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A role for deregulated c-Myc expression in apoptosis of Epstein-Barr virus-immortalized B cells. 总被引:10,自引:0,他引:10 下载免费PDF全文
B W Cherney K Bhatia G Tosato 《Proceedings of the National Academy of Sciences of the United States of America》1994,91(26):12967-12971
When deprived of autocrine growth factors, Epstein-Barr virus (EBV)-immortalized B cells stop growing and die. In this study, we show that death of EBV-immortalized cells deprived of autocrine growth factors occurred by apoptosis. Cycloheximide, a protein synthesis inhibitor, inhibited apoptosis, suggesting that de novo protein synthesis is required. Because p53, Bcl-2, and c-Myc were previously implicated in the induction or prevention of apoptosis in other systems, we assessed their possible involvement here. Unlike normal cells that respond to growth factor deprivation by down-regulating c-Myc expression, EBV-immortalized cells continued to express c-Myc, p53, and Bcl-2 at levels comparable to those measured prior to starvation. Consistent with data demonstrating that c-Myc expression is sufficient to drive quiescent cells into the cell cycle, autocrine growth factor-deprived EBV-immortalized cells did not undergo growth arrest but rather continued to proliferate until death, which occurred randomly throughout the cell cycle. In contrast to EBV-immortalized B cells, normal peripheral blood B cells activated in vitro with anti-CD40 monoclonal antibody and interleukin 4 rapidly down-regulated c-Myc expression and underwent growth arrest in response to growth factors and serum deprivation. These findings demonstrated that c-Myc expression is deregulated in EBV-immortalized cells. Addition of antisense oligonucleotides to c-Myc specifically promoted the survival of starved EBV-immortalized cells and suppressed growth of nonstarved EBV-immortalized cells. Thus, deregulated expression of c-Myc in EBV-immortalized cells promotes proliferation and apoptosis following autocrine growth factor deprivation. 相似文献
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J Martín de Pablos M Santano Domínguez A Blanco Yun J Sánchez Calero 《Revista española de enfermedades digestivas》1992,82(3):189-191
We report a case of a primary gastric Burkitt's lymphoma in a 8-year-old child, which first symptoms were abdominal pain, dysphagia, melena and a constitutional syndrome. The differential characteristics of this case are its peculiar gastric infiltration and the existence of oesophageal extension, which is very infrequent among this kind of tumors. 相似文献
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Seung Hyun Lee Hyung Joon Kim Jang Sik Mun Hyoung-Chul Oh Hyun Woong Lee Chang Hwan Choi Jeong Wook Kim Jae Hyuk Do Jae Gyu Kim Sae Kyung Chang Mi Kyung Kim 《Taehan Sohwagi Hakhoe chi》2008,51(4):259-264
Burkitt's lymphoma is a rare disease that belongs to the aggressive non-Hodgkin's lymphoma. Herein, we report a case of primary hepatic Burkitt's lymphoma. A 19-year-old man visited the hospital for right upper quadrant pain. He felt fatigue for two months. Physical examination revealed hepatomegaly and no palpable lymph node. He had no fever, weight loss, or night sweating. Laboratory finding showed mild anemia (hemoglobin, 12.4 g/dL), mild elevated transaminase (ALT, 52 IU/L), elevated lactate dehydrogenase (LDH, 437 IU/L), and alkaline phosphatase (ALP, 129 IU/L). The viral marker was positive for HBsAg, HBeAg, anti-HBs, and anti-HBc (IgG), and negative for anti-HBe, anti-HCV, and anti-HIV. CEA, AFP, and CA19-9 levels were within normal ranges. The HBV DNA quantitation was 1.3 x 10(9) copies/ml. Abdominal-Pelvis CT scan and abdominal MRI finding were compatible with malignant lymphoma. Liver biopsy examination confirmed Burkitt's lymphoma. No metastasis was detected in the thoracic cavity, bone marrow, and spinal fluid. The patient was treated with the combination regimen of cyclophosphamide, doxorubicin, vincristine, prednisone and high dose methotrexate. Cytosine arabinoside and methotrexate were added for CNS prophylaxis by intrathecal installation. Chemotherapy was administered every 3 weeks for fifteen cycles. Serial follow-up CT scan showed a marked decrease in the size of hepatic lesions. Follow-up CT scan and PET-CT scan were performed 4 weeks after the final cycle disclosed no definite residual or active lesion confirming the state of complete remission. 相似文献
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Egi Y Fujimoto H Kondo M Shirota T Hayashi T 《[Rinshō ketsueki] The Japanese journal of clinical hematology》1999,40(2):140-144
We report a case of Burkitt's lymphoma originating in gluteal muscle tissue. A 61-year-old Japanese man was admitted to our hospital due to painful swelling of the left femur and gluteal region in October 1996. A laboratory examination disclosed elevated levels of serum lactate dehydrogenase and soluble interleukin 2 receptor. Gallium scintigraphy demonstrated accumulations in the left femur and gluteal region. Magnetic resonance imaging yielded intense signals and disclosed swelling of muscle tissue in the same region. Pathological examination of biopsy specimens from the left femur revealed a starry-sky pattern, and a chromosomal analysis revealed t(2;8)(p11;q24). Heightened concentrations of antibody for Epstein-Barr virus were not detected. Non-African type Burkitt's lymphoma was diagnosed on the basis of these findings. CHOP therapy and irradiation of the affected region were initially effective, but the disease eventually became resistant to treatment. The patient died of cerebral hemorrhage. As far as we know, this is the first report in Japan of Burkitt's lymphoma originating in muscle tissue. 相似文献
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Schattner EJ; Mascarenhas J; Bishop J; Yoo DH; Chadburn A; Crow MK; Friedman SM 《Blood》1996,88(4):1375-1382
Cytotoxic function of CD4+ Th1 cells is mediated by Fas (CD95, APO-1) and its ligand (Fas ligand). Recent studies using nontransformed B cells and the Ramos Burkitt's lymphoma (BL) B-cell line cells show that CD40 ligation at the B-cell surface by activated, CD40 ligand (CD40L)- bearing, CD4+ T cells upregulates Fas expression on B cells and primes B cells for Fas-mediated death signals. In this work, we examine whether this CD4+ T-cell-dependent molecular pathway for Fas upregulation and B-cell apoptosis reflects a peculiarity of the Ramos B- cell line or is applicable to other Burkitt's tumors as well. In 5 of the 6 Epstein-Barr virus-negative BL cell lines examined, the cells constitutively express undetectable or low levels of Fas and are resistant to Fas-mediated signals induced by monoclonal anti-Fas antibody. All 6 of the BL cell line B cells upregulate Fas in response to CD40 ligation, and in 4 of the cases they become sensitive to Fas- mediated death signals. In one BL cell line, the cells are constitutively sensitive to Fas-mediated cytolysis and are unaffected by CD40 signals. Next, we applied these immunologic manipulations to cells from a refractory clinical sample and observed that the tumor cells could be induced to express Fas and undergo apoptosis in our system. These results establish CD4+ T cells and the Fas-Fas ligand system as important immune regulators of Burkitt's lymphoma B cells and indicate that the susceptibility of tumor cells to Fas-mediated death signals can be modulated by specific activation events at the cell surface. 相似文献
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Regression of experimental Burkitt's lymphoma induced by Epstein-Barr virus-immortalized human B cells 总被引:3,自引:1,他引:3
Tosato G; Sgadari C; Taga K; Jones KD; Pike SE; Rosenberg A; Sechler JM; Magrath IT; Love LA; Bhatia K 《Blood》1994,83(3):776-784
Epstein-Barr virus (EBV)-immortalized human B cells survive only transiently when injected subcutaneously into athymic mice, whereas Burkitt's lymphoma cells give rise to progressively growing subcutaneous tumors. In this study, we tested whether these Burkitt's tumors could be induced to regress via a bystander effect induced by EBV-immortalized B cells. Simultaneous inoculation of EBV-immortalized B cells and Burkitt's lymphoma cells in the same subcutaneous site resulted in tumors that regressed with necrosis and scarring. Similarly, simultaneous inoculation of EBV-immortalized B cells and Burkitt's lymphoma cells in separate subcutaneous sites resulted in regression of a proportion of the Burkitt's tumors. Furthermore, most of the established human Burkitt's tumors regressed with necrosis and scarring after intratumor inoculations with EBV-immortalized B cells. The EBV-immortalized B cells continued to exert this antitumor effect even when killed with irradiation. The experimental approach to Burkitt's lymphoma treatment described here exploits the ability of athymic mice to reject EBV-immortalized B cells to target an effective antitumor response to malignant cells normally incapable of eliciting it. 相似文献
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A clonally distinct recurrence of Burkitt's lymphoma at 15 years 总被引:2,自引:0,他引:2
A human immunodeficiency virus-negative male was successfully treated for two occurrences of Burkitt's lymphoma, 15 years apart. As consolidation of his second remission, he underwent high-dose chemotherapy with peripheral blood stem cell transplantation. In an effort to prove whether the second lymphoma was a relapse of the first or a second primary lymphoma, we obtained paraffin-embedded material from both lymphomas. DNA was extracted from this material and amplified by polymerase chain reaction (PCR) using consensus JH and VH region primers. Analysis of the PCR products, which mostly reflects VDJ joints, showed two sharp bands of different molecular size, proving the monoclonal nature of the lymphomas and suggesting that each had different Ig gene rearrangements. Sequencing of both PCR products showed a marked dissimilarity in nucleotide sequence in the clonally unique VDJ joint region, providing strong evidence for the separate cellular genesis of each lymphoma. These results suggest that late relapses of Burkitt's lymphoma should be examined for clonal distinctiveness. If the second lymphoma is distinct from the primary one, it might be treated as a primary lymphoma rather than as recurrent disease. 相似文献
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Etodolac inhibits EBER expression and induces Bcl-2-regulated apoptosis in Burkitt's lymphoma cells 总被引:6,自引:0,他引:6
Kobayashi M Nakamura S Shibata K Sahara N Shigeno K Shinjo K Naito K Ohnishi K 《European journal of haematology》2005,75(3):212-220
Cyclooxygenase-2 (COX-2) is reported to be an important cellular target for therapy in malignancies. The growth inhibitory effects of COX-2 inhibitors on malignancies have been demonstrated to be through not only COX-2 dependent, but also independent mechanisms. In this study, we showed that etodolac, COX-2 inhibitor, induced apoptosis via COX-2 independent pathway, and investigated the molecular details of etodolac-induced apoptosis in Burkitt's lymphoma cells. In Daudi and Raji Burkitt's lymphoma cell lines, which expressed no COX-2 enzyme, etodolac more strongly induced apoptosis compared to meloxicam. Moreover, etodolac did not induce apoptosis to normal B-lymphocytes. For the pathway of etodolac-induced apoptosis, reduction of anti-apoptotic bcl-2 mRNA and Bcl-2 protein, activation of Caspase-9 and -3, down-regulation of caspase inhibitors, c-IAP-1 and Survivin were involved. Moreover, EBER-1 and -2 expression in Epstein-Barr virus positive Daudi and Raji cells were reduced to result in down-regulation of Bcl-2 by treatment with etodolac. It has been reported that etodolac has stereoisomers, R- and S-etodolac. We found that racemate of etodolac more strongly induced apoptosis in Daudi and Raji cells compared to R- or S-etodolac. In conclusion, our findings indicated etodolac inhibited EBERs expression and induced apoptosis via a Bcl-2-regulated pathway. Moreover, racemate of etodolac more effectively induced apoptosis than R- and/or S-etodolac. Therefore, these activities of etodolac potentially extend to the treatment of patients with Burkitt's lymphoma resistant to chemotherapy. 相似文献
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Zahava Vadasz Tharwat Haj Alexandra Balbir Regina Peri Itzhak Rosner Gleb Slobodin Aharon Kessel Elias Toubi 《Seminars in arthritis and rheumatism》2014