This site is intended for
Healthcare Professionals only.

For Patients


BCR-ABL interacting with ATP and ADP expressed on a tumor cell diagram

The expression of BCR-ABL fusion protein in tumor cells promotes tumor growth and increases resistance to apoptosis.

  • BCR-ABL is a tyrosine kinase fusion protein, and is the result of the chromosomal translocation that produces the Philadelphia chromosome1
  • BCR-ABL is expressed in tumor cells, and most frequently observed in chronic myelogenous leukemia (CML), acute lymphoblastic leukemia (ALL), and with less frequency (0.5%-3%) in acute myeloid leukemia (AML)2-4
  • BCR-ABL expressing cells have increased DNA damage and genetic aberrations2
    • This is further associated with the generation of genetic instability2
  • BCR-ABL is constitutively active in cancers like CML, ALL and occasionally AML, and converts ATP to ADP4-6
    • BCR-ABL expression promotes tumor cell proliferation and increases their resistance to apoptosis7
    • Preclinical data using a mouse model of CML have shown that BCR-ABL may lead to the premature release of myeloid cells in the bone marrow, further contributing to the pathogenesis of CML8

Get I-O Resources

Order or download
educational tools for your
patients and practice

See all resources

Clinical Trials

Learn more about our
current clinical trials

Learn more


1. Talpaz M, Shah NP, Kantarjian H, et al. Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias. N Engl J Med. 2006;354(24):2531-2541. 2. Burke BA, Carroll M. BCR-ABL: a multi-faceted promoter of DNA mutation in chronic myelogeneous leukemia. Leukemia. 2010;24(6):1105-1112.
3. López-Andrade B, Sartori F, Gutiérrez A, et al. Acute lymphoblastic leukemia with e1a3 BCR/ABL fusion protein. A report of two cases. Exp Hematol Oncol. 2015;5:21. doi:10.1186/s40164-016-0049-y. 4. Neuendorff NR, Burmeister T, Dörken B, Westermann J. BCR-ABL-positive acute myeloid leukemia: a new entity? Analysis of clinical and molecular features. Ann Hematol. 2016;95(8):1211-1221. 5. Hantschel O. Structure, regulation, signaling, and targeting of abl kinases in cancer. Genes Cancer. 2012;3(5-6):436-446. 6. Cuellar S, Vozniak M, Rhodes J, Forcello N, Olszta D. BCR-ABL1 tyrosine kinase inhibitors for the treatment of chronic myeloid leukemia. J Oncol Pharm Pract. 2018;24(6):433-452. 7. Greuber EK, Smith-Pearson P, Wang J, Pendergast AM. Role of ABL family kinases in cancer: from leukaemia to solid tumours. Nat Rev Cancer. 2013;13(8):559-571. 8. Pelletier SD, Hong DS, Hu Y, Liu Y, Li S. Lack of the adhesion molecules P-selectin and intercellular adhesion molecule-1 accelerate the development of BCR/ABL-induced chronic myeloid leukemia-like myeloproliferative disease in mice. Blood. 2004;104(7):2163-2171. 9. La Rosée P, O’Dwyer ME, Druker BJ. Insights from pre-clinical studies for new combination treatment regimens with the Bcr-Abl kinase inhibitor imatinib mesylate (Gleevec/Glivec) in chronic myelogenous leukemia: a translational perspective. Leukemia. 2002;16(7):1213-1219. 10. Mumprecht S, Schürch C, Schwaller J, Solenthaler M, Ochsenbein AF. Programmed death 1 signaling on chronic myeloid leukemia-specific T cells results in T-cell exhaustion and disease progression. Blood. 2009;114(8):1528-1536. 11. Manlove LS, Schenkel JM, Manlove KR, et al. Heterologous vaccination and checkpoint blockade synergize to induce antileukemia immunity. J Immunol. 2016;196(11):4793-4804.