Bosutinib for the treatment of chronic myeloid leukemia

Doan, Vi; Wang, Alice; Prescott, Hillary

doi:10.2146/ajhp140221

Cited by 16 publications

(10 citation statements)

References 29 publications

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“…Bosutinib is a dual inhibitor of Abl and Src kinases [ 100 , 101 ]. Bosutinib has a high anti-proliferative activity, can inhibit the proliferation and survival of CML cells [ 102 ]. It can inhibit the activity of CML graft in vivo, making K562 tumor transplant cells subsided in nude mice.…”

Section: Tkis Biologymentioning

confidence: 99%

Advances in studies of tyrosine kinase inhibitors and their acquired resistance

et al. 2018

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Protein tyrosine kinase (PTK) is one of the major signaling enzymes in the process of cell signal transduction, which catalyzes the transfer of ATP-γ-phosphate to the tyrosine residues of the substrate protein, making it phosphorylation, regulating cell growth, differentiation, death and a series of physiological and biochemical processes. Abnormal expression of PTK usually leads to cell proliferation disorders, and is closely related to tumor invasion, metastasis and tumor angiogenesis. At present, a variety of PTKs have been used as targets in the screening of anti-tumor drugs. Tyrosine kinase inhibitors (TKIs) compete with ATP for the ATP binding site of PTK and reduce tyrosine kinase phosphorylation, thereby inhibiting cancer cell proliferation. TKI has made great progress in the treatment of cancer, but the attendant acquired acquired resistance is still inevitable, restricting the treatment of cancer. In this paper, we summarize the role of PTK in cancer, TKI treatment of tumor pathways and TKI acquired resistance mechanisms, which provide some reference for further research on TKI treatment of tumors.

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Section: Tkis Biologymentioning

confidence: 99%

Advances in studies of tyrosine kinase inhibitors and their acquired resistance

et al. 2018

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“…Bosutinib is effective in most imatinib-resistant mutations except T315I and V299L [3]. Bosutinib also demonstrated confirmed CHR (50%-83%) and MCyR (14%-67%) in baseline mutations associated with clinical resistance to dasatinib (F317L) and nilotinib (Y253H and F359C/I/V) [2].…”

Section: Introductionmentioning

confidence: 88%

“…Bosutinib is primarily metabolized by cytochrome P-450 isoenzyme 3A4; therefore concomitant use of strong or moderate CYP3A4 inhibitors and inducers should be avoided [3]. Concomitant use of PPI is not recommended in patients receiving bosutinib.…”

Section: Pharmacokinetic Datamentioning

confidence: 99%

The Efficacy and Safety of Bosutinib in Chronic Myeloid Leukemia

Hamed¹

2018

CTOIJ

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“…Dasatinib increases expression of inhibitory KIR2DL1 receptors that can suppress NK cell toxicity against CML cells [ 164 ]. Similar to dasatinib, bosutinib inhibits BCR-ABL1 and SRC family kinases, while is minimally active against KIT and PDGFR [ 165 ] . Radotinib (RAD) is also a novel potent second-generation TKI with high inhibitory capacity for the BCR-ABL1 oncoprotein [ 166 ].…”

Section: Therapeutic Implications Of CML Lscsmentioning

confidence: 99%

Chronic myeloid leukemia stem cells: targeting therapeutic implications

2021

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Chronic myeloid leukemia (CML) is a clonal myeloproliferative neoplasm driven by BCR-ABL1 oncoprotein, which plays a pivotal role in CML pathology, diagnosis, and treatment as confirmed by the success of tyrosine kinase inhibitor (TKI) therapy. Despite advances in the development of more potent tyrosine kinase inhibitors, some mechanisms particularly in terms of CML leukemic stem cell (CML LSC) lead to intrinsic or acquired therapy resistance, relapse, and disease progression. In fact, the maintenance CML LSCs in patients who are resistance to TKI therapy indicates the role of CML LSCs in resistance to therapy through survival mechanisms that are not completely dependent on BCR-ABL activity. Targeting therapeutic approaches aim to eradicate CML LSCs through characterization and targeting genetic alteration and molecular pathways involving in CML LSC survival in a favorable leukemic microenvironment and resistance to apoptosis, with the hope of providing a functional cure. In other words, it is possible to develop the combination therapy of TKs with drugs targeting genes or molecules more specifically, which is required for survival mechanisms of CML LSCs, while sparing normal HSCs for clinical benefits along with TKIs.

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Bosutinib for the treatment of chronic myeloid leukemia

Abstract: Bosutinib is a safe and effective second-line treatment option for select patients with Ph-positive CML who were intolerant or resistant to prior TKI therapy.

Cited by 16 publications

References 29 publications

Advances in studies of tyrosine kinase inhibitors and their acquired resistance

Advances in studies of tyrosine kinase inhibitors and their acquired resistance

The Efficacy and Safety of Bosutinib in Chronic Myeloid Leukemia

Chronic myeloid leukemia stem cells: targeting therapeutic implications

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