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==References==
==References==
1. Diekmann D. et al. (1991). Bcr encodes a GTPase-activating protein for p21rac. Nature 35: 400-2. PMID 1903516 DOI: 10.1038/351400a0
1. Drucker, BJ et al. (2001). Activity of a Specific Inhibitor of the BCR-ABL Tyrosine Kinase in the Blast Crisis of Chronic Myeloid Leukemia and Acute Lymphoblastic Leukemia with the Philadelphia Chromosome. NEJM 344:1038-1042 PMID 11287973. DOI: 10.1056/NEJM200104053441402
2. Faderl, S et al. (1999). The Biology of Chronic Myeloid Leukemia. NEJM 341:164-172. PMID 10403855. DOI: 10.1056/NEJM199907153410306
3. Wong S and Witte ON. (2004). The BCR-ABL story: bench to bedside and back. Annu Rev Immunol. 22:247-306. PMID 15032571 DOI: 10.1146/annurev.immunol.22.012703.104753
4. Soverini, S. et al. (2014). Drug resistance and BCR-ABL kinase domain mutations in Philadelphia chromosome-positive acute lymphoblastic leukemia from the imatinib to the second-generation tyrosine kinase inhibitor era: The main changes are in the type of mutations, but not in the frequency of mutation involvement. Cancer 120:1002-9, PMID 24382642 DOI: 10.1002/cncr.28522
5. Drucker, B. J., et al. (2001). Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. New England Journal of Medicine 344, 1031–1037. PMID 11287972 DOI: 10.1056/NEJM200104053441401
6. Greuber, E.K. et al. (2013). Role of ABL family kinases in cancer: from leukaemia to solid tumours. Nat. Rev. Cancer 13: 559–571. PMID 23842646 DOIi: 10.1038/nrc3563
7. Quintás-Cardama, A. and Cortes, J. (2008). Therapeutic Options Against BCR-ABL1 T315I-Positive Chronic Myelogenous Leukemia. Clinical Cancer Research 14: 4392-9. PMID 18628453 DOI: 10.1158/1078-0432.CCR-08-0117
8. Redaelli S. et al. (2009). Activity of bosutinib, dasatinib, and nilotinib against 18 imatinib-resistant BCR/ABL mutants. J Clin Oncol. 27: 469-71. PMID 19075254 DOI: 10.1200/JCO.2008.19.8853
9. Diekmann D. et al. (1991). Bcr encodes a GTPase-activating protein for p21rac. Nature 35: 400-2. PMID 1903516 DOI: 10.1038/351400a0
== Notes ==
== Notes ==
<nowiki>*</nowiki>Primary authors will typically be those that initially create and complete the content of a page. If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the CCGA coordinators (contact information provided on the homepage). Additional global feedback or concerns are also welcome.
<nowiki>*</nowiki>Primary authors will typically be those that initially create and complete the content of a page. If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the CCGA coordinators (contact information provided on the homepage). Additional global feedback or concerns are also welcome.