Biological characteristics of myelodysplastic syndrome patients who demonstrated high versus no intramedullary apoptosis
: Spontaneous intramedullary apoptosis was measured in bone marrow (BM) biopsies of 175 patients with myelodysplastic syndromes (MDS) using in situ end‐labeling (ISEL) of fragmented DNA. Two groups of high (n = 71) versus low (n = 43) levels of apoptosis were identified while 61 patients were ISEL‐...
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| Veröffentlicht in: | European journal of haematology 1999-02, Vol.62 (2), p.90-94 |
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| creator | Dar, Saleem Mundle, Suneel Andric, Tanja Qawi, Huma Shetty, Vilasini Reza, Samina Mativi, B. Yifwayimare Allampallam, Krishnan Ali, Ambereen Venugopal, Parameswaren Gezer, Sefer Broady-Robinson, LaTanya Cartlidge, John Showel, Margaret Hussaini, Seema Ragasa, Deborah Ali, Irfan Chaudhry, Ambreen Waggoner, Samina Lisak, Laurie Huang, Ray-Win Raza, Azra |
| description | : Spontaneous intramedullary apoptosis was measured in bone marrow (BM) biopsies of 175 patients with myelodysplastic syndromes (MDS) using in situ end‐labeling (ISEL) of fragmented DNA. Two groups of high (n = 71) versus low (n = 43) levels of apoptosis were identified while 61 patients were ISEL‐negative. Semiquantitative assessment of 3 cytokines, the number of macrophages and in vivo labeling indices (LI) were also determined from consecutive sections of the biopsy. Patients with high apoptosis levels tended to have a high LI (p = 0.013), more macrophages in their BM biopsies (p = 0.006) and higher tumor necrosis factor alpha (TNF‐α) levels (not significant) compared to patients with no apoptosis. In addition, low risk MDS patients had significantly lower rates of apoptosis (p = 0.047) and lower levels of TNF‐α (p = 0.055) compared to high‐risk MDS patients. We conclude that the genesis of cytopenias in MDS is of multifactorial origin and that cytokine‐associated apoptosis clearly identifies a distinct biological subgroup of patients who may benefit selectively by use of anti‐cytokine therapies. |
| doi_str_mv | 10.1111/j.1600-0609.1999.tb01727.x |
| format | Article |
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Yifwayimare ; Allampallam, Krishnan ; Ali, Ambereen ; Venugopal, Parameswaren ; Gezer, Sefer ; Broady-Robinson, LaTanya ; Cartlidge, John ; Showel, Margaret ; Hussaini, Seema ; Ragasa, Deborah ; Ali, Irfan ; Chaudhry, Ambreen ; Waggoner, Samina ; Lisak, Laurie ; Huang, Ray-Win ; Raza, Azra</creator><creatorcontrib>Dar, Saleem ; Mundle, Suneel ; Andric, Tanja ; Qawi, Huma ; Shetty, Vilasini ; Reza, Samina ; Mativi, B. Yifwayimare ; Allampallam, Krishnan ; Ali, Ambereen ; Venugopal, Parameswaren ; Gezer, Sefer ; Broady-Robinson, LaTanya ; Cartlidge, John ; Showel, Margaret ; Hussaini, Seema ; Ragasa, Deborah ; Ali, Irfan ; Chaudhry, Ambreen ; Waggoner, Samina ; Lisak, Laurie ; Huang, Ray-Win ; Raza, Azra</creatorcontrib><description>: Spontaneous intramedullary apoptosis was measured in bone marrow (BM) biopsies of 175 patients with myelodysplastic syndromes (MDS) using in situ end‐labeling (ISEL) of fragmented DNA. Two groups of high (n = 71) versus low (n = 43) levels of apoptosis were identified while 61 patients were ISEL‐negative. Semiquantitative assessment of 3 cytokines, the number of macrophages and in vivo labeling indices (LI) were also determined from consecutive sections of the biopsy. Patients with high apoptosis levels tended to have a high LI (p = 0.013), more macrophages in their BM biopsies (p = 0.006) and higher tumor necrosis factor alpha (TNF‐α) levels (not significant) compared to patients with no apoptosis. In addition, low risk MDS patients had significantly lower rates of apoptosis (p = 0.047) and lower levels of TNF‐α (p = 0.055) compared to high‐risk MDS patients. We conclude that the genesis of cytopenias in MDS is of multifactorial origin and that cytokine‐associated apoptosis clearly identifies a distinct biological subgroup of patients who may benefit selectively by use of anti‐cytokine therapies.</description><identifier>ISSN: 0902-4441</identifier><identifier>EISSN: 1600-0609</identifier><identifier>DOI: 10.1111/j.1600-0609.1999.tb01727.x</identifier><identifier>PMID: 10052711</identifier><identifier>CODEN: EJHAEC</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Aged ; Apoptosis ; Biological and medical sciences ; Biomarkers ; bone marrow ; Bone Marrow - pathology ; Female ; Hematologic and hematopoietic diseases ; human disease ; Humans ; in vivo ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; macrophage ; Male ; Medical sciences ; myelodysplastic syndromes (MDS) ; Myelodysplastic Syndromes - blood ; Myelodysplastic Syndromes - pathology ; Myelodysplastic Syndromes - physiopathology ; proliferation ; tumor necrosis factor (TNF-α) ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>European journal of haematology, 1999-02, Vol.62 (2), p.90-94</ispartof><rights>Munksgaard 1999</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4387-273611fd27c6ded316a257d9b6c27dbd22b6e5d00a93464d0814a3281d50bf4c3</citedby><cites>FETCH-LOGICAL-c4387-273611fd27c6ded316a257d9b6c27dbd22b6e5d00a93464d0814a3281d50bf4c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1600-0609.1999.tb01727.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1600-0609.1999.tb01727.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1652489$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10052711$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dar, Saleem</creatorcontrib><creatorcontrib>Mundle, Suneel</creatorcontrib><creatorcontrib>Andric, Tanja</creatorcontrib><creatorcontrib>Qawi, Huma</creatorcontrib><creatorcontrib>Shetty, Vilasini</creatorcontrib><creatorcontrib>Reza, Samina</creatorcontrib><creatorcontrib>Mativi, B. Yifwayimare</creatorcontrib><creatorcontrib>Allampallam, Krishnan</creatorcontrib><creatorcontrib>Ali, Ambereen</creatorcontrib><creatorcontrib>Venugopal, Parameswaren</creatorcontrib><creatorcontrib>Gezer, Sefer</creatorcontrib><creatorcontrib>Broady-Robinson, LaTanya</creatorcontrib><creatorcontrib>Cartlidge, John</creatorcontrib><creatorcontrib>Showel, Margaret</creatorcontrib><creatorcontrib>Hussaini, Seema</creatorcontrib><creatorcontrib>Ragasa, Deborah</creatorcontrib><creatorcontrib>Ali, Irfan</creatorcontrib><creatorcontrib>Chaudhry, Ambreen</creatorcontrib><creatorcontrib>Waggoner, Samina</creatorcontrib><creatorcontrib>Lisak, Laurie</creatorcontrib><creatorcontrib>Huang, Ray-Win</creatorcontrib><creatorcontrib>Raza, Azra</creatorcontrib><title>Biological characteristics of myelodysplastic syndrome patients who demonstrated high versus no intramedullary apoptosis</title><title>European journal of haematology</title><addtitle>Eur J Haematol</addtitle><description>: Spontaneous intramedullary apoptosis was measured in bone marrow (BM) biopsies of 175 patients with myelodysplastic syndromes (MDS) using in situ end‐labeling (ISEL) of fragmented DNA. Two groups of high (n = 71) versus low (n = 43) levels of apoptosis were identified while 61 patients were ISEL‐negative. Semiquantitative assessment of 3 cytokines, the number of macrophages and in vivo labeling indices (LI) were also determined from consecutive sections of the biopsy. Patients with high apoptosis levels tended to have a high LI (p = 0.013), more macrophages in their BM biopsies (p = 0.006) and higher tumor necrosis factor alpha (TNF‐α) levels (not significant) compared to patients with no apoptosis. In addition, low risk MDS patients had significantly lower rates of apoptosis (p = 0.047) and lower levels of TNF‐α (p = 0.055) compared to high‐risk MDS patients. We conclude that the genesis of cytopenias in MDS is of multifactorial origin and that cytokine‐associated apoptosis clearly identifies a distinct biological subgroup of patients who may benefit selectively by use of anti‐cytokine therapies.</description><subject>Aged</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Biomarkers</subject><subject>bone marrow</subject><subject>Bone Marrow - pathology</subject><subject>Female</subject><subject>Hematologic and hematopoietic diseases</subject><subject>human disease</subject><subject>Humans</subject><subject>in vivo</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>macrophage</subject><subject>Male</subject><subject>Medical sciences</subject><subject>myelodysplastic syndromes (MDS)</subject><subject>Myelodysplastic Syndromes - blood</subject><subject>Myelodysplastic Syndromes - pathology</subject><subject>Myelodysplastic Syndromes - physiopathology</subject><subject>proliferation</subject><subject>tumor necrosis factor (TNF-α)</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0902-4441</issn><issn>1600-0609</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkVFv1SAYhonRuLPpXzDEGO9agVIo3pi5zU1zMr2Y8ZJQoDsc21Khdaf_XpqeTG_lBvLx8PLxAMBrjHKcxrt9jhlCGWJI5FgIkY81wpzw_PAEbB63noINEohklFJ8Ak5j3COEiMD8OTjBCJWEY7wBh4_Ot_7eadVCvVNB6dEGF0enI_QN7GbbejPHoVVLDca5N8F3Fg5qdLYfI3zYeWhs5_s4BjVaA3fufgd_2xCnCHsPXZ_qnTVT26owQzX4YfTRxRfgWaPaaF8e5zPw_dPV3cVNtv16_fnifJtpWlQ8I7xgGDeGcM2MNQVmipTciJppwk1tCKmZLQ1CShSUUYMqTFVBKmxKVDdUF2fg7Zo7BP9rsnGUnYvapm5666comUjCaFkl8P0K6uBjDLaRQ3Bd6lliJBfvci8XuXKRKxfv8uhdHtLhV8dbpjo99p-jq-gEvDkCKibXTVC9dvEvx0pCK5GwDyv24Fo7_0cH8urLzbJKCdmakD7RHh4TVPgpGS94KX_cXsuyvOPb28tvEhV_AISRsiM</recordid><startdate>199902</startdate><enddate>199902</enddate><creator>Dar, Saleem</creator><creator>Mundle, Suneel</creator><creator>Andric, Tanja</creator><creator>Qawi, Huma</creator><creator>Shetty, Vilasini</creator><creator>Reza, Samina</creator><creator>Mativi, B. 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Yifwayimare ; Allampallam, Krishnan ; Ali, Ambereen ; Venugopal, Parameswaren ; Gezer, Sefer ; Broady-Robinson, LaTanya ; Cartlidge, John ; Showel, Margaret ; Hussaini, Seema ; Ragasa, Deborah ; Ali, Irfan ; Chaudhry, Ambreen ; Waggoner, Samina ; Lisak, Laurie ; Huang, Ray-Win ; Raza, Azra</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4387-273611fd27c6ded316a257d9b6c27dbd22b6e5d00a93464d0814a3281d50bf4c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Aged</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Biomarkers</topic><topic>bone marrow</topic><topic>Bone Marrow - pathology</topic><topic>Female</topic><topic>Hematologic and hematopoietic diseases</topic><topic>human disease</topic><topic>Humans</topic><topic>in vivo</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>macrophage</topic><topic>Male</topic><topic>Medical sciences</topic><topic>myelodysplastic syndromes (MDS)</topic><topic>Myelodysplastic Syndromes - blood</topic><topic>Myelodysplastic Syndromes - pathology</topic><topic>Myelodysplastic Syndromes - physiopathology</topic><topic>proliferation</topic><topic>tumor necrosis factor (TNF-α)</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dar, Saleem</creatorcontrib><creatorcontrib>Mundle, Suneel</creatorcontrib><creatorcontrib>Andric, Tanja</creatorcontrib><creatorcontrib>Qawi, Huma</creatorcontrib><creatorcontrib>Shetty, Vilasini</creatorcontrib><creatorcontrib>Reza, Samina</creatorcontrib><creatorcontrib>Mativi, B. 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Yifwayimare</au><au>Allampallam, Krishnan</au><au>Ali, Ambereen</au><au>Venugopal, Parameswaren</au><au>Gezer, Sefer</au><au>Broady-Robinson, LaTanya</au><au>Cartlidge, John</au><au>Showel, Margaret</au><au>Hussaini, Seema</au><au>Ragasa, Deborah</au><au>Ali, Irfan</au><au>Chaudhry, Ambreen</au><au>Waggoner, Samina</au><au>Lisak, Laurie</au><au>Huang, Ray-Win</au><au>Raza, Azra</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Biological characteristics of myelodysplastic syndrome patients who demonstrated high versus no intramedullary apoptosis</atitle><jtitle>European journal of haematology</jtitle><addtitle>Eur J Haematol</addtitle><date>1999-02</date><risdate>1999</risdate><volume>62</volume><issue>2</issue><spage>90</spage><epage>94</epage><pages>90-94</pages><issn>0902-4441</issn><eissn>1600-0609</eissn><coden>EJHAEC</coden><abstract>: Spontaneous intramedullary apoptosis was measured in bone marrow (BM) biopsies of 175 patients with myelodysplastic syndromes (MDS) using in situ end‐labeling (ISEL) of fragmented DNA. Two groups of high (n = 71) versus low (n = 43) levels of apoptosis were identified while 61 patients were ISEL‐negative. Semiquantitative assessment of 3 cytokines, the number of macrophages and in vivo labeling indices (LI) were also determined from consecutive sections of the biopsy. Patients with high apoptosis levels tended to have a high LI (p = 0.013), more macrophages in their BM biopsies (p = 0.006) and higher tumor necrosis factor alpha (TNF‐α) levels (not significant) compared to patients with no apoptosis. In addition, low risk MDS patients had significantly lower rates of apoptosis (p = 0.047) and lower levels of TNF‐α (p = 0.055) compared to high‐risk MDS patients. We conclude that the genesis of cytopenias in MDS is of multifactorial origin and that cytokine‐associated apoptosis clearly identifies a distinct biological subgroup of patients who may benefit selectively by use of anti‐cytokine therapies.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>10052711</pmid><doi>10.1111/j.1600-0609.1999.tb01727.x</doi><tpages>5</tpages></addata></record> |
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| subjects | Aged Apoptosis Biological and medical sciences Biomarkers bone marrow Bone Marrow - pathology Female Hematologic and hematopoietic diseases human disease Humans in vivo Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis macrophage Male Medical sciences myelodysplastic syndromes (MDS) Myelodysplastic Syndromes - blood Myelodysplastic Syndromes - pathology Myelodysplastic Syndromes - physiopathology proliferation tumor necrosis factor (TNF-α) Tumor Necrosis Factor-alpha - metabolism |
| title | Biological characteristics of myelodysplastic syndrome patients who demonstrated high versus no intramedullary apoptosis |
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