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Antonino Carbone - One of the best experts on this subject based on the ideXlab platform.
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NEOPLASIA Gene expression profile analysis of AIDS-related primary effusion Lymphoma (PEL) suggests a plasmablastic derivation and identifies PEL-specific transcripts
2016Co-Authors: Ulf Klein, Annunziata Gloghini, Gianluca Gaidano, Amy Chadburn, Ethel Cesarman, Riccardo Dalla-favera, Antonino CarboneAbstract:AIDS-related primary effusion Lymphoma (PEL) is an HIV-associated malignancy characterized by the ability of the tumor cells to specifically home in the serous body cavities. Here we used gene expres-sion profile analysis (about 12 000 genes) to further define the phenotype of PEL and to investigate the Lymphoma relation-ship to normal B cells and to other tumor subtypes, including non-Hodgkin lympho-mas (NHLs) of immunocompetent hosts and AIDS-associated NHL (AIDS-NHL). The results showed that PEL displayed a common gene expression profile that is clearly distinct from all NHLs of immuno-competent hosts and AIDS-NHL subtypes and, in contrast to those, is not related to germinal center (GC) or memory B cells. The gene expression profile of PEL was defined as plasmablastic because it showed features of both immunoblasts identified by Epstein-Barr virus (EBV)– transformed lymphoblastoid cell lines and AIDS Immunoblastic Lymphoma, and plasma cells, as defined by multiple my-eloma cell lines. Finally, our results iden-tify a set of genes specifically expressed in PEL tumor cells. Their expression was validated at the protein level, suggesting their potential pathogenetic and clinical significance. (Blood. 2003;101:4115-4121) © 2003 by The American Society of Hematolog
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Clinica l Features and Outcome of Primary Ef fus ion Lymphoma in HIV-Infected Pat ients: A Single- Inst i tut ion Study
2016Co-Authors: Cecilia Simonelli, Antonino Carbone, Michele Spina, Roberta Cinelli, Renato Talamini, Rosamaria Tedeschi, Annunziata Gloghini, Emanuela Vaccher, Umberto TirelliAbstract:Purpose: To describe the clinical features and outcome of HIV-associated primary effusion Lymphoma (PEL) and to compare them with those of the other HIV-associated non-Hodgkin’s Lymphomas (NHLs). Patients and Methods: From April 1987 to June 2002, 277 patients with HIV infection and systemic NHL were diagnosed and treated in our institution. Clinical features and outcome of PEL patients were compared with the fea-tures and outcomes of 162 patients belonging to the follow-ing histologic subtypes: plasmoblastic Lymphoma of oral cavity (PBLOC, n 11), Immunoblastic Lymphoma (IBL, n 76), and centroblastic B-cell Lymphoma (CBCL, n 75)
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clinical features and outcome of primary effusion Lymphoma in hiv infected patients a single institution study
Journal of Clinical Oncology, 2003Co-Authors: Cecilia Simonelli, Antonino Carbone, Michele Spina, Roberta Cinelli, Renato Talamini, Rosamaria Tedeschi, Annunziata Gloghini, Emanuela Vaccher, Umberto TirelliAbstract:Purpose: To describe the clinical features and outcome of HIV-associated primary effusion Lymphoma (PEL) and to compare them with those of the other HIV-associated non-Hodgkin’s Lymphomas (NHLs). Patients and Methods: From April 1987 to June 2002, 277 patients with HIV infection and systemic NHL were diagnosed and treated in our institution. Clinical features and outcome of PEL patients were compared with the features and outcomes of 162 patients belonging to the following histologic subtypes: plasmoblastic Lymphoma of oral cavity (PBLOC, n = 11), Immunoblastic Lymphoma (IBL, n = 76), and centroblastic B-cell Lymphoma (CBCL, n = 75). Results: Among the 277 NHL patients, PEL was diagnosed in 11 patients (4%). Eight of 11 patients were treated with a cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP)–like regimen. Complete remission was reached in 42% of patients, with a median survival time of 6 months. When the clinical features and outcome of 11 PEL patients were compared with the other th...
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gene expression profile analysis of aids related primary effusion Lymphoma pel suggests a plasmablastic derivation and identifies pel specific transcripts
Blood, 2003Co-Authors: Ulf Klein, Annunziata Gloghini, Gianluca Gaidano, Amy Chadburn, Ethel Cesarman, Riccardo Dallafavera, Antonino CarboneAbstract:AIDS-related primary effusion Lymphoma (PEL) is an HIV-associated malignancy characterized by the ability of the tumor cells to specifically home in the serous body cavities. Here we used gene expression profile analysis (about 12 000 genes) to further define the phenotype of PEL and to investigate the Lymphoma relationship to normal B cells and to other tumor subtypes, including non-Hodgkin Lymphomas (NHLs) of immunocompetent hosts and AIDS-associated NHL (AIDS-NHL). The results showed that PEL displayed a common gene expression profile that is clearly distinct from all NHLs of immunocompetent hosts and AIDS-NHL subtypes and, in contrast to those, is not related to germinal center (GC) or memory B cells. The gene expression profile of PEL was defined as plasmablastic because it showed features of both immunoblasts identified by Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines and AIDS Immunoblastic Lymphoma, and plasma cells, as defined by multiple myeloma cell lines. Finally, our results identify a set of genes specifically expressed in PEL tumor cells. Their expression was validated at the protein level, suggesting their potential pathogenetic and clinical significance.
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expression profile of mum1 irf4 bcl 6 and cd138 syndecan 1 defines novel histogenetic subsets of human immunodeficiency virus related Lymphomas
Blood, 2001Co-Authors: Antonino Carbone, Annunziata Gloghini, Umberto Tirelli, Riccardo Dallafavera, Luigi Maria Larocca, Daniela Capello, Francesco Pierconti, Vincenzo Canzonieri, Gianluca GaidanoAbstract:This study was aimed at defining the histogenesis of the pathologic spectrum of Lymphoma arising in the context of human immunodeficiency virus (HIV) infection. Toward this aim, 87 AIDS-related non-Hodgkin Lymphomas (AIDS-NHL) and 16 Hodgkin Lymphomas arising in HIV + patients (HIV-HL) were comparatively analyzed for the expression pattern of several B-cell histogenetic markers, including BCL-6 (expressed by centroblasts and centrocytes), MUM1/IRF4 (expressed by late centrocytes and post–germinal center [GC] B cells), and CD138/syn-1 (expressed by post-GC B cells). Expression of MUM1, BCL-6, and syn-1 segregated 3 major phenotypic patterns among AIDS-NHL and HIV-HL: (1) the BCL-6 + /MUM1 − /syn-1 − pattern, selectively clustering with a large fraction of AIDS-Burkitt Lymphoma (17 of 19) and of systemic AIDS–diffuse large cell Lymphoma (12 of 16); (2) the BCL-6 − /MUM1 + /syn-1 − pattern, associated with a fraction of AIDS-Immunoblastic Lymphoma (8 of 24); and (3) the BCL-6 − /MUM1 + /syn-1 + pattern, associated with systemic and primary central nervous system Immunoblastic Lymphoma (14 of 24) and with primary effusion Lymphoma (10 of 10), plasmablastic Lymphoma of the oral cavity (7 of 7), and HIV-HL (15 of 16). Analysis of nonneoplastic lymph nodes showed that the 3 phenotypic patterns detected in AIDS-NHL and HIV-HL correspond to distinct stages of physiologic B-cell development—centroblasts (BCL-6 + /MUM1 − /syn-1 − ), late GC/early post-GC B cells (BCL-6 − /MUM1 + /syn-1 − ), and post-GC B cells (BCL-6 − /MUM1 + /syn-1 + ). Expression of the Epstein-Barr virus-encoded latent membrane protein-1 clustered with the BCL-6 − /MUM1 + /syn-1 + profile throughout the clinicopathologic spectrum of AIDS-NHL and HIV-HL. Overall, these results define novel histogenetic subsets of AIDS-NHL and HIV-HL and may provide novel tools for refining the diagnosis of these disorders.
James J Goedert - One of the best experts on this subject based on the ideXlab platform.
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immune deficiency and risk for malignancy among persons with aids
Journal of Acquired Immune Deficiency Syndromes, 2003Co-Authors: Sam M Mbulaiteye, James J Goedert, Robert J Biggar, Eric A EngelsAbstract:Background: People with AIDS have an elevated risk for cancer. We studied the relationship between cancer risk and AIDS-related immunosuppression as measured by CD4 count at AIDS onset. Methods: We linked records from AIDS and cancer registries in 11 US regions (1990-1996). We studied 82,217 (86.6%) adults who had a CD4 count measured at AIDS onset and survived into the follow-up period. We calculated standardized incidence ratios (SIRs) for AIDS-defining (Kaposi sarcoma [KS], non-Hodgkin Lymphoma [NHL] and cervical cancer) as well as non-AIDS-defining cancers in the 2 years after AIDS onset. For each cancer, the change in SIRs across CD4 counts (0-49 cells/mm 3 , 50-99 cells/mm 3 , 100-199 cells/mm 3 , and ≥200 cells/mm 3 ) was modeled using Poisson regression. Results: The SIRs for KS, NHL, and cervical cancer were 258, 78, and 8.8, respectively. For each fall of 100 CD4 cells/mm 3 , RRs were 1.36 (95% CI: 1.29-1.43) for KS and 1.48 (95% CI: 1.37-1.59) for NHL. Among NHL subtypes, the association with lower CD4 counts was strongest for Immunoblastic Lymphoma (RR = 1.64, 95% CI: 1.37-1.96, per decline of 100 CD4 cells/mm 3 ) and central nervous system Lymphoma (RR = 2.29, 95% CI: 1.95-2.69). The SIR for cervical cancer did not vary with CD4 count (p =.74). For non-AIDS-defining cancers (overall SIR = 2.1), neither the combined risk nor the risk of specific types was associated with declining CD4 counts. Conclusions: KS and NHL risk increased with level of immunosuppression at AIDS onset. Risks for other cancers, including cervical cancer, were unrelated to CD4 counts. Elevated risks for non-AIDS cancers may be a result of lifestyle factors.
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Immunoblastic Lymphoma in persons with AIDS-associated Kaposi's sarcoma: a role for Kaposi's sarcoma-associated herpesvirus.
Modern Pathology, 2003Co-Authors: Eric A Engels, Stefania Pittaluga, Denise Whitby, Charles S. Rabkin, Yoshiyasu Aoki, Elaine S. Jaffe, James J GoedertAbstract:Kaposi's sarcoma–associated herpesvirus, the viral agent of Kaposi's sarcoma, is associated with two lymphoproliferative disorders: primary effusion Lymphoma and multicentric Castleman's disease. To identify other lymphoproliferative conditions linked with Kaposi's sarcoma–associated herpesvirus, we studied non-Hodgkin's Lymphomas arising in individuals with AIDS-associated Kaposi's sarcoma. Formalin-fixed tissues from 24 such Lymphomas were examined. As expected, two primary effusion Lymphomas were Kaposi's sarcoma–associated herpesvirus–positive, with immunohistochemistry demonstrating the Kaposi's sarcoma–associated herpesvirus latency-associated nuclear antigen in the nuclei of all neoplastic cells. Additionally, three of seven evaluable cases of the Immunoblastic variant of diffuse large B-cell Lymphoma (Immunoblastic Lymphoma) showed similar latency-associated nuclear antigen staining. These Kaposi's sarcoma–associated herpesvirus–positive Immunoblastic Lymphomas resembled primary effusion Lymphoma histologically but were not known to involve body cavities (sites included lymph nodes, soft tissues of the neck, and spleen). Notably, 5–20% of the neoplastic cells in the Kaposi's sarcoma–associated herpesvirus–positive Immunoblastic Lymphomas also showed cytoplasmic staining for viral interleukin-6, a biologically active cytokine homologue found in primary effusion Lymphoma. We conclude that Kaposi's sarcoma–associated herpesvirus is present in some Immunoblastic Lymphomas in persons with AIDS-associated Kaposi's sarcoma.
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cancers associated with kaposi s sarcoma ks in aids a link between ks herpesvirus and Immunoblastic Lymphoma
British Journal of Cancer, 2001Co-Authors: Eric A Engels, Philip S Rosenberg, Morten Frisch, James J GoedertAbstract:Kaposi's sarcoma (KS), common among persons with acquired immunodeficiency syndrome (AIDS), is caused by KS herpesvirus (KSHV) but whether KSHV causes other malignancies is uncertain. Using linked United States AIDS and cancer registries, we measured the incidence of specific malignancies in persons with AIDS (4–27 months after AIDS onset). We identified associations with KSHV by calculating a relative risk: cancer incidence in persons with KS (all were KSHV-infected) divided by incidence in persons without KS. Using Poisson regression, relative risks were adjusted for human immunodeficiency virus risk group, gender, age, race, and calendar year. We included 189 159 subjects (26 972 with KS). Immunoblastic Lymphoma was significantly associated with KS (506 cases; relative risks: unadjusted 2.44, 95%CI 2.00–2.96, adjusted 1.58, 95%CI 1.29–1.93). Only one Immunoblastic Lymphoma had pleura as primary site. None of 37 other specified malignancies (other non-Hodgkin Lymphomas, haematological malignancies, solid tumours) was significantly associated with KS. In summary, the association of Immunoblastic Lymphoma with KS was specific among examined malignancies and remained significant after statistical adjustment. Our findings, and the previously demonstrated presence of KSHV in the histologically related primary effusion Lymphoma, suggest that KSHV is involved in the pathogenesis of some Immunoblastic Lymphomas. © 2001 Cancer Research Campaign
Annunziata Gloghini - One of the best experts on this subject based on the ideXlab platform.
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NEOPLASIA Gene expression profile analysis of AIDS-related primary effusion Lymphoma (PEL) suggests a plasmablastic derivation and identifies PEL-specific transcripts
2016Co-Authors: Ulf Klein, Annunziata Gloghini, Gianluca Gaidano, Amy Chadburn, Ethel Cesarman, Riccardo Dalla-favera, Antonino CarboneAbstract:AIDS-related primary effusion Lymphoma (PEL) is an HIV-associated malignancy characterized by the ability of the tumor cells to specifically home in the serous body cavities. Here we used gene expres-sion profile analysis (about 12 000 genes) to further define the phenotype of PEL and to investigate the Lymphoma relation-ship to normal B cells and to other tumor subtypes, including non-Hodgkin lympho-mas (NHLs) of immunocompetent hosts and AIDS-associated NHL (AIDS-NHL). The results showed that PEL displayed a common gene expression profile that is clearly distinct from all NHLs of immuno-competent hosts and AIDS-NHL subtypes and, in contrast to those, is not related to germinal center (GC) or memory B cells. The gene expression profile of PEL was defined as plasmablastic because it showed features of both immunoblasts identified by Epstein-Barr virus (EBV)– transformed lymphoblastoid cell lines and AIDS Immunoblastic Lymphoma, and plasma cells, as defined by multiple my-eloma cell lines. Finally, our results iden-tify a set of genes specifically expressed in PEL tumor cells. Their expression was validated at the protein level, suggesting their potential pathogenetic and clinical significance. (Blood. 2003;101:4115-4121) © 2003 by The American Society of Hematolog
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Clinica l Features and Outcome of Primary Ef fus ion Lymphoma in HIV-Infected Pat ients: A Single- Inst i tut ion Study
2016Co-Authors: Cecilia Simonelli, Antonino Carbone, Michele Spina, Roberta Cinelli, Renato Talamini, Rosamaria Tedeschi, Annunziata Gloghini, Emanuela Vaccher, Umberto TirelliAbstract:Purpose: To describe the clinical features and outcome of HIV-associated primary effusion Lymphoma (PEL) and to compare them with those of the other HIV-associated non-Hodgkin’s Lymphomas (NHLs). Patients and Methods: From April 1987 to June 2002, 277 patients with HIV infection and systemic NHL were diagnosed and treated in our institution. Clinical features and outcome of PEL patients were compared with the fea-tures and outcomes of 162 patients belonging to the follow-ing histologic subtypes: plasmoblastic Lymphoma of oral cavity (PBLOC, n 11), Immunoblastic Lymphoma (IBL, n 76), and centroblastic B-cell Lymphoma (CBCL, n 75)
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clinical features and outcome of primary effusion Lymphoma in hiv infected patients a single institution study
Journal of Clinical Oncology, 2003Co-Authors: Cecilia Simonelli, Antonino Carbone, Michele Spina, Roberta Cinelli, Renato Talamini, Rosamaria Tedeschi, Annunziata Gloghini, Emanuela Vaccher, Umberto TirelliAbstract:Purpose: To describe the clinical features and outcome of HIV-associated primary effusion Lymphoma (PEL) and to compare them with those of the other HIV-associated non-Hodgkin’s Lymphomas (NHLs). Patients and Methods: From April 1987 to June 2002, 277 patients with HIV infection and systemic NHL were diagnosed and treated in our institution. Clinical features and outcome of PEL patients were compared with the features and outcomes of 162 patients belonging to the following histologic subtypes: plasmoblastic Lymphoma of oral cavity (PBLOC, n = 11), Immunoblastic Lymphoma (IBL, n = 76), and centroblastic B-cell Lymphoma (CBCL, n = 75). Results: Among the 277 NHL patients, PEL was diagnosed in 11 patients (4%). Eight of 11 patients were treated with a cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP)–like regimen. Complete remission was reached in 42% of patients, with a median survival time of 6 months. When the clinical features and outcome of 11 PEL patients were compared with the other th...
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gene expression profile analysis of aids related primary effusion Lymphoma pel suggests a plasmablastic derivation and identifies pel specific transcripts
Blood, 2003Co-Authors: Ulf Klein, Annunziata Gloghini, Gianluca Gaidano, Amy Chadburn, Ethel Cesarman, Riccardo Dallafavera, Antonino CarboneAbstract:AIDS-related primary effusion Lymphoma (PEL) is an HIV-associated malignancy characterized by the ability of the tumor cells to specifically home in the serous body cavities. Here we used gene expression profile analysis (about 12 000 genes) to further define the phenotype of PEL and to investigate the Lymphoma relationship to normal B cells and to other tumor subtypes, including non-Hodgkin Lymphomas (NHLs) of immunocompetent hosts and AIDS-associated NHL (AIDS-NHL). The results showed that PEL displayed a common gene expression profile that is clearly distinct from all NHLs of immunocompetent hosts and AIDS-NHL subtypes and, in contrast to those, is not related to germinal center (GC) or memory B cells. The gene expression profile of PEL was defined as plasmablastic because it showed features of both immunoblasts identified by Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines and AIDS Immunoblastic Lymphoma, and plasma cells, as defined by multiple myeloma cell lines. Finally, our results identify a set of genes specifically expressed in PEL tumor cells. Their expression was validated at the protein level, suggesting their potential pathogenetic and clinical significance.
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expression profile of mum1 irf4 bcl 6 and cd138 syndecan 1 defines novel histogenetic subsets of human immunodeficiency virus related Lymphomas
Blood, 2001Co-Authors: Antonino Carbone, Annunziata Gloghini, Umberto Tirelli, Riccardo Dallafavera, Luigi Maria Larocca, Daniela Capello, Francesco Pierconti, Vincenzo Canzonieri, Gianluca GaidanoAbstract:This study was aimed at defining the histogenesis of the pathologic spectrum of Lymphoma arising in the context of human immunodeficiency virus (HIV) infection. Toward this aim, 87 AIDS-related non-Hodgkin Lymphomas (AIDS-NHL) and 16 Hodgkin Lymphomas arising in HIV + patients (HIV-HL) were comparatively analyzed for the expression pattern of several B-cell histogenetic markers, including BCL-6 (expressed by centroblasts and centrocytes), MUM1/IRF4 (expressed by late centrocytes and post–germinal center [GC] B cells), and CD138/syn-1 (expressed by post-GC B cells). Expression of MUM1, BCL-6, and syn-1 segregated 3 major phenotypic patterns among AIDS-NHL and HIV-HL: (1) the BCL-6 + /MUM1 − /syn-1 − pattern, selectively clustering with a large fraction of AIDS-Burkitt Lymphoma (17 of 19) and of systemic AIDS–diffuse large cell Lymphoma (12 of 16); (2) the BCL-6 − /MUM1 + /syn-1 − pattern, associated with a fraction of AIDS-Immunoblastic Lymphoma (8 of 24); and (3) the BCL-6 − /MUM1 + /syn-1 + pattern, associated with systemic and primary central nervous system Immunoblastic Lymphoma (14 of 24) and with primary effusion Lymphoma (10 of 10), plasmablastic Lymphoma of the oral cavity (7 of 7), and HIV-HL (15 of 16). Analysis of nonneoplastic lymph nodes showed that the 3 phenotypic patterns detected in AIDS-NHL and HIV-HL correspond to distinct stages of physiologic B-cell development—centroblasts (BCL-6 + /MUM1 − /syn-1 − ), late GC/early post-GC B cells (BCL-6 − /MUM1 + /syn-1 − ), and post-GC B cells (BCL-6 − /MUM1 + /syn-1 + ). Expression of the Epstein-Barr virus-encoded latent membrane protein-1 clustered with the BCL-6 − /MUM1 + /syn-1 + profile throughout the clinicopathologic spectrum of AIDS-NHL and HIV-HL. Overall, these results define novel histogenetic subsets of AIDS-NHL and HIV-HL and may provide novel tools for refining the diagnosis of these disorders.
Eric A Engels - One of the best experts on this subject based on the ideXlab platform.
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immune deficiency and risk for malignancy among persons with aids
Journal of Acquired Immune Deficiency Syndromes, 2003Co-Authors: Sam M Mbulaiteye, James J Goedert, Robert J Biggar, Eric A EngelsAbstract:Background: People with AIDS have an elevated risk for cancer. We studied the relationship between cancer risk and AIDS-related immunosuppression as measured by CD4 count at AIDS onset. Methods: We linked records from AIDS and cancer registries in 11 US regions (1990-1996). We studied 82,217 (86.6%) adults who had a CD4 count measured at AIDS onset and survived into the follow-up period. We calculated standardized incidence ratios (SIRs) for AIDS-defining (Kaposi sarcoma [KS], non-Hodgkin Lymphoma [NHL] and cervical cancer) as well as non-AIDS-defining cancers in the 2 years after AIDS onset. For each cancer, the change in SIRs across CD4 counts (0-49 cells/mm 3 , 50-99 cells/mm 3 , 100-199 cells/mm 3 , and ≥200 cells/mm 3 ) was modeled using Poisson regression. Results: The SIRs for KS, NHL, and cervical cancer were 258, 78, and 8.8, respectively. For each fall of 100 CD4 cells/mm 3 , RRs were 1.36 (95% CI: 1.29-1.43) for KS and 1.48 (95% CI: 1.37-1.59) for NHL. Among NHL subtypes, the association with lower CD4 counts was strongest for Immunoblastic Lymphoma (RR = 1.64, 95% CI: 1.37-1.96, per decline of 100 CD4 cells/mm 3 ) and central nervous system Lymphoma (RR = 2.29, 95% CI: 1.95-2.69). The SIR for cervical cancer did not vary with CD4 count (p =.74). For non-AIDS-defining cancers (overall SIR = 2.1), neither the combined risk nor the risk of specific types was associated with declining CD4 counts. Conclusions: KS and NHL risk increased with level of immunosuppression at AIDS onset. Risks for other cancers, including cervical cancer, were unrelated to CD4 counts. Elevated risks for non-AIDS cancers may be a result of lifestyle factors.
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Immunoblastic Lymphoma in persons with AIDS-associated Kaposi's sarcoma: a role for Kaposi's sarcoma-associated herpesvirus.
Modern Pathology, 2003Co-Authors: Eric A Engels, Stefania Pittaluga, Denise Whitby, Charles S. Rabkin, Yoshiyasu Aoki, Elaine S. Jaffe, James J GoedertAbstract:Kaposi's sarcoma–associated herpesvirus, the viral agent of Kaposi's sarcoma, is associated with two lymphoproliferative disorders: primary effusion Lymphoma and multicentric Castleman's disease. To identify other lymphoproliferative conditions linked with Kaposi's sarcoma–associated herpesvirus, we studied non-Hodgkin's Lymphomas arising in individuals with AIDS-associated Kaposi's sarcoma. Formalin-fixed tissues from 24 such Lymphomas were examined. As expected, two primary effusion Lymphomas were Kaposi's sarcoma–associated herpesvirus–positive, with immunohistochemistry demonstrating the Kaposi's sarcoma–associated herpesvirus latency-associated nuclear antigen in the nuclei of all neoplastic cells. Additionally, three of seven evaluable cases of the Immunoblastic variant of diffuse large B-cell Lymphoma (Immunoblastic Lymphoma) showed similar latency-associated nuclear antigen staining. These Kaposi's sarcoma–associated herpesvirus–positive Immunoblastic Lymphomas resembled primary effusion Lymphoma histologically but were not known to involve body cavities (sites included lymph nodes, soft tissues of the neck, and spleen). Notably, 5–20% of the neoplastic cells in the Kaposi's sarcoma–associated herpesvirus–positive Immunoblastic Lymphomas also showed cytoplasmic staining for viral interleukin-6, a biologically active cytokine homologue found in primary effusion Lymphoma. We conclude that Kaposi's sarcoma–associated herpesvirus is present in some Immunoblastic Lymphomas in persons with AIDS-associated Kaposi's sarcoma.
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cancers associated with kaposi s sarcoma ks in aids a link between ks herpesvirus and Immunoblastic Lymphoma
British Journal of Cancer, 2001Co-Authors: Eric A Engels, Philip S Rosenberg, Morten Frisch, James J GoedertAbstract:Kaposi's sarcoma (KS), common among persons with acquired immunodeficiency syndrome (AIDS), is caused by KS herpesvirus (KSHV) but whether KSHV causes other malignancies is uncertain. Using linked United States AIDS and cancer registries, we measured the incidence of specific malignancies in persons with AIDS (4–27 months after AIDS onset). We identified associations with KSHV by calculating a relative risk: cancer incidence in persons with KS (all were KSHV-infected) divided by incidence in persons without KS. Using Poisson regression, relative risks were adjusted for human immunodeficiency virus risk group, gender, age, race, and calendar year. We included 189 159 subjects (26 972 with KS). Immunoblastic Lymphoma was significantly associated with KS (506 cases; relative risks: unadjusted 2.44, 95%CI 2.00–2.96, adjusted 1.58, 95%CI 1.29–1.93). Only one Immunoblastic Lymphoma had pleura as primary site. None of 37 other specified malignancies (other non-Hodgkin Lymphomas, haematological malignancies, solid tumours) was significantly associated with KS. In summary, the association of Immunoblastic Lymphoma with KS was specific among examined malignancies and remained significant after statistical adjustment. Our findings, and the previously demonstrated presence of KSHV in the histologically related primary effusion Lymphoma, suggest that KSHV is involved in the pathogenesis of some Immunoblastic Lymphomas. © 2001 Cancer Research Campaign
Fernando Cabanillas - One of the best experts on this subject based on the ideXlab platform.
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alternating triple therapy for the treatment of intermediate grade and Immunoblastic Lymphoma
Annals of Oncology, 1998Co-Authors: Fernando Cabanillas, Peter Mclaughlin, Fredrick B Hagemeister, Jorge E Romaguera, Maria A Rodriguez, Rodriguezdiaz J Pavon, K Dong, T MoonAbstract:Summary Background CHOP is currently considered the gold standard of treatment for intermediate grade Lymphomas. We designed a new regimen known as ‘ATT’ (alternating triple therapy) which uses three non-cross resistant combinations in alternating sequence for nine cycles. Materials and methods This is a phase II clinical trial with comparison to CHOP/CMED historical controls using prognostic factors. The tumor score system was used to evaluate the results of this trial. Two hundred sixty-eight eligible patients who had one or more of the following adverse features: bulky disease, elevated LDH or > 1 extranodal site were analyzed. Outcome measures consist of survival and failure free survival. Results At a median follow-up of 32 months, there was no statistically significant difference in survival for those with favorable prognostic factors (tumor score ≤ 2). However, there was a statistically significant difference in favor of ATT for those with unfavorable tumor scores. When we examined the failure-free survival of those with unfavorable tumor scores, we again observed a superiority for the ATT regimen over CHOP/CMED but the opposite was true for those with favorable tumor scores. We also found a statistically significant difference in favor of the ATT regimen when compared with CHOP/CMED for patients ≤ 60 years old with a tumor score ≥ 3, while no advantage was found for those > 60 years. Conclusions ATT appears more effective but only for patients 60 years with unfavorable tumor scores neither ATT or CHOP/CMED were adequate treatment. Because of the phase II nature of this study, these conclusions should be considered as hypotheses which require prospective testing.
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the clinical relevance of t 14 18 bcl 2 rearrangement and del 6q in diffuse large cell Lymphoma and Immunoblastic Lymphoma
Annals of Oncology, 1993Co-Authors: J E Romaguera, William C Pugh, Rajyalakshmi Luthra, A M Goodacre, Fernando CabanillasAbstract:Summary Background t(14; 18)/bcl-2 gene rearrangement (R) is claimed to impart a worse rate of complete remission and disease-free survival in diffuse large cell Lymphoma (DLCL). DEL 6q has also been associated with poor outcome. Design Retrospective study of 54 patients with either diffuse large cell or Immunoblastic Lymphoma who had cytogenetics and/or molecular studies performed. Results Patient characteristics, complete remission rate, and time to treatment failure (TTF) were similar at three year follow-up for groups with and without t(14; 18)/BCL-2R Survival was worse for the former but the difference was not statistically significant. For DEL 6q, patient characteristics and survival rates were similar at three year follow-up for patients with and without the abnormality. TTF was worse for the former but this was not statistically significant. Conclusions This study, with equal or greater number of patients with t(14; 18) than previous reports, fails to show a worse prognosis for patients with the t(14; 18) chromosomal abnormality. A definite association will await further accrual of patients and a meaningul multivariate analysis.
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original article a proposal for a simple staging system for intermediate grade Lymphoma and Immunoblastic Lymphoma based on the tumor score
Annals of Oncology, 1992Co-Authors: Jesus Castanon Rodriguez, Fernando Cabanillas, Peter Mclaughlin, Fredrick B Hagemeister, Maria A Rodriguez, F Swan, Jorge E RomagueraAbstract:A new staging system for intermediate grade Lymphomas and Immunoblastic Lymphomas is described. This system is based on the tumor score which consists of assigning a point to each one of five variables that have been previously shown to have a high prognostic value. Ann Arbor stages III-IV, presence of bulky mass, elevation of B-2 microglobulin and LDH as well as presence of 'B' symptoms are the variables utilized in this system. When we applied this tumor score system to a population of 144 patients uniformly treated with CHOP/Bleo/CMED protocol, we observed that this system can accurately divide the population into two prognostic groups without an intermediate category. The first group is made up of those patients with a score of 0-2 points while the second group consists of patients with a score of > or = 3 points. The first group has a time-to-treatment failure (TTF) of 83% at three years in contrast to the second group whose TTF was 24%. If we compare this system with other commonly used systems in our institution, such as Ann Arbor, M.D. Anderson clinical staging system, and M.D. Anderson serological staging system, we observed that the tumor score system is not only more specific and sensitive than the others but also was capable of eliminating an intermediate risk group, thus facilitating therapeutic choices. This tumor score system is easy to apply and potentially reproducible in any institution.
