The lymphocyte immunophenotypical pattern in chronic lymphocytic leukemia associated with hepatitis viral infections
Chronic lymphoproliferative disorders (CLD) are frequently found in patients with hepatitis viral infections, which can lead to changes in pathogenesis. Hepatitis viruses are hepatotrope viruses, potentially lymphotrope and also potentially oncogenic (hepatocellular carcinoma) viruses. HBV and HCV a...
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| Veröffentlicht in: | Journal of medicine and life 2011-08, Vol.4 (3), p.256-263 |
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| creator | Bumbea, H Vladareanu, A M Vintilescu, A Radesi, S Ciufu, C Onisai, M Baluta, C Begu, M Dobrea, C Arama, V Streinu-Cercel, A Arama, S |
| description | Chronic lymphoproliferative disorders (CLD) are frequently found in patients with hepatitis viral infections, which can lead to changes in pathogenesis. Hepatitis viruses are hepatotrope viruses, potentially lymphotrope and also potentially oncogenic (hepatocellular carcinoma) viruses. HBV and HCV are involved in autoimmune disorders and in the ethiopathogeny of chronic lymphoproliferative disorders.
Detection of immunophenotype changes of malignant lymphocytes in CLD--especially CLL--associated with hepatitis viral infections.
Bone marrow aspirate, peripheral blood samples on EDTA were available for analysis from 58 patients from a follow-up schedule of the Department of Hematology SUUB from March 2008 until June 2009. The patients were diagnosed with chronic lymphoproliferative disorders associated with hepatitis virus B/C/D infections. A group of 28 consecutive unselected patients with CLL who met the diagnostic criteria of the National Cancer Institute-Working Group (NCI NCIWG), and associated hepatitis viral infection (v-CLL) were studied for the expression of several immunophenotypical markers, in comparison to CLL patients without viral infection (control group). Immunophenotyping analysis was performed on a FACS Calibur flowcytometer with a large panel according to EGIL/WHO recommendations. The diagnosis was completed after the histological and immunochemical analysis from tumoral lesions.
Demographics characteristics--male/female ratio 1/2, average age 64 years. Disease type: 90% B-CLD, 5% T-CLD, 5% Hodgkin's disease. The viral infections: 58.53% HCV, 34.41% HBV, 2.43% HBV+HDV, 2.43% HCV+HDV, 2.43% HBV+HCV+HDV. We found in CLL with viral coinfection (v-CLL) cases an elevated expression of B-cell markers--CD19 (Md95/92), CD20 (Md 90/39), CD79b (Md58/31), CD23 (Md67/37). Poor prognosis markers have a higher expression in v-CLL: CD38 (Md49/24), Bcl2 (Md 46/5), cyclin D19 (Md 11/0.5). No change in ZAP-70 expression was observed: Md 59.5/59.1.
Hepatitis viruses could be involved in the pathogenesis of CLD, but as a trigger for a more aggressive outcome. Higher expression of B-cell markers CD19, CD20 in CLL with viral infection suggests a change to atypical CLL, sustained by elevated expression of known poor prognosis markers bcl-2, cyclin D1 and CD38. Lack of ZAP-70 expression could be explained by a strong correlation with a basic unmutated IgVH status, not related to the viral infection. We found a higher frequency of HCV infection in patients with C |
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Detection of immunophenotype changes of malignant lymphocytes in CLD--especially CLL--associated with hepatitis viral infections.
Bone marrow aspirate, peripheral blood samples on EDTA were available for analysis from 58 patients from a follow-up schedule of the Department of Hematology SUUB from March 2008 until June 2009. The patients were diagnosed with chronic lymphoproliferative disorders associated with hepatitis virus B/C/D infections. A group of 28 consecutive unselected patients with CLL who met the diagnostic criteria of the National Cancer Institute-Working Group (NCI NCIWG), and associated hepatitis viral infection (v-CLL) were studied for the expression of several immunophenotypical markers, in comparison to CLL patients without viral infection (control group). Immunophenotyping analysis was performed on a FACS Calibur flowcytometer with a large panel according to EGIL/WHO recommendations. The diagnosis was completed after the histological and immunochemical analysis from tumoral lesions.
Demographics characteristics--male/female ratio 1/2, average age 64 years. Disease type: 90% B-CLD, 5% T-CLD, 5% Hodgkin's disease. The viral infections: 58.53% HCV, 34.41% HBV, 2.43% HBV+HDV, 2.43% HCV+HDV, 2.43% HBV+HCV+HDV. We found in CLL with viral coinfection (v-CLL) cases an elevated expression of B-cell markers--CD19 (Md95/92), CD20 (Md 90/39), CD79b (Md58/31), CD23 (Md67/37). Poor prognosis markers have a higher expression in v-CLL: CD38 (Md49/24), Bcl2 (Md 46/5), cyclin D19 (Md 11/0.5). No change in ZAP-70 expression was observed: Md 59.5/59.1.
Hepatitis viruses could be involved in the pathogenesis of CLD, but as a trigger for a more aggressive outcome. Higher expression of B-cell markers CD19, CD20 in CLL with viral infection suggests a change to atypical CLL, sustained by elevated expression of known poor prognosis markers bcl-2, cyclin D1 and CD38. Lack of ZAP-70 expression could be explained by a strong correlation with a basic unmutated IgVH status, not related to the viral infection. We found a higher frequency of HCV infection in patients with CLD and especially in CLL patients, which were analyzed extensively for immunophenotypical changes. In the present study, we demonstrated that this CD5+ B cell population with clonal expansion, defining CLL patients, has a different immunophenotype, probably related to the hepatitis viral infection.</description><identifier>ISSN: 1844-122X</identifier><identifier>EISSN: 1844-3117</identifier><identifier>PMID: 22567048</identifier><language>eng</language><publisher>Romania: Carol Daila University Foundation</publisher><subject>Antigens, Neoplasm - immunology ; Biomarkers, Tumor - immunology ; Female ; Hepatitis - complications ; Hepatitis - epidemiology ; Hepatitis - immunology ; Hepatitis - virology ; Humans ; Immunophenotyping ; Incidence ; Leukemia, Lymphocytic, Chronic, B-Cell - complications ; Leukemia, Lymphocytic, Chronic, B-Cell - epidemiology ; Leukemia, Lymphocytic, Chronic, B-Cell - immunology ; Leukemia, Lymphocytic, Chronic, B-Cell - virology ; Lymphocytes - immunology ; Male ; Middle Aged ; Original ; Prevalence</subject><ispartof>Journal of medicine and life, 2011-08, Vol.4 (3), p.256-263</ispartof><rights>Copyright Carol Davila University Foundation Jul-Sep 2011</rights><rights>Carol Davila University Press 2011</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3168828/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3168828/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22567048$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bumbea, H</creatorcontrib><creatorcontrib>Vladareanu, A M</creatorcontrib><creatorcontrib>Vintilescu, A</creatorcontrib><creatorcontrib>Radesi, S</creatorcontrib><creatorcontrib>Ciufu, C</creatorcontrib><creatorcontrib>Onisai, M</creatorcontrib><creatorcontrib>Baluta, C</creatorcontrib><creatorcontrib>Begu, M</creatorcontrib><creatorcontrib>Dobrea, C</creatorcontrib><creatorcontrib>Arama, V</creatorcontrib><creatorcontrib>Streinu-Cercel, A</creatorcontrib><creatorcontrib>Arama, S</creatorcontrib><title>The lymphocyte immunophenotypical pattern in chronic lymphocytic leukemia associated with hepatitis viral infections</title><title>Journal of medicine and life</title><addtitle>J Med Life</addtitle><description>Chronic lymphoproliferative disorders (CLD) are frequently found in patients with hepatitis viral infections, which can lead to changes in pathogenesis. Hepatitis viruses are hepatotrope viruses, potentially lymphotrope and also potentially oncogenic (hepatocellular carcinoma) viruses. HBV and HCV are involved in autoimmune disorders and in the ethiopathogeny of chronic lymphoproliferative disorders.
Detection of immunophenotype changes of malignant lymphocytes in CLD--especially CLL--associated with hepatitis viral infections.
Bone marrow aspirate, peripheral blood samples on EDTA were available for analysis from 58 patients from a follow-up schedule of the Department of Hematology SUUB from March 2008 until June 2009. The patients were diagnosed with chronic lymphoproliferative disorders associated with hepatitis virus B/C/D infections. A group of 28 consecutive unselected patients with CLL who met the diagnostic criteria of the National Cancer Institute-Working Group (NCI NCIWG), and associated hepatitis viral infection (v-CLL) were studied for the expression of several immunophenotypical markers, in comparison to CLL patients without viral infection (control group). Immunophenotyping analysis was performed on a FACS Calibur flowcytometer with a large panel according to EGIL/WHO recommendations. The diagnosis was completed after the histological and immunochemical analysis from tumoral lesions.
Demographics characteristics--male/female ratio 1/2, average age 64 years. Disease type: 90% B-CLD, 5% T-CLD, 5% Hodgkin's disease. The viral infections: 58.53% HCV, 34.41% HBV, 2.43% HBV+HDV, 2.43% HCV+HDV, 2.43% HBV+HCV+HDV. We found in CLL with viral coinfection (v-CLL) cases an elevated expression of B-cell markers--CD19 (Md95/92), CD20 (Md 90/39), CD79b (Md58/31), CD23 (Md67/37). Poor prognosis markers have a higher expression in v-CLL: CD38 (Md49/24), Bcl2 (Md 46/5), cyclin D19 (Md 11/0.5). No change in ZAP-70 expression was observed: Md 59.5/59.1.
Hepatitis viruses could be involved in the pathogenesis of CLD, but as a trigger for a more aggressive outcome. Higher expression of B-cell markers CD19, CD20 in CLL with viral infection suggests a change to atypical CLL, sustained by elevated expression of known poor prognosis markers bcl-2, cyclin D1 and CD38. Lack of ZAP-70 expression could be explained by a strong correlation with a basic unmutated IgVH status, not related to the viral infection. We found a higher frequency of HCV infection in patients with CLD and especially in CLL patients, which were analyzed extensively for immunophenotypical changes. In the present study, we demonstrated that this CD5+ B cell population with clonal expansion, defining CLL patients, has a different immunophenotype, probably related to the hepatitis viral infection.</description><subject>Antigens, Neoplasm - immunology</subject><subject>Biomarkers, Tumor - immunology</subject><subject>Female</subject><subject>Hepatitis - complications</subject><subject>Hepatitis - epidemiology</subject><subject>Hepatitis - immunology</subject><subject>Hepatitis - virology</subject><subject>Humans</subject><subject>Immunophenotyping</subject><subject>Incidence</subject><subject>Leukemia, Lymphocytic, Chronic, B-Cell - complications</subject><subject>Leukemia, Lymphocytic, Chronic, B-Cell - epidemiology</subject><subject>Leukemia, Lymphocytic, Chronic, B-Cell - immunology</subject><subject>Leukemia, Lymphocytic, Chronic, B-Cell - virology</subject><subject>Lymphocytes - immunology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Original</subject><subject>Prevalence</subject><issn>1844-122X</issn><issn>1844-3117</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdUU1LxDAQDaK4y7p_QYInL4U2SZP0IsjiFyx42YO3kk2nNmub1CZd6b834vo5MMyDmfd4M3OE5plkLKFZJo4POCPkaYaW3u_SGCznnNNTNCMk5yJlco7CpgHcTl3fOD0FwKbrRuv6BqwLU2-0anGvQoDBYmOxbgZnjf4hfGAYX6AzCivvnTYqQIXfTGhwA5FpgvF4b4aoY2wNOhhn_Rk6qVXrYXmoC7S5vdms7pP1493D6nqd9CSVIWGkZikRrMgFY1KpWvMiq2gtCNlyiLVgVKdbwSrQfMu4Ai0gEtJU5FVV0wW6-pTtx20HlQYboo-yH0ynhql0ypR_O9Y05bPblzTjUhIZBS4PAoN7HcGHsjNeQ9sqC270ZZZm8cpUMBpHL_6N7tw42LhdKWVRcJrHXKDz34a-nXy9g74DN5yMdA</recordid><startdate>20110815</startdate><enddate>20110815</enddate><creator>Bumbea, H</creator><creator>Vladareanu, A M</creator><creator>Vintilescu, A</creator><creator>Radesi, S</creator><creator>Ciufu, C</creator><creator>Onisai, M</creator><creator>Baluta, C</creator><creator>Begu, M</creator><creator>Dobrea, C</creator><creator>Arama, V</creator><creator>Streinu-Cercel, A</creator><creator>Arama, S</creator><general>Carol Daila University Foundation</general><general>Carol Davila University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BYOGL</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20110815</creationdate><title>The lymphocyte immunophenotypical pattern in chronic lymphocytic leukemia associated with hepatitis viral infections</title><author>Bumbea, H ; Vladareanu, A M ; Vintilescu, A ; Radesi, S ; Ciufu, C ; Onisai, M ; Baluta, C ; Begu, M ; Dobrea, C ; Arama, V ; Streinu-Cercel, A ; Arama, S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p208t-42f40274957448aafc691d3f722b6e3f7943c0b74dec6b46aec7e0270075ddf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Antigens, Neoplasm - immunology</topic><topic>Biomarkers, Tumor - immunology</topic><topic>Female</topic><topic>Hepatitis - complications</topic><topic>Hepatitis - epidemiology</topic><topic>Hepatitis - immunology</topic><topic>Hepatitis - virology</topic><topic>Humans</topic><topic>Immunophenotyping</topic><topic>Incidence</topic><topic>Leukemia, Lymphocytic, Chronic, B-Cell - complications</topic><topic>Leukemia, Lymphocytic, Chronic, B-Cell - epidemiology</topic><topic>Leukemia, Lymphocytic, Chronic, B-Cell - immunology</topic><topic>Leukemia, Lymphocytic, Chronic, B-Cell - virology</topic><topic>Lymphocytes - immunology</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Original</topic><topic>Prevalence</topic><toplevel>online_resources</toplevel><creatorcontrib>Bumbea, H</creatorcontrib><creatorcontrib>Vladareanu, A M</creatorcontrib><creatorcontrib>Vintilescu, A</creatorcontrib><creatorcontrib>Radesi, S</creatorcontrib><creatorcontrib>Ciufu, C</creatorcontrib><creatorcontrib>Onisai, M</creatorcontrib><creatorcontrib>Baluta, C</creatorcontrib><creatorcontrib>Begu, M</creatorcontrib><creatorcontrib>Dobrea, C</creatorcontrib><creatorcontrib>Arama, V</creatorcontrib><creatorcontrib>Streinu-Cercel, A</creatorcontrib><creatorcontrib>Arama, S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>East Europe, Central Europe Database</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of medicine and life</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bumbea, H</au><au>Vladareanu, A M</au><au>Vintilescu, A</au><au>Radesi, S</au><au>Ciufu, C</au><au>Onisai, M</au><au>Baluta, C</au><au>Begu, M</au><au>Dobrea, C</au><au>Arama, V</au><au>Streinu-Cercel, A</au><au>Arama, S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The lymphocyte immunophenotypical pattern in chronic lymphocytic leukemia associated with hepatitis viral infections</atitle><jtitle>Journal of medicine and life</jtitle><addtitle>J Med Life</addtitle><date>2011-08-15</date><risdate>2011</risdate><volume>4</volume><issue>3</issue><spage>256</spage><epage>263</epage><pages>256-263</pages><issn>1844-122X</issn><eissn>1844-3117</eissn><abstract>Chronic lymphoproliferative disorders (CLD) are frequently found in patients with hepatitis viral infections, which can lead to changes in pathogenesis. Hepatitis viruses are hepatotrope viruses, potentially lymphotrope and also potentially oncogenic (hepatocellular carcinoma) viruses. HBV and HCV are involved in autoimmune disorders and in the ethiopathogeny of chronic lymphoproliferative disorders.
Detection of immunophenotype changes of malignant lymphocytes in CLD--especially CLL--associated with hepatitis viral infections.
Bone marrow aspirate, peripheral blood samples on EDTA were available for analysis from 58 patients from a follow-up schedule of the Department of Hematology SUUB from March 2008 until June 2009. The patients were diagnosed with chronic lymphoproliferative disorders associated with hepatitis virus B/C/D infections. A group of 28 consecutive unselected patients with CLL who met the diagnostic criteria of the National Cancer Institute-Working Group (NCI NCIWG), and associated hepatitis viral infection (v-CLL) were studied for the expression of several immunophenotypical markers, in comparison to CLL patients without viral infection (control group). Immunophenotyping analysis was performed on a FACS Calibur flowcytometer with a large panel according to EGIL/WHO recommendations. The diagnosis was completed after the histological and immunochemical analysis from tumoral lesions.
Demographics characteristics--male/female ratio 1/2, average age 64 years. Disease type: 90% B-CLD, 5% T-CLD, 5% Hodgkin's disease. The viral infections: 58.53% HCV, 34.41% HBV, 2.43% HBV+HDV, 2.43% HCV+HDV, 2.43% HBV+HCV+HDV. We found in CLL with viral coinfection (v-CLL) cases an elevated expression of B-cell markers--CD19 (Md95/92), CD20 (Md 90/39), CD79b (Md58/31), CD23 (Md67/37). Poor prognosis markers have a higher expression in v-CLL: CD38 (Md49/24), Bcl2 (Md 46/5), cyclin D19 (Md 11/0.5). No change in ZAP-70 expression was observed: Md 59.5/59.1.
Hepatitis viruses could be involved in the pathogenesis of CLD, but as a trigger for a more aggressive outcome. Higher expression of B-cell markers CD19, CD20 in CLL with viral infection suggests a change to atypical CLL, sustained by elevated expression of known poor prognosis markers bcl-2, cyclin D1 and CD38. Lack of ZAP-70 expression could be explained by a strong correlation with a basic unmutated IgVH status, not related to the viral infection. We found a higher frequency of HCV infection in patients with CLD and especially in CLL patients, which were analyzed extensively for immunophenotypical changes. In the present study, we demonstrated that this CD5+ B cell population with clonal expansion, defining CLL patients, has a different immunophenotype, probably related to the hepatitis viral infection.</abstract><cop>Romania</cop><pub>Carol Daila University Foundation</pub><pmid>22567048</pmid><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antigens, Neoplasm - immunology Biomarkers, Tumor - immunology Female Hepatitis - complications Hepatitis - epidemiology Hepatitis - immunology Hepatitis - virology Humans Immunophenotyping Incidence Leukemia, Lymphocytic, Chronic, B-Cell - complications Leukemia, Lymphocytic, Chronic, B-Cell - epidemiology Leukemia, Lymphocytic, Chronic, B-Cell - immunology Leukemia, Lymphocytic, Chronic, B-Cell - virology Lymphocytes - immunology Male Middle Aged Original Prevalence |
| title | The lymphocyte immunophenotypical pattern in chronic lymphocytic leukemia associated with hepatitis viral infections |
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