e8a2 BCR–ABL: more frequent than other atypical BCR–ABL variants?
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P. Paschka | G. Martinelli | A. Hochhaus | M. Deininger | S. Demehri | S. Branford | T. Koizumi | L. Lim | B. Schultheis | T. Lange | B. Druker | T. Sugimoto | T. Kegel
[1] J. Melo,et al. BCR-ABL with an e6a2 fusion in a CML patient diagnosed in blast crisis , 2003, Leukemia.
[2] M. Shibuya,et al. The Dbl Homology Domain of BCR Is Not a Simple Spacer in P210BCR-ABL of the Philadelphia Chromosome* , 2001, The Journal of Biological Chemistry.
[3] M. Lemmon,et al. Signal-dependent membrane targeting by pleckstrin homology (PH) domains. , 2000, The Biochemical journal.
[4] R. Collins,et al. Treatment of T prolymphocytic leukemia with allogeneic bone marrow transplantation , 1998, Bone Marrow Transplantation.
[5] M. White,et al. Role of substrates and products of PI 3-kinase in regulating activation of Rac-related guanosine triphosphatases by Vav. , 1998, Science.
[6] J. Melo,et al. The diversity of BCR-ABL fusion proteins and their relationship to leukemia phenotype. , 1996, Blood.
[7] G M Bokoch,et al. Abr and Bcr are multifunctional regulators of the Rho GTP-binding protein family. , 1995, Proceedings of the National Academy of Sciences of the United States of America.
[8] O. Witte,et al. Tyrosine kinase activity and transformation potency of bcr-abl oncogene products. , 1990, Science.
[9] M. Baccarani,et al. Novel types of bcr-abl transcript with breakpoints in BCR exon 8 found in Philadelphia positive patients with typical chronic myeloid leukemia retain the sequence encoding for the DBL- and CDC24 homology domains but not the pleckstrin homology one. , 2002, Haematologica.