The Superior Cytotoxicity of Dual Targeting of BCR/ABL and PI3K in K562 Cells: Proposing a Novel Therapeutic Potential for the Treatment of CML
Author:
Funder
Shahid Beheshti University of Medical Sciences
Publisher
Springer Science and Business Media LLC
Subject
Hematology
Link
https://link.springer.com/content/pdf/10.1007/s12288-021-01434-9.pdf
Reference40 articles.
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2. Höglund M, Sandin F, Hellström K, Björeman M, Björkholm M, Brune M et al (2013) Tyrosine kinase inhibitor usage, treatment outcome, and prognostic scores in CML: report from the population-based Swedish CML registry. Blood J Am SocHematol 122(7):1284–1292
3. Chopade P, Akard LP (2018) Improving outcomes in chronic myeloid leukemia over time in the era of tyrosine kinase inhibitors. Clin Lymphoma Myeloma Leuk 18(11):710–723
4. Gesbert F, Sellers WR, Signoretti S, Loda M, Griffin JD (2000) BCR/ABL regulates expression of the cyclin-dependent kinase inhibitor p27Kip1 through the phosphatidylinositol 3-Kinase/AKT pathway. J Biol Chem 275(50):39223–39230
5. Li Q, Wu Y, Fang S, Wang L, Qi H, Zhang Y et al (2015) BCR/ABL oncogene-induced PI3K signaling pathway leads to chronic myeloid leukemia pathogenesis by impairing immuno-modulatory function of hemangioblasts. Cancer Gene Ther 22(5):227–237
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