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International journal of hematology 25건

  1. [해외논문]   Pathogenesis of thrombosis in patients with malignancy.  

    Falanga, A , Donati, M B
    International journal of hematology v.73 no.2 ,pp. 137 - 144 , 2001 , 0925-5710 ,

    초록

    Cancer cells can contribute to activation of the clotting system by their capacity to produce and release procoagulant/fibrinolytic substances and inflammatory cytokines, and by their interaction with host cells (endothelial, monocytes, platelets, and neutrophils). Moreover, anticancer drugs (chemotherapy/hormone therapy) may greatly affect the risk of thromboembolic complications in cancer patients by similar mechanisms, eg, through the release of procoagulants by tumor cells, through endothelial damage, or stimulation of tissue factor production by host cells. The interactions between cancer/metastatic processes and thrombosis have been reviewed here from the pathogenetic viewpoint. We hope that better knowledge of these pathogenetic pathways will lead to the development of more targeted strategies to prevent thromboembolism in cancer patients.

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  2. [해외논문]   The role of the hemostatic system in tumor growth, metastasis, and angiogenesis: tissue factor is a bifunctional molecule capable of inducing both fibrin deposition and angiogenesis in cancer.  

    Rickles, F R , Shoji, M , Abe, K
    International journal of hematology v.73 no.2 ,pp. 145 - 150 , 2001 , 0925-5710 ,

    초록

    Cancer patients are prone to venous thromboembolism (VTE), and this hypercoagulability favors tumor growth and metastasis. After a brief review of the clinical aspects of VTE and cancer, we discuss the pathogenesis of hypercoagulability with an emphasis on the role of tissue factor (TF). The discovery that, in addition to tumor cells, TF is expressed by tumor-associated macrophages and tumor-associated endothelial cells led to studies of the role of TF in the regulation of tumor angiogenesis. In human lung cancer, melanoma, and breast cancer, TF and vascular endothelial growth factor (VEGF) co-localize in tumor cells; a close correlation exists between TF and VEGF synthesis (P = .001) in tumor cell lines and with angiogenesis in vivo in a severe, combined immunodeficient mouse model. Transfection of a TF/VEGF low-producing human tumor cell line with full length TF complementary DNA (cDNA) results in conversion to a high producer of TF and VEGF; transfection of a deletion-mutant TF cDNA lacking cytoplasmic serine residues restores full TF procoagulant activity but not VEGF synthesis to the cells. These results suggest that the cytoplasmic tail of TF is necessary for tumor cell VEGF synthesis. Targeting of TF in tumors and tumor-associated blood vessels is discussed as a strategy for drug delivery and rational anti-cancer and anti-angiogenesis drug design.

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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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  3. [해외논문]   Hemostatic changes in patients with malignancy.  

    Goldsmith, G H
    International journal of hematology v.73 no.2 ,pp. 151 - 156 , 2001 , 0925-5710 ,

    초록

    Alterations of hemostasis commonly accompany the progression of malignant disease and every known component of the hemostatic mechanism may be affected by this disease process. Nearly all patients with an active neoplasm will exhibit at least subtle biochemical changes in hemostasis, and a minority of these patients will also develop clinical thrombosis or hemorrhage. In this paper, we will review intravascular coagulation and fibrinolysis, thrombocytopenia, and thrombocytosis, as well as more rare thrombotic and hemorrhagic events resulting from the direct interactions of neoplasms, or of their products, with the individual elements of hemostatic mechanisms. Thrombotic and hemorrhagic events resulting from the induction of autoimmune or thrombotic microangiopathic syndromes are also discussed. This review focuses on the clinical thrombotic and bleeding syndromes that may occur as a result of this interaction between neoplasia and hemostasis.

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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]   Treatment of cancer with anticoagulants: rationale in the treatment of melanoma.  

    Ornstein, D L , Zacharski, L R
    International journal of hematology v.73 no.2 ,pp. 157 - 161 , 2001 , 0925-5710 ,

    초록

    The blood coagulation mechanism regulates the growth and dissemination of malignancy by multiple mechanisms, and anticoagulant drugs have been shown to inhibit the progression of certain cancers. Although progress has been slow, there is ample information on the effects of anticoagulants in various tumors that suggests that the use of anticoagulants has considerable potential in the treatment of some cancers. For example, melanoma is one of a small number of human tumor types in which the tumor is associated with an intact coagulation pathway leading to thrombin generation and conversion of fibrinogen to fibrin in situ immediately adjacent to viable tumor cells. Observations in experimental models combined with the limited clinical trial data on this subject suggest that inhibition of tumor cell thrombin generation may improve outcomes in melanoma cases. Thus, we postulate that pharmacological interruption of the tumor cell-associated coagulation pathway at any one step or even at multiple levels might constitute effective therapy for this disease. Drugs that block the activity of tissue factor, factor Xa, or thrombin are available for clinical testing and, if effective, offer the prospect of a relatively nontoxic, novel treatment for this aggressive tumor.

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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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  5. [해외논문]   Clinical gene therapy in hematology: past and future.  

    Richter, J , Karlsson, S
    International journal of hematology v.73 no.2 ,pp. 162 - 169 , 2001 , 0925-5710 ,

    초록

    Gene transfer into hematopoietic cells using viral vectors has focused mostly on lymphocytes and hematopoietic stem cells (HSCs). HSCs have been considered particularly important as target cells because of their pluripotency and ability to reconstitute hematopoiesis after myeloablation and transplantation. HSCs are believed to have the ability to live a long time, perhaps a lifetime, in the recipient following bone marrow transplantation. Genetic correction of HSCs can therefore potentially last a lifetime and permanently cure hematologic disorders in which genetic deficiencies cause the pathology. Oncoretroviral vectors have been the main vectors used for HSCs because of their ability to integrate into the chromosomes of their target cells. Gene-transfer efficiency of murine HSCs is high using oncoretroviral vectors. In contrast, gene-transfer efficiency using the same viral vectors to transduce human HSCs or HSCs from large animals has been much lower. Although these difficulties may have several causes, the main reason for the low efficiency of human HSC transduction with oncoretroviral vectors is probably because of the nondividing nature of HSCs. Murine HSCs can be easily stimulated to divide in culture, whereas it is more problematic to stimulate human HSCs to divide rapidly in vitro. Because oncoretroviral vectors require dividing target cells for successful nuclear import of the preintegration complex and subsequent integration of the provirus, only the dividing fraction of the target cells can be transduced. This review focuses on gene transfer into human hematopoietic cells, particularly human HSCs. We review the clinical studies that have been reported, including the recent successful gene therapy for X-linked severe combined immunodeficiency. We discuss how the gene-transfer efficiency of human HSCs can be improved using oncoretroviral and lentiviral vectors.

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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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  6. [해외논문]   The pathogenesis of chronic myeloproliferative diseases.  

    Tefferi, A
    International journal of hematology v.73 no.2 ,pp. 170 - 176 , 2001 , 0925-5710 ,

    초록

    Chronic myeloproliferative disorders are operationally classified to include essential thrombocythemia, polycythemia vera, and agnogenic myeloid metaplasia. In most cases, clonal hematopoiesis, involving all 3 myeloid lineages, can be demonstrated. However, the underlying molecular lesions that are responsible for disease initiation and progression remain elusive. There are ongoing efforts to clarify the pathogenetic role of cytokines, bone marrow stromal cells and molecules, and intracellular aberrations in either signal transduction or apoptosis. This review discusses some of the current and past observations regarding the pathogenesis of chronic myeloproliferative disorders.

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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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  7. [해외논문]   Wilms' tumor gene WT1: its oncogenic function and clinical application.  

    Sugiyama, H
    International journal of hematology v.73 no.2 ,pp. 177 - 187 , 2001 , 0925-5710 ,

    초록

    The Wilms' tumor gene WT1 is a gene responsible for the childhood renal tumor. Wilms' tumor, and is defined as a tumor suppressor gene. However, the wild-type WT1 gene is highly expressed in leukemic blast cells of myeloid and lymphoid origin, and thus, WT1 messenger RNA provides a novel tumor marker for detection of minimal residual disease of leukemias and for monitoring disease progression of myelodysplastic syndromes. The WT1 gene exerts an oncogenic function rather than a tumor-suppressor gene function in solid tumors as well as leukemias, and the WT1 gene product is an attractive tumor antigen capable of eliciting cytotoxic T lymphocytes against WT1-expressing tumors.

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  8. [해외논문]   Detection of red blood cell-bound immunoglobulin G by flow cytometry and its application in the diagnosis of autoimmune hemolytic anemia.  

    Wang, Z , Shi, J , Zhou, Y , Ruan, C
    International journal of hematology v.73 no.2 ,pp. 188 - 193 , 2001 , 0925-5710 ,

    초록

    Detection of autoantibodies to erythrocytes is of fundamental importance in the diagnosis of autoimmune hemolytic anemia (AIHA). The routinely used direct antiglobulin test (DAT) has the disadvantage of low sensitivity. In this study, we investigated the optimal test conditions of measurement of red blood cell (RBC)-bound immunoglobulin (Ig) G by flow cytometry (FCM). We studied 64 patients with AIHA, 30 anemic patients diagnosed with other diseases, and 36 healthy individuals. In 33 AIHA patients who were found to have RBC-bound IgG, both the mean fluorescence intensity (MFI) and percentage of fluorescence-activated RBCs were remarkably increased and results of both were considered positive. In the remaining 31 AIHA patients who had positive results for RBC-bound complement C3d, the MFI and the percentage of fluorescence-activated RBCs was also increased and 17 patients (54.8%) were considered to have a positive result by this method. In anemic patients with negative DATs the results of FCM were always negative. These results could be confirmed by enzyme-linked immunosorbent assay (ELISA), and the values obtained by FCM and ELISA corresponded to titration scores of the DAT. Additionally, in 3 of the other 8 patients who were suspected to have DAT-negative AIHA, RBC-bound IgG was detected by FCM and ELISA. Our investigation demonstrates that FCM is a precise, reliable, and sensitive method of detecting RBC-bound autoantibodies and could be used as a new routine diagnostic technique for AIHA and other immune hemolytic anemias.

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

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  9. [해외논문]   Primary chronic myelofibrosis: clinical and prognostic evaluation in 336 Japanese patients.  

    Okamura, T , Kinukawa, N , Niho, Y , Mizoguchi, H
    International journal of hematology v.73 no.2 ,pp. 194 - 198 , 2001 , 0925-5710 ,

    초록

    We retrospectively analyzed 336 patients with primary chronic myelofibrosis from 203 medical institutes in Japan. Notwithstanding their heterogeneous treatments, the median survival in 298 patients that could be evaluated was 10.0 years. Average age at onset was 60.7 years. Men were affected 1.4 times more frequently than women. The factors associated with shorter survival included anemia, leukocytosis/leukocytopenia, thrombocytopenia, and increased blasts in the peripheral blood, and sex (male), age (>60), and the presence of symptoms. A new scoring system based on the peripheral blood findings (hemoglobin [Hb] level, platelet count, and rate of blast formation) at initial diagnosis clearly correlated with survival rate. Accordingly, patients could be categorized into 3 groups by severity grading. Through stepwise multivariate survival analysis, the significant prognostic factors were identified as the severity grading based on the new scoring system (P = .0002), age (P = .0024), sex (P = .0153), and Hb (P = .0198). Chromosomal abnormalities were found in 58 of 154 patients (38%), although these did not influence survival.

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  10. [해외논문]   Effect of granulocyte colony-stimulating factor on chemotherapeutic activity of cytosine arabinoside in acute leukemic cell lines.  

    Cha, K E , Yoon, S Y , Lee, K N
    International journal of hematology v.73 no.2 ,pp. 199 - 205 , 2001 , 0925-5710 ,

    초록

    Recent studies have shown the presence of receptors for granulocyte colony-stimulating factor (G-CSF) on lymphoid leukemic cells. To determine the effect of G-CSF on chemotherapeutic activity of cytosine arabinoside (Ara-C) on lymphoid as well as myeloid leukemic cells, we evaluated cell counts, apoptosis, and growth inhibition in HL-60, KG-1, Molt-4, Jijoye, and CCRF-CEM cell lines after incubation with Ara-C (0.1 and 1 micromol/L) and/or 5 ng/mL G-CSE G-CSF potentiated the effect of Ara-C on 2 of 3 lymphoid leukemic cell lines (Molt-4 and Jijoye), whereas it decreased the apoptosis and the effect of Ara-C on myeloid cell lines (HL-60 and KG-1).

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