverfasser: Masuya, Masahiro, Kita, Kenkichi, Shimizu, Noriko, Ohishi, Kohshi, Katayama, Naoyuki, Sekine, Takao, Otsuji, Akira, Miwa, Hiroshi, Shirakawa, Shigeru
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container_end_page 3394
container_issue 12
container_start_page 3388
container_title Blood
container_volume 81
creator Masuya, Masahiro
Kita, Kenkichi
Shimizu, Noriko
Ohishi, Kohshi
Katayama, Naoyuki
Sekine, Takao
Otsuji, Akira
Miwa, Hiroshi
Shirakawa, Shigeru
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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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 (&lt; 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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