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Ph+ CML Information
Ph+ CML Treatment Goals
Ongoing Management and Monitoring

Ph+ CML INFORMATION

Ph+ CML is a disease of BCR-ABL

Ph+ CML is a myeloproliferative disease characterized by the presence of the abnormal Philadelphia chromosome in hematopoietic stem cells.1

The Philadelphia chromosome results from a reciprocal translocation of sections of chromosomes 9 and 22.1,2 This translocation fuses portions of the BCR and ABL genes, resulting in the BCR-ABL oncogene that encodes the BCR-ABL fusion protein.2 This protein possesses a constitutively active tyrosine kinase domain, which promotes cell proliferation, suppresses apoptosis, and diminishes cell adhesion.2,3 Evidence confirms that this unregulated activity of the Abl tyrosine kinase in BCR-ABL is the cause of Ph+ CML. For this reason, the BCR-ABL tyrosine kinase domain remains ideal for a targeted therapeutic approach.4

To see a video demonstrating the role of BCR-ABL in Ph+ CML, visit TASIGNA mechanism of action.

Keeping patients in the chronic phase is vital5

Survival after progression to AP/BC in ENESTnd (N=846)5*
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*All patients were followed for survival and progression after study drug discontinuation.

As the ENESTnd study demonstrated, the median survival of patients who progressed to AP/BC was only 10.5 months, illustrating the importance of maintaining Ph+ CML patients in the chronic phase.


References:
1. Faderl S, Talpaz M, Estrov Z, O’Brien S, Kurzrock R, Kantarjian HM. The biology of chronic myeloid leukemia. N Engl J Med. 1999;341(3):164-172.
2. Sawyers CL. Chronic myeloid leukemia. N Engl J Med. 1999;340(17):1330-1340.
3. Ren R. Mechanisms of BCR-ABL in the pathogenesis of chronic myelogenous leukaemia. Nat Rev Cancer. 2005;5(3):172-183.
4. Hughes T, Branford S. Molecular monitoring of BCR–ABL as a guide to clinical management in chronic myeloid leukaemia. Blood Rev. 2006;20(1):29-41.
5. Larson RA, Hochhaus A, Hughes TP, et al. Nilotinib vs imatinib in patients with newly diagnosed Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase: ENESTnd 3-year follow-up. Leukemia. 2012;26(10):2197-2203.
6. Weisberg E, Manley PW, Cowan-Jacob SW, Hochhaus A, Griffin JD. Second generation inhibitors of BCR-ABL for the treatment of imatinib-resistant chronic myeloid leukaemia. Nat Rev Cancer. 2007;7(5):345-356.
7. TASIGNA® (nilotinib) Summary of Product Characteristics. Basel, Switzerland: Novartis Pharma AG; September 2012.

TASIGNA Interactive Game

To see how TASIGNA is an optimized BCR-ABL inhibitor that was designed to improve on imatinib, go to TASIGNA mechanism of action6

ENESTnd showed that TASIGNA significantly reduces progression to AP/BC vs imatinib in patients with newly diagnosed Ph+ CML7