20
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Etiological factors in primary hepatic B-cell lymphoma

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Sixty-four cases of malignant lymphoma involving the liver were examined. Of these, 20 cases were histologically confirmed to be primary hepatic B-cell lymphoma. Twelve of these 20 cases were diffuse large B-cell lymphoma (DLBCL) and eight cases were mucosa-associated lymphoid tissue (MALT) lymphoma. Of the 12 cases of DLBCL, six were immunohistologically positive for CD10 and/or Bcl6 (indicating a germinal center phenotype), six were positive for Bcl2, and five were positive for CD25. Eight of the 12 DLBCL cases (66.7%) and two of the eight MALT lymphoma cases (25%) had serum anti-hepatitis C virus (HCV) antibodies and HCV RNA. The incidence of HCV infection was significantly higher in the hepatic DLBCL cases than in systemic intravascular large B-cell cases with liver involvement (one of 11 cases, 9.1%) and T/NK-cell lymphoma cases (one of 19 cases, 5.3%) ( p < 0.01 for both). Two hepatic DLBCL cases (16.7%) had rheumatoid arthritis treated with methotrexate, and four MALT lymphoma cases (50%) had Sjögren’s syndrome, primary biliary cirrhosis, or autoimmune hepatitis; one case in each of these two groups was complicated by chronic HCV-seropositive hepatitis. Although primary hepatic lymphoma is rare, persistent inflammatory processes associated with HCV infection or autoimmune disease may play independent roles in the lymphomagenesis of hepatic B cells.

          Related collections

          Most cited references58

          • Record: found
          • Abstract: found
          • Article: not found

          Report on a workshop convened to discuss the pathological and staging classifications of gastrointestinal tract lymphoma.

          It was considered timely to review the pathological and staging classifications of GI tract lymphoma. This meeting specifically did not address the question of treatment; the management of GI tract lymphoma could perhaps form the basis for a further workshop. The following recommendations were made: to adopt the Isaacson histological classification, that all patients with GI tract lymphoma be investigated uniformly, to record the prognostic factors described above, to use the staging classification shown above. It is hoped that these recommendations will be taken into account in the design of future clinical trials of therapy for GI tract lymphoma.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Regression of splenic lymphoma with villous lymphocytes after treatment of hepatitis C virus infection.

            Some epidemiologic studies suggest a link between hepatitis C virus (HCV) infection and some B-cell non-Hodgkin's lymphomas. We undertook this study after a patient with splenic lymphoma with villous lymphocytes had a hematologic response after antiviral treatment of HCV infection. Nine patients who had splenic lymphoma with villous lymphocytes and HCV infection were treated with interferon alfa-2b (3 million IU three times per week) alone or in combination with ribavirin (1000 to 1200 mg per day). The outcomes were compared with those of six similarly treated patients with splenic lymphoma with villous lymphocytes who tested negative for HCV infection. Of the nine patients with HCV infection who received interferon alfa, seven had a complete remission after the loss of detectable HCV RNA. The other two patients had a partial and a complete remission after the addition of ribavirin and the loss of detectable HCV RNA. One patient had a relapse when the HCV RNA load again became detectable in blood. In contrast, none of the six HCV-negative patients had a response to interferon therapy. In patients with splenic lymphoma with villous lymphocytes who are infected with HCV, treatment with interferon can lead to regression of the lymphoma.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Hepatitis C virus induces a mutator phenotype: enhanced mutations of immunoglobulin and protooncogenes.

              Hepatitis C virus (HCV) is a nonretroviral oncogenic RNA virus, which is frequently associated with hepatocellular carcinoma (HCC) and B cell lymphoma. We demonstrated here that acute and chronic HCV infection caused a 5- to 10-fold increase in mutation frequency in Ig heavy chain, BCL-6, p53, and beta-catenin genes of in vitro HCV-infected B cell lines and HCV-associated peripheral blood mononuclear cells, lymphomas, and HCCs. The nucleotide-substitution pattern of p53 and beta-catenin was different from that of Ig heavy chain in HCV-infected cells, suggesting two different mechanisms of mutation. In addition, the mutated protooncogenes were amplified in HCV-associated lymphomas and HCCs, but not in lymphomas of nonviral origin or HBV-associated HCC. HCV induced error-prone DNA polymerase zeta, polymerase iota, and activation-induced cytidine deaminase, which together, contributed to the enhancement of mutation frequency, as demonstrated by the RNA interference experiments. These results indicate that HCV induces a mutator phenotype and may transform cells by a hit-and-run mechanism. This finding provides a mechanism of oncogenesis for an RNA virus.
                Bookmark

                Author and article information

                Contributors
                +81-92-8011011 , +81-92-861-7300 , m-take@adm.fukuoka-u.ac.jp
                Journal
                Virchows Arch
                Virchows Arch
                Virchows Archiv
                Springer-Verlag (Berlin/Heidelberg )
                0945-6317
                1432-2307
                7 March 2012
                7 March 2012
                April 2012
                : 460
                : 4
                : 379-387
                Affiliations
                [1 ]Departments of Pathology and Internal Medicine, Faculty of Medicine, Fukuoka University, Nanakuma 7-45-1, Johnan-ku, Fukuoka, Japan
                [2 ]Pathological Laboratory, National Organization Kokura Hospital, Harugaoko 10-1, Kokura minmi-ku, Kitakyushu, Japan
                [3 ]Pathological Laboratory, Matsuyama Red-Cross Hospital, Bunkyo-cho, 1-1, Matsuyama, Japan
                [4 ]Pathological Laboratory, Nihon Steel Yawata Memorial Hospital, Horunomachi 1-1-1, Yawata nishi-ku, Kitakyushu, Japan
                [5 ]Pathological Laboratory, Kumamoto University Hospital, Honjyo 1-1-1, Kumamoto, Japan
                [6 ]Hematology Laboratory and Pathological Laboratory, National Organization Kyushu Medical Center, Jigyohama 1-8-1, Chuo-ku, Fukuoka, Japan
                [7 ]Pathological Laboratory, Saint Mary Hospital, Tsufukumotomachi 422, Kurume, Japan
                [8 ]Hematology Laboratory, National Organization Kyushu Cancer Center, Notamo 3-1-1, Minami-ku, Fukuoka, Japan
                [9 ]Pathological Laboratory, Kokura Memorial Hospital, Kisencho 1-1, Kokura kita-ku, Kitakyushu, Japan
                [10 ]Pathological Laboratory, Municipal Kitakyushu Medical Center, Bashaku 2-1-1, Kokura kita-ku, Kitakyushu, Japan
                Article
                1199
                10.1007/s00428-012-1199-x
                3320708
                22395482
                bed8122e-e395-4406-9951-81aec80e1397
                © The Author(s) 2012
                History
                : 12 November 2011
                : 8 January 2012
                : 19 January 2012
                Categories
                Original Article
                Custom metadata
                © Springer-Verlag 2012

                Pathology
                autoimmune disease,malignant lymphoma,liver,hcv
                Pathology
                autoimmune disease, malignant lymphoma, liver, hcv

                Comments

                Comment on this article