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Lymphoma Development (lymphoma + development)
Selected AbstractsAutoimmune and inflammatory disorders and risk of malignant lymphomas , an updateJOURNAL OF INTERNAL MEDICINE, Issue 6 2008K. E. Smedby Abstract. As specific autoimmune disorders now constitute established risk factors for malignant lymphomas, we describe this association. We review reported risk levels, risk determinants, lymphoma subtypes and biological mechanisms in autoimmunity/inflammation, emphasizing on recent findings. Whilst numerous reports describe average lymphoma risks in large patient groups, there's a recent shift of focus to risk determinants and the role of inflammatory activity. Studies highlight associations with diffuse large B-cell lymphoma, apart from lymphoma development in target organs of inflammation. Future studies of high-risk patient subsets using detailed assessments of autoimmunity/inflammation and lymphoma may give important clues to lymphomagenesis. [source] Do rheumatoid arthritis and lymphoma share risk factors?: A comparison of lymphoma and cancer risks before and after diagnosis of rheumatoid arthritisARTHRITIS & RHEUMATISM, Issue 5 2010Karin Hellgren Objective Patients with rheumatoid arthritis (RA), in particular those with the most severe disease, are at increased risk of developing malignant lymphoma. Whether this increase is entirely a consequence of the RA disease and/or its treatment or is reflective of shared susceptibility to the two diseases remains unclear. We undertook this study to assess whether patients with RA are already at increased risk of lymphoma or of other cancers before the diagnosis of RA, and if the relative risk increases with time since RA diagnosis. Methods Patients with incident RA (symptom duration <1 year) (n = 6,745) registered in the Swedish Early Arthritis Registry from 1997 through 2006 were identified. For each patient, 5 general population controls were randomly matched by sex, age, marital status, and residence (n = 33,657). For all study subjects, inclusion in the nationwide Swedish Cancer Register in 1958,2006 was determined. Relative risks (RRs) (with 95% confidence intervals [95% CIs]) of lymphoma and of cancer overall, before and after diagnosis of RA, were estimated using conditional logistic regression and Cox regression, respectively. Results Before diagnosis of RA, there was no observed increase in the risk of lymphoma (RR [odds ratio] 0.67 [95% CI 0.37,1.23]) or other cancers (RR 0.78 [95% CI 0.70,0.88]). During the first 10 years following diagnosis of RA, the overall RR (hazard ratio) of lymphoma development was 1.75 (95 % CI 1.04,2.96). Conclusion These findings indicate that overall, a history of cancer, including lymphoma, does not increase the risk of subsequent RA development. Shared susceptibility to RA and lymphoma may thus be of limited importance. In contrast, increased lymphoma risks were observed within the first decade following RA diagnosis. [source] Tumor necrosis factor antagonist therapy and lymphoma development: Twenty-six cases reported to the Food and Drug Administration,ARTHRITIS & RHEUMATISM, Issue 12 2002S. Lori Brown PhD Objective Etanercept and infliximab are tumor necrosis factor (TNF) antagonists that have been recently approved for the treatment of rheumatoid arthritis (RA) and Crohn's disease (CD). This study was undertaken to investigate the occurrence of lymphoproliferative disorders in patients treated with these agents. Methods Relevant data in the MedWatch postmarket adverse event surveillance system run by the US Food and Drug Administration were reviewed. Results We identified 26 cases of lymphoproliferative disorders following treatment with etanercept (18 cases) or infliximab (8 cases). The majority of cases (81%) were non-Hodgkin's lymphomas. The interval between initiation of therapy with etanercept or infliximab and the development of lymphoma was very short (median 8 weeks). In 2 instances (1 infliximab, 1 etanercept), lymphoma regression was observed following discontinuation of anti-TNF treatment, in the absence of specific cytotoxic therapy directed toward the lymphoma. Conclusion Although data from a case series such as this cannot establish a clear causal relationship between exposure to these medications and the risk of lymphoproliferative disease, the known predisposition of patients with RA and CD to lymphoma, the known excess of lymphoma in other immunosuppressed populations, and the known immunosuppressive effects of the anti-TNF drugs provide a biologic basis for concern and justification for the initiation of additional epidemiologic studies to formally evaluate this possible association. [source] Diversity of genome profiles in malignant lymphomaCANCER SCIENCE, Issue 3 2010Masao Seto (Cancer Sci 2010; 101: 573,578) Characteristic chromosome translocations are associated with specific disease entities, and are known to play a pivotal role in lymphoma development. Chromosome translocation alone, however, is not sufficient to produce tumors. Factors including the microenvironment and epigenetic and genetic alterations other than chromosome translocations have been shown to play a role in lymphoma development. Follicular lymphoma cells proliferate in close contact with follicular dendritic cells. Mucosa-associated lymphoid tissue (MALT) lymphoma cells proliferate at the marginal zone area of reactive follicles which are formed by preceding chronic inflammation. The importance of genetic alterations other than chromosome translocation has been recognized since the introduction of array comparative genomic hybridization (array CGH). Variations in the genomic profile among patients with the same disease entity have been found by array CGH analyses. These variations indicate that multiple genetic pathways leading to the development of lymphomas may exist and hence result in the variable clinicopathological features observed. [source] Immunity against mouse thymus-leukemia antigen (TL) protects against development of lymphomas induced by a chemical carcinogen, N -butyl- N -nitrosoureaCANCER SCIENCE, Issue 11 2004Kunio Tsujimura Mouse thymus-leukemia antigens (TL) are aberrantly expressed on T lymphomas in C57BL/6 (B6) and C3H/He (C3H) mice, while they are not expressed on normal T lymphocytes in these strains. When N -butyl- N -nitrosourea (NBU), a chemical carcinogen, was administered orally to B6 and C3H strains, lymphoma development was slower than in T3b -TL gene-transduced counterpart strains expressing TL ubiquitously as self-antigens, suggesting that anti-TL immunity may play a protective role. In addition, the development of lymphomas was slightly slower in C3H than in B6, which seems to be in accordance with the results of skin graft experiments indicating that both cellular and humoral immunities against TL were stronger in C3H than B6 mice. The interesting finding that B lymphomas derived from a T3b -TL transgenic strain (C3H background) expressing a very high level of TL were rejected in C3H, but not in H-2Kb transgenic mice (C3H background), raises the possibility that TL-specific effector T cell populations are eliminated and/or anergized to a certain extent by interacting with H-2Kb molecules. [source] Genetic and epigenetic factors involved in B-cell lymphomagenesisCANCER SCIENCE, Issue 9 2004Masao Seto Malignant lymphomas have been classified by the WHO into disease categories based not only on histological features, but also on cell surface markers, cytogenetic and clinical features. It is known that chromosome translocation plays an important role in lymphoma development, but it is not entirely clear yet why a given type of chromosome translocation is associated with a specific type of lymphoma. This review deals with molecular mechanisms of B-cell lymphoma development in association with chromosome translocations. The outcome of chromosome translo-cations can be categorized into three factors: enhancement of proliferation, inhibition of differentiation and anti-apoptotic activity. It is well known that chromosome translocation by itself cannot cause cells to become malignant because it is only one of the growth advantages leading to malignancy, while additional genetic and epigenetic alterations are required for cells to become fully malignant. Mucosa-associated lymphoid tissue (MALT) lymphomas of the stomach are unique in that a majority can be cured by Helicobacter pylori eradication, although 20 to 30% remain resistant. Others as well as we have demonstrated that the presence of the API2-MALT1 chimeric gene correlates well with resistance to H. pylori eradication treatment. These characteristics have led to the speculation that the classification of MALT lymphoma falls somewhere between tumor and inflammation. Although MALT lymphoma seems to have unique features in comparison with other types of B-cell lymphomas, it shares common molecular mechanisms with B-cell lymphoma development. [source] | ||||||||||