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Start Over Author "Steurer, M." Topic chronic lymphocytic leukemia
5 results on '"Steurer, M."'

1. Alemtuzumab in chronic lymphocytic leukemia: final results of a large observational multicenter study in mostly pretreated patients

Author

Fiegl, M., Stauder, R., Steurer, M., Mian, M., Hopfinger, G., Brychtova, Y., Skrabs, C., Zabernigg, A., Schmid, F., Haslbaur, F., Winder, G., Walder, A., Lang, A., Voskova, D., Greil, R., Mayer, J., Gastl, G., and for The Austrian Collaborative Study Group on Alemtuzumab in Chronic Lymphocytic Leukemia, in cooperation with The Czech Leukemia Study Group for Life, CELL

Published
2014
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2. Systematic review of purine analog treatment for chronic lymphocytic leukemia: lessons for future trials

Author

Bauduer, M., Gribben, J., Herrmann, R., Thiel, E., Rai, K., Larson, R., Ferrara, F., Barnard, J., Pearce, H., Taylor, C., Brillant, B., Steurer, M., Weingart, O., Flinn, W., Funkhouser, A., Nallman, M., Sun, Z., Jakšić, Branimir, Suciou, S., Chevret, S., Dighiero, G., Leporrier, M., Frankel, S.R., Sirard, C., Hillmen, P., Trehu, B., Felder, M., Busch, R., Eichorst, B., Mallek, M., Stilgenbauer, S., Pangalis, G., Bezares, R., van Oers, M.H.J., van Putten, W., Gobbi, M., Spriano, M., Mabed, M., Catovsky, D., Richards, S., Wade, R., Abdelhamid, T., Dearden, C., Knauf, W., Blonski, J., Jamroziak, K., Robak, T., Mauro, F., Hiddeman, W., Johnson, S.A., Longthorne, G., Rummel, M.J., Juliusson, G., Pulluqui, P., Zinzani, P.L., Pozzato, G., Reynolds, C, Furman, R.R., Durrant, J., Elphinstone, P., Evans, V., Gettins, .L, Hicks, C., James, S., Clarke, M., MacKinnon, L., McHugh, T.M., Morris, P., Read, S., Gregory, C., Pozzato, Gabriele, Bauduer M, Gribben J, Herrmann R, Thiel E, Rai K, Larson R, Ferrara F, Barnard J, Pearce H, Taylor C, Brillant C, Steurer M, Weingart O, Flinn IW, Funkhouser A, Tallman M, Sun Z, Jaksic B, Suciu S, Chevret S, Dighiero G, Leporrier M, Frankel SR, Sirard C, Hillmen P, Trehu B, Felder M, Busch R, Eichhorst B, Hallek M, Stilgenbauer S, Pangalis G, Bezares R, van Oers MH, van Putten W, Gobbi M, Spriano M, Mabed M, Catovsky D, Richards S, Wade R, Abdelhamid T, Dearden C, Knauf W, Blonski J, Jamroziak K, Robak T, Mauro F, Hiddeman W, Johnson SA, Longthorne G, Juliusson G, Pulluqi P, Zinzani PL, Pozzato G, Oncology US, Reynolds C, Furman RR, Durrant J, Elphinstone P, Evans V, Gettins L, Hicks C, James S, Clarke M, MacKinnon L, McHugh TM, Morris P, Read S, and Gregory C. CLL Trialists’ Collaborative Group

Subjects
Oncology, medicine.medical_specialty, review, Purine analogue, chronic lymphocytic leukemia, fludarabine, clinical trial, Pharmacology, Disease-Free Survival, combination therapy, purine analog, Internal medicine, Antineoplastic Combined Chemotherapy Protocols, Medicine, Humans, Progression-free survival, Cladribine, Antineoplastic Agents, Alkylating, Chlorambucil, business.industry, Hematology, Odds ratio, Leukemia, Lymphocytic, Chronic, B-Cell, Fludarabine, Clinical trial, Treatment Outcome, CLL, cyclophosphamide, Purines, Original Articles and Brief Reports, business, Untreated Chronic Lymphocytic Leukemia, medicine.drug
Abstract

Background. A systematic review of purine analogs revealed heterogeneity between trials in treatment effects on response and progression free survival, but not survival, perhaps partly due to variations in analysis methods. In addition, combination treatments required evaluation. Design and Methods. Individual patient data were sought for all randomized trials in untreated chronic lymphocytic leukemia which involved a purine analog, but not including antibody therapies. Results. Sixteen trials were found, addressing seven comparisons. Eight trials, with 2753 patients, showed that single agent purine analog improved progression free survival (Odds ratio = 0.71; 95% confidence interval =0.63-0.79). Heterogeneity remained substantial. Three trials, with 1403 patients, showed that progression free survival was further improved by the addition of cyclophosphamide (Odds ratio = 0.54; 0.47-0.62). Fewer data were available on the addition of other drugs to purine analog, and none showed clear benefit. Two trials, with 544 patients, suggested cladribine improved progression free survival compared to fludarabine (Odds ratio = 0.77; 0.63-0.95). No differences were seen in overall survival for any comparisons. Conclusions. Purine analogs, particularly combined with cyclophosphamide, significantly improve progression free survival but not survival. Some groups, such as the elderly, may not see the same benefits and maximising doses may be important for all treatments, including chlorambucil. Longer follow-up, consistent definitions and detailed reporting of trials should be encouraged.

Published
2012

3. Actinomycin D induces p53-independent cell death and prolongs survival in high-risk chronic lymphocytic leukemia.

Author

Merkel, O, Wacht, N, Sifft, E, Melchardt, T, Hamacher, F, Kocher, T, Denk, U, Hofbauer, J P, Egle, A, Scheideler, M, Schlederer, M, Steurer, M, Kenner, L, and Greil, R

Subjects
ACTINOMYCIN, CELL death, CHRONIC lymphocytic leukemia, APOPTOSIS, TRANSGENIC mice
Abstract

Chronic lymphocytic leukemia (CLL) is the most prevalent lymphoid malignancy in the elderly of the Western world. Although treatment options have improved over the past two decades, 10-15% of patients still have a poor prognosis and are often resistant to therapy. Aberrations in the p53 pathway, such as a deleted (del17p13) or mutated p53 gene, are highly enriched in this class of patients. In an extensive screen for p53-independent apoptosis inducers, actinomycin D was identified from 1496 substances and shown to induce apoptosis in primary CLL cells derived from high-risk patients including those with aberrant p53, revealing a novel p53-independent mechanism of action. Both pro-survival genes BCL2 and MCL1 are targeted by actinomycin D, in contrast to fludarabine the backbone of current treatment schedules. In the well-established TCL1 transgenic mouse model for high-risk CLL, actinomycin D treatment was more effective in reducing tumor load than fludarabine, with no evidence of resistance after three treatment cycles and an overall survival increase of over 300%. Tumor load reduction was coupled to BCL2 downregulation. Our results identify the clinically approved compound actinomycin D as a potentially valuable treatment option for CLL high-risk patients. [ABSTRACT FROM AUTHOR]

Published
2012
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5. Reduction of complement factor H binding to CLL cells improves the induction of rituximab-mediated complement-dependent cytotoxicity.

Author

Hörl, S, Bánki, Z, Huber, G, Ejaz, A, Windisch, D, Muellauer, B, Willenbacher, E, Steurer, M, and Stoiber, H

Subjects
CANCER cells, CHRONIC lymphocytic leukemia, RITUXIMAB
Abstract

A correction to the article "Reduction of complement factor H binding to CLL cells improves the induction of rituximab-mediated complement-dependent cytotoxicity" by D. Windisch and B. Muellauer that was published in the previous issue.

Published
2013
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