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International journal of hematology 22건

  1. [해외논문]   The pathogenetic role of oncogenes deregulated by chromosomal translocation in B-cell malignancies.  

    Dyer, Martin J S
    International journal of hematology v.77 no.4 ,pp. 315 - 320 , 2003 , 0925-5710 ,

    초록

    Chromosomal translocations involving the immunoglobulin (IG) loci play a pivotal role in the pathogenesis of many subtypes of mature B-cell malignancy. Although all the common IG translocations have been cloned, cloning of rare but nonetheless recurrent translocations continues to allow identification of genes of importance to the development of both normal and malignant B-cells. Clustering of breakpoints within the IG gene segments has allowed development of polymerase chain reaction methods that facilitate cloning. IG translocations result in overexpression of a wide variety of genes ranging from cell surface receptors to transcriptional repressors. Genes recently shown to be involved in such translocations include BCL11A and MALT1. As with the acute leukemias, different translocations in B-cell lymphomas may target different proteins that interact directly. A common endpoint for several translocations is activation of the nuclear factor kappaB pathway. Analysis of the mechanisms of transformation may define new therapeutic strategies.

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  2. [해외논문]   Diffuse large B-cell lymphoma: insights gained from gene expression profiling.  

    Lossos, Izidore S , Levy, Ronald
    International journal of hematology v.77 no.4 ,pp. 321 - 329 , 2003 , 0925-5710 ,

    초록

    Analysis of global gene expression with DNA microarrays has great potential to improve the understanding of tumorigenesis advance tumor diagnosis and classification, and affect cancer treatment. Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin's lymphoma. However, we now realize that the disease is extremely heterogeneous. This review summarizes the progress in understanding DLBCL that has been made as a result of the application of gene expression profiling.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  3. [해외논문]   The molecular basis for the generation of Hodgkin and Reed-Sternberg cells in Hodgkin's lymphoma.  

    Lee, Im-Soon , Kim, Seok Hyung , Song, Hyung Geun , Park, Seong Hoe
    International journal of hematology v.77 no.4 ,pp. 330 - 335 , 2003 , 0925-5710 ,

    초록

    Hodgkin's lymphoma (HL) is a lymphoid neoplasm with a low frequency of malignant tumor cells, known as Hodgkin and Reed-Sternberg (H-RS) cells, in a background of mixed cellular infiltrates. Despite extensive studies on H-RS cells, the molecular mechanisms of their growth and regulation have remained uncertain for a long period. Recently, constitutively activated nuclear factor-kappaB (NF-kappaB) was reported to be a unique and common characteristic of H-RS cells that prevents the cells from undergoing apoptosis. NF-kappaB triggers proliferation and provides a molecular basis for these cells' aberrant growth and cytokine gene expression. In HL pathogenesis associated with Epstein-Barr virus infection, the activation of NF-kappaB is induced by viral latent membrane protein 1 (LMP1). Coupled with recent insights into the molecular mechanisms of activation of NF-kappaB signaling in H-RS cells, this review discusses a linkage between LMP1 and HL via CD99, which has recently been reported to be down-regulated by LMP1 through the NF-kappaB signaling pathway. This down-regulation leads to the generation of cells with H-RS phenotypes related to the clinical and histologic characteristics of HL.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  4. [해외논문]   Immunodeficient mouse models of lymphoid tumors.  

    Imada, Kazunori
    International journal of hematology v.77 no.4 ,pp. 336 - 341 , 2003 , 0925-5710 ,

    초록

    Severe combined immunodeficient (SCID) mice lack functional T- and B-cells and readily accept human xenografts, including hematopoietic malignancies. Accordingly, SCID mice have been used to study the growth and behavior of lymphoid tumors in vivo. The SCID mouse models of disease mimic human diseases and have provided valuable information. However, this mouse strain has some residual immunity that somewhat limits posttransplantation growth of human xenografts. Recently, the SCID mutation was backcrossed onto the nonobese diabetic (NOD) strain background. The result was an animal with additional immunological defects beyond those seen in SCID mice. The NOD/SCID strain appears to be more promising as a tool for xenotransplantation of lymphoid tumors. Moreover, these SCID and NOD/SCID mouse models have been used to develop novel therapeutic strategies. Results from such studies may also help to elucidate the pathogenesis of lymphoid tumors.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  5. [해외논문]   Oxidative stress and the myelodysplastic syndromes.  

    Farquhar, Morag J , Bowen, David T
    International journal of hematology v.77 no.4 ,pp. 342 - 350 , 2003 , 0925-5710 ,

    초록

    The evolution of higher organisms from anaerobic to aerobic living has promoted an elaborate mechanism of defense against potentially toxic oxidants. Many environmental toxicants implicated in the pathogenesis of myelodysplastic syndromes (MDS), including benzene and ionizing radiation, exert toxicity via pro-oxidant mechanisms. The emerging data suggest a probable genetic susceptibility to environmental carcinogenesis through functional polymorphic variants in enzymes that metabolize toxicants and/or protect against oxidative stress. The most studied enzyme is NAD(P)H:quinone oxidoreductase (NQO1). CD34+ cells from individuals homozygous for the NQO1 C609T nonfunctional allelic variant are incapable of enzyme induction following exposure to benzene, thus potentially increasing the hematotoxicity of benzene metabolites. Serologic and molecular markers of oxidative stress are present in many patients with MDS and include an increased concentration of the lipid peroxidation product malondialdehyde and the presence of oxidized bases in CD34+ cells. Potential mechanisms of oxidative stress include mitochondrial dysfunction via iron overload and mitochondrial DNA mutation, systemic inflammation, and bone marrow stromal defects. The biological activity of the antioxidant aminothiol amifostine in vivo suggests that these pathways may be meaningful targets for future therapy in MDS patients.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  6. [해외논문]   Relationship between temperature and apoptosis of human peripheral blood mononuclear cells.  

    Bergman, M , Bessler, H , Salman, H , Djaldetti, M
    International journal of hematology v.77 no.4 ,pp. 351 - 353 , 2003 , 0925-5710 ,

    초록

    To examine the effect of various incubation temperatures on the apoptotic death of human peripheral blood mononuclear cells (PBMC), we incubated cells at 37 degrees C, 22 degrees C, and 4 degrees C for 1 and 24 hours. In addition, cells incubated at 4 degrees C for 3, 6, and 9 hours were rewarmed to 37 degrees C until a total incubation time of 24 hours was reached. The percentage of apoptotic cells was detected by a flow cytometric assay using propidium iodide staining. Incubation of PBMC at the above-mentioned temperatures for 1 hour did not affect the percentage of apoptotic cells. However, incubation at 4 degrees C for 24 hours resulted in the lowest percentage of apoptotic cells compared to those incubated at 22 degrees C and 37 degrees C. Rewarming of the cells to 37 degrees C increased the percentage of apoptotic cells to a level similar to that of the controls (incubated at 37 degrees C). Because PBMC are closely involved in the normal function of the immune system, the results of the study should be considered in cases in which these cells are exposed to various thermal conditions.

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    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  7. [해외논문]   Pure Red Cell Aplasia in a Patient with Trrisomy X Chromosome Abnormality and Reactivated Epstein-Barr Virus Infection  

    Daibata, Masanori , Machida, Hisanori , Nemoto, Yuiko , Taguchi, Hirokuni
    International journal of hematology v.77 no.4 ,pp. 354 - 358 , 2003 , 0925-5710 ,

    초록

    To examine the effect of various incubation temperatures on the apoptotic death of human peripheral blood mononuclear cells (PBMC), we incubated cells at 37 degrees C, 22 degrees C, and 4 degrees C for 1 and 24 hours. In addition, cells incubated at 4 degrees C for 3, 6, and 9 hours were rewarmed to 37 degrees C until a total incubation time of 24 hours was reached. The percentage of apoptotic cells was detected by a flow cytometric assay using propidium iodide staining. Incubation of PBMC at the above-mentioned temperatures for 1 hour did not affect the percentage of apoptotic cells. However, incubation at 4 degrees C for 24 hours resulted in the lowest percentage of apoptotic cells compared to those incubated at 22 degrees C and 37 degrees C. Rewarming of the cells to 37 degrees C increased the percentage of apoptotic cells to a level similar to that of the controls (incubated at 37 degrees C). Because PBMC are closely involved in the normal function of the immune system, the results of the study should be considered in cases in which these cells are exposed to various thermal conditions.

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  8. [해외논문]   Pure red cell aplasia in a patient with trisomy X chromosome abnormality and reactivated Epstein-Barr virus infection.  

    Daibata, Masanori ; Machida, Hisanori ; Nemoto, Yuiko ; Taguchi, Hirokuni
    International journal of hematology v.77 no.4 ,pp. 354 - 358 , 2003 , 0925-5710 ,

    초록

    We describe a woman with a congenital chromosome anomaly, 47,XXX, who developed chronic pure red cell aplasia (PRCA). The patient had serologic reactivity consistent with that of reactivated Epstein-Barr virus (EBV) infection, as judged by high titers for anti-EBV viral capsid antigen (VCA) immunoglobulin G (IgG) and anti-early antigen (EA) IgG. Detection of EBV genome in peripheral blood cells and cell-free serum also supported the diagnosis. Although EBV infection has been implicated in the pathogenesis of acute PRCA, the viral infection rarely results in a chronic disease state. So far, only 1 case of EBV-associated chronic PRCA has been reported, to the best of our knowledge. Chronic PRCA also is known to occur on an autoimmune basis. Individuals carrying an extra X chromosome, such as XXY and XXX, are prone to development of immune abnormalities. Our patient had an anti-DNA autoantibody and a positive result of the direct Coombs test. The pathogenesis of PRCA in this case seemed to involve multiple factors. In addition to the infectious agent, host factors may have played a role. Although the etiologic link between chronic PRCA and trisomy X remains to be elucidated, our findings suggest the importance of karyotype analysis as well as search for infectious agents in patients with chronic PRCA.

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    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  9. [해외논문]   Expression of apoptosis-associated protein RCAS1 in macrophages of histiocytic necrotizing lymphadenitis.  

    Abe, Yasunobu , Ohshima, Koichi , Nakashima, Manabu , Hara, Keiichi , Matsushima, Takamitsu , Choi, Ilseung , Nishimura, Junji , Kikuchi, Masahiro , Nawata, Hajime , Watanabe, Takeshi , Muta, Koichiro
    International journal of hematology v.77 no.4 ,pp. 359 - 363 , 2003 , 0925-5710 ,

    초록

    Receptor-binding cancer antigen expressed on SiSo cells (RCAS1), which is recognized by the 22-1-1 monoclonal antibody (MoAb) against human uterine adenocarcinoma cell line SiSo, has been identified on various kinds of cancer cells. RCAS1 appears to be an apoptosis-associated protein that induces apoptosis in activated T-cells and erythroid progenitor cells. We previously demonstrated that monocytes/macrophages express RCAS1. In the present study, we investigated RCAS1 expression by 22-1-1 MoAb in histiocytic necrotizing lymphadenitis (HNL), which is characterized by necrotic lesions consisting of T-cells undergoing apoptosis and macrophages in proliferation. Expression of RCAS1 was analyzed by immunohistochemical staining in 9 cases of HNL and in 9 cases of reactive lymphadenitis used as a control. The ratio of RCAS1+ cells to CD68+ cells (monocytes/macrophages) was significantly higher in the patients with HNL than in the patients with reactive lymphadenitis (P = .0002; paired t test). Our findings suggest that RCAS1 expressed on macrophages may play an important role in the induction of activated T-cell apoptosis in cases of HNL.

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    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  10. [해외논문]   Constitutive activation of extracellular signal-regulated kinase and p38 mitogen-activated protein kinase in B-cell lymphoproliferative disorders.  

    Ogasawara, Toshie , Yasuyama, Masako , Kawauchi, Kiyotaka
    International journal of hematology v.77 no.4 ,pp. 364 - 370 , 2003 , 0925-5710 ,

    초록

    Signaling molecules such as p21(ras) (Ras), mitogen-activated protein kinase (MAPK), and Akt kinase play pivotal roles in the proliferation and survival of lymphoid cells in response to many kinds of stimulation. It is not fully understood, however, how these molecules participate in the growth of malignant lymphoid cells. We determined whether Ras, MAPKs such as extracellular signal-regulated kinase (ERK), c-Jun amino-terminal kinase (JNK), and p38 MAPK, and Akt kinase are activated in B-cell tumors, including acute lymphoblastic leukemia, chronic lymphocytic leukemia, Burkitt-like lymphoma, diffuse large B-cell lymphoma, and plasma cell leukemia. We found that Lyn protein tyrosine kinase was constitutively phosphorylated on tyrosine, and that ERK and p38 MAPK were constitutively active in all cases of the B-cell tumor. In contrast, activation of Ras and Akt kinase was found in limited cases, and JNK kinase activity was not observed in any case. These results suggest that ERK and p38 play roles in the oncogenesis of B-cell tumors.

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