The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.
A phase 1 study of SU11248 in the treatment of patients with refractory or resistant acute myeloid leukemia (AML) or not amenable to conventional therapy for the disease
Abstract
Fifteen patients with refractory AML were treated in a phase 1 study with SU11248, an oral kinase inhibitor of fms-like tyrosine kinase 3 (Flt3), Kit, vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF) receptors. Separate cohorts of patients received SU11248 for 4-week cycles followed by either a 2- or a 1-week rest period. At the starting dose level of 50 mg (n = 13), no dose-limiting toxicities were observed. The most frequent grade 2 toxicities were edema, fatigue, and oral ulcerations. Two fatal bleedings possibly related to the disease, one from a concomitant lung cancer and one cerebral bleeding, were observed. At the 75 mg dose level (n = 2), one case each of grade 4 fatigue, hypertension, and cardiac failure was observed, and this dose level was abandoned. All patients with FLT3 mutations (n = 4) had morphologic or partial responses compared with 2 of 10 evaluable patients with wild-type FLT3. Responses, although longer in patients with mutated FLT3, were of short duration. Reductions of cellularity and numbers of Ki-67+, phospho-Kit+, phospho–kinase domain–containing receptor–positive (phospho-KDR+), phospho–signal transducer and activator of transcription 5–positive (phospho-STAT5+), and phospho-Akt+ cells were detected in bone marrow histology analysis. In summary, monotherapy with SU11248 induced partial remissions of short duration in acute myeloid leukemia (AML) patients. Further evaluation of this compound, for example in combination with chemotherapy, is warranted.
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Druker, B. J., Talpaz, M., Resta, D. J., Peng, B., Buchdunger, E., Ford, J. M., Lydon, N. B., Kantarjian, H., Capdeville, R., Ohno-Jones, S., et al. (2001) · New England Journal of Medicine · doi:10.1056/nejm200104053441401 · Cited by 5,243
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Self-citationThiede, C., Steudel, C., Mohr, B., Schaich, M., Schäkel, U., Platzbecker, U., Wermke, M., Bornhäuser, M., Ritter, M., Neubauer, A., et al. (2002) · Blood · doi:10.1182/blood.v99.12.4326 · Cited by 1,735
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Activating mutation of D835 within the activation loop of FLT3 in human hematologic malignancies
Yamamoto, Y. (2001) · Blood · doi:10.1182/blood.v97.8.2434 · Cited by 1,150
Schnittger, S., Schoch, C., Dugas, M., Kern, W., Staib, P., Wuchter, C., Löffler, H., Sauerland, C. M., Serve, H., Büchner, T., et al. (2002) · Blood · doi:10.1182/blood.v100.1.59 · Cited by 973
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Self-citationSU11248 is a novel FLT3 tyrosine kinase inhibitor with potent activity in vitro and in vivo
O'Farrell, A.-M., Abrams, T. J., Yuen, H. A., Ngai, T. J., Louie, S. G., Yee, K. W. H., Wong, L. M., Hong, W., Lee, L. B., Town, A., et al. (2003) · Blood · doi:10.1182/blood-2002-07-2307 · Cited by 864
Self-citationCheson, B. D., Cassileth, P. A., Head, D. R., Schiffer, C. A., Bennett, J. M., Bloomfield, C. D., Brunning, R., Gale, R. P., Grever, M. R., & Keating, M. J. (1990) · Journal of Clinical Oncology · doi:10.1200/jco.1990.8.5.813 · Cited by 770
Cited by
Döhner, H., Estey, E. H., Amadori, S., Appelbaum, F. R., Büchner, T., Burnett, A. K., Dombret, H., Fenaux, P., Grimwade, D., Larson, R. A., et al. (2010) · Blood · doi:10.1182/blood-2009-07-235358 · Cited by 3,373
Motzer, R. J., Michaelson, M. D., Redman, B. G., Hudes, G. R., Wilding, G., Figlin, R. A., Ginsberg, M. S., Kim, S. T., Baum, C. M., DePrimo, S. E., et al. (2006) · Journal of Clinical Oncology · doi:10.1200/jco.2005.02.2574 · Cited by 1,634
Self-citationCardiotoxicity associated with tyrosine kinase inhibitor sunitinib
Chu, T. F., Rupnick, M. A., Kerkela, R., Dallabrida, S. M., Zurakowski, D., Nguyen, L., Woulfe, K., Pravda, E., Cassiola, F., Desai, J., et al. (2007) · The Lancet · doi:10.1016/s0140-6736(07)61865-0 · Cited by 1,083
Inhibition of drug-resistant mutants of ABL, KIT, and EGF receptor kinases
Carter, T. A., Wodicka, L. M., Shah, N. P., Velasco, A. M., Fabian, M. A., Treiber, D. K., Milanov, Z. V., Atteridge, C. E., Biggs, W. H., Edeen, P. T., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0504952102 · Cited by 554
Possible molecular mechanisms involved in the toxicity of angiogenesis inhibition
Verheul, H. M. W., & Pinedo, H. M. (2007) · Nature Reviews Cancer · doi:10.1038/nrc2152 · Cited by 503
Metadata
- Authors
- Fiedler, W., Serve, H., Döhner, H., Schwittay, M., Ottmann, O. G., O'Farrell, A.-M., Bello, C. L., Allred, R., Manning, W. C., Cherrington, J. M., Louie, S. G., Hong, W., Brega, N. M., Massimini, G., Scigalla, P., Berdel, W. E., & Hossfeld, D. K.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2005-02-01
- Volume
- 105
- Issue
- 3
- Pages
- 986-993
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2164886552
- Cited by
- 490
- References
- 30
- FWCI
- 34.80
- Type
- journal article
- Language
- en
- Open access
- closed
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- Fiedler, W., Serve, H., Döhner, H., Schwittay, M., Ottmann, O. G., O'Farrell, A.-M., Bello, C. L., Allred, R., Manning, W. C., Cherrington, J. M., Louie, S. G., Hong, W., Brega, N. M., Massimini, G., Scigalla, P., Berdel, W. E., & Hossfeld, D. K. (2005). A phase 1 study of SU11248 in the treatment of patients with refractory or resistant acute myeloid leukemia (AML) or not amenable to conventional therapy for the disease. Blood. https://doi.org/10.1182/blood-2004-05-1846
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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