Treatment of sporadic Burkitt lymphoma in adults, a retrospective comparison of four treatment regimens

Oosten, L.; Chamuleau, Martine E.D.; Thielen, Frederick W.; Wreede, L.C. de; Siemes, Claire; Doorduijn, Jeanette K.; Smeekes, Oscar S.; Kersten, Marie José; Hardi, Lizan; Baars, Joke W.; Demandt, Astrid M P; Stevens, Wendy B C; Nijland, Marcel; Imhoff, Gustaaf W. van; Brouwer, Rolf E.; Groot, Carin A. Uyl–de; Kluin, Philippus; Jong, Daphne de; Veelken, Hendrik

doi:10.1007/s00277-017-3167-7

Cited by 36 publications

(38 citation statements)

References 33 publications

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“…The relationship between HIF-1α expression and patient prognosis was examined using the SurvExpress database and show enhanced expression of Survivin and decreased expression of Bim. In Burkitt's lymphoma patients, the melphalan-containing regimen of the Haemato Oncology Foundation for Adults in The Netherlands (HOVON), with 69% of complete response, performed as well as other regimens, such as the French Lymphome Malins B (LMB) regimen and the German Berlin-Frankfurt-Munster (BFM) regimen, but with refractory disease of 21% and relapse rate of 9% [57]. In addition, patients with low Bim expression presented lower complete remission rate (24%) and shorter overall survival, and Burkitt's lymphoma patients with high Survivin expression responded poorly to chemotherapy [58,59].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of HIF-1α contributes to melphalan resistance in multiple myeloma cells by activation of ERK1/2, Akt, and NF-κB

Tsubaki

Takeda

Tomonari

et al. 2019

Laboratory Investigation

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Multiple myeloma (MM) commonly displays multidrug resistance and is associated with poor prognosis. Therefore, it is important to identify the mechanisms by which MM cells develop multidrug resistance. Our previous study showed that multidrug resistance is correlated with overexpression of multidrug resistance protein 1 (MDR1) and Survivin, and downregulation of Bim expression in melphalan-resistant RPMI8226/L-PAM cells; however, the underlying mechanism of multidrug resistance remains unclear. In the present study, we investigated the mechanism of multidrug resistance in melphalan-resistant cells. We found that RPMI8226/L-PAM and ARH-77/L-PAM cells showed increased phosphorylation of extracellular signal-regulated protein kinase 1/2 (ERK1/2) and Akt, and nuclear localization of nuclear factor κB (NF-κB). The combination of ERK1/2, Akt, and NF-κB inhibitors with melphalan reversed melphalan resistance via suppression of Survivin expression and enhanced Bim expression in melphalan-resistant cells. In addition, RPMI8226/L-PAM and ARH-77/L-PAM cells overexpressed hypoxia-inducible factor 1α (HIF-1α) via activation of ERK1/2, Akt, and NF-κB. Moreover, suppression of HIF-1α by echinomycin or HIF-1α siRNA resensitized RPMI8226/L-PAM cells to melphalan through downregulation of Survivin expression and upregulation of Bim expression. These results indicate that enhanced Survivin expression and decreased Bim expression by HIF-1α via activation of ERK1/2, Akt, and NF-κB play a critical role in melphalan resistance. Our findings suggest that HIF-1α, ERK1/2, Akt, and NF-κB inhibitors are potentially useful as anti-MDR agents for the treatment of melphalan-resistant MM.

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Section: Discussionmentioning

confidence: 99%

Overexpression of HIF-1α contributes to melphalan resistance in multiple myeloma cells by activation of ERK1/2, Akt, and NF-κB

Tsubaki

Takeda

Tomonari

et al. 2019

Laboratory Investigation

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“…Patients were regarded as high-risk based on the following features: stage I and abdominal mass or extra-abdominal mass > 10 cm or Ann Arbor stage II-IV. Patients not meeting these criteria were regarded as low-risk [19].…”

Section: Patientsmentioning

confidence: 99%

DA-EPOCH-R is more effective and less toxic than modified CODOX-M/IVAC-R for treating Chinese HIV-infected patients with Burkitt lymphoma: an uncontrolled retrospective clinical trial

Ding¹,

Sun²,

Shen³

et al. 2020

Preprint

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BACKGROUND Burkitt lymphoma (BL), commonly associated with human immuno-deficiency virus (HIV) in China, is an aggressive B-cell lymphoma with a poor prognosis. Current treatments are insufficient and have severe side effects in adult patients with immunodeficiency. METHODS We retrospectively studied HIV-positive patients with untreated BL from December 2011 to June 2019. We compared a low-intensity treatment regimen comprising infused etoposide, doxorubicin, and cyclophosphamide with vincristine, prednisone, and rituximab (dose-adjusted EPOCH-R, study group) and a dose-intensive regimen comprising cyclophosphamide, vincristine, doxorubicin, high-dose methotrexate/ifosfamide, etoposide, high-dose cytarabine, and rituximab (CODOX-M/IVAC-R, control group). Differences in survival outcomes, toxicity, and survival-associated factors were analyzed.RESULTS Twenty-eight consecutive patients were enrolled with integrated clinical data, with 18 patients in the DA-EPOCH-R group and 10 in the modified CODOX-M/IVAC-R group. The median age of patients was 40 years (range: 21–60 years). The median baseline absolute CD4+ cell count was 243.5 cells/µL. All patients had high-risk diseases. Overall, grade 3–4 toxicity was observed at least once in 22 patients. The principal grade 3–4 toxic events, namely leukopenia (100% vs. 50%), febrile neutropenia (90% vs. 22.2%), and thrombocytopenia (80% vs. 16.7%), were significantly higher in the control group than in the study group. One patient in the control group died of septic shock induced by pneumonia. The median follow-up time was 19 months, and the median overall survival (OS) was significantly improved in the study group compared with that in the control group [18.0 months (95% confidence interval [CI], 14.0–22.0 months) vs. 7.9 months (95% CI, 4.8–11.0 months), respectively; P = 0.032]. Treatment with DA-R-EPOCH was a favorable prognostic factor for OS (HR: 0.19 [95% CI: 0.05–0.68]; P = 0.011).CONCLUSIONS DA-EPOCH-R may be an alternative to modified CODOX-M/IVAC-R, with better efficacy and lower toxicity, for treating Chinese patients with high-risk HIV-associated BL.

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“…Chemotherapy presents with a number of side effects, and the prognosis for patients undergoing this treatment is poor. Therefore, the identification of a low-toxic and effective treatment method for Burkitt's lymphoma is urgently required (3,4). Targeted therapy is currently considered to be the best available treatment option.…”

Section: Introductionmentioning

confidence: 99%

Role and mechanism of PTEN in Burkitt's lymphoma

Xin

et al. 2020

Oncol Rep

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The aim of the present study was to explore the possible mechanisms of phosphatase and tensin homolog (PTEN) in the pathogenesis of Burkitt's lymphoma, and provide novel information that can be used in the targeted treatment of this disease. PTEN lentiviral overexpression vector and short-hairpin PTEN silencing vectors were constructed. The effect of PTEN on the growth and proliferation of CA46 and RAJI cells was analyzed using a Cell Counting Kit-8 assay. Apoptosis was detected by Hoechst 33342 and propidium iodide double staining. Flow cytometry was used to analyze the cell cycle. A Transwell chamber was used to detect cell migration and invasion abilities. Western blot analysis was used to detect related protein changes. The mechanism of the effect of PTEN on the biological characteristics of Burkitt's lymphoma cells was subsequently analyzed. The results revealed that PTEN inhibited the proliferation of CA46 and RAJI cells by downregulating the expression of p-AKT, It was indicated that the upregulation of proapoptotic proteins (including Bad and Bax) induced apoptosis, regulated cyclin (including P53, P21, CDK4, CDK6, cyclin D3 and cyclin H) to inhibit cell cycle progression, and mediated epithelial-mesenchymal transition-like cell markers (including E-cadherin, N-cadherin, β-catenin, TCF-8, vimentin, Slug and Snail) to inhibit cell migration and invasion. In conclusion, the tumor-suppressor gene PTEN inhibited the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway and inhibited the proliferation and migration of Burkitt's lymphoma cells, induced apoptosis and cell cycle arrest, thus playing a crucial role in the pathogenesis of Burkitt's lymphoma.

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Treatment of sporadic Burkitt lymphoma in adults, a retrospective comparison of four treatment regimens

Cited by 36 publications

References 33 publications

Overexpression of HIF-1α contributes to melphalan resistance in multiple myeloma cells by activation of ERK1/2, Akt, and NF-κB

Overexpression of HIF-1α contributes to melphalan resistance in multiple myeloma cells by activation of ERK1/2, Akt, and NF-κB

DA-EPOCH-R is more effective and less toxic than modified CODOX-M/IVAC-R for treating Chinese HIV-infected patients with Burkitt lymphoma: an uncontrolled retrospective clinical trial

Role and mechanism of PTEN in Burkitt's lymphoma

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