PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32340449-4 2020 In this study, we used ABL kinase (target) as a model, and synthesized a fluorescent probe (Cy3-dasatinib) with an affinity to the target using ABL inhibitor dasatinib as a precursor. Dasatinib 96-105 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 23-26 32266142-6 2020 He was then treated with the ABL1 tyrosine kinase inhibitor dasatinib and achieved complete remission within 2 weeks. Dasatinib 60-69 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 29-33 32094501-6 2020 Lastly, in patients administered with dasatinib for the treatment of BCR-ABL-positive leukemias, we provided the proof of concept that the kinase inhibitor also influences the two innate T-cell subsets in humans, as attested by their increased frequency in the peripheral blood. Dasatinib 38-47 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 69-76 31014138-0 2019 Response to single agent dasatinib post allogeneic transplant in B-cell acute lymphoblastic leukemia with NUP214-ABL1. Dasatinib 25-34 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 113-117 31539241-3 2019 Herein, we described the design, synthesis, and evaluation of novel proteolysis-targeting chimeric (PROTAC) small molecules targeting BCR-ABL which connect dasatinib and VHL E3 ubiquitin ligase ligand by extensive optimization of linkers. Dasatinib 156-165 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 134-141 30879266-4 2019 However, CML relapsed 4 months after starting dasatinib due to increased BCR-ABL fusion signals in the peripheral blood. Dasatinib 46-55 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 73-80 30546081-6 2019 Notably, the dasatinib-containing combination led to treatment- and leukemia-free long-term survival in a BCR-ABL + mouse model. Dasatinib 13-22 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 106-113 30568173-5 2019 Furthermore, NUP98-NSD1+/FLT3-ITD+ patient cells were also very sensitive to BCL2-inhibitor navitoclax, although the highest select sensitivity was found to SRC/ABL-inhibitor dasatinib (mean IC50 = 2.2 nM). Dasatinib 175-184 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 161-164 30568173-8 2019 We found that SRC/ABL-inhibitor dasatinib is highly synergistic with BCL2-inhibitor navitoclax in NUP98-NSD1+/FLT3-ITD+ cells. Dasatinib 32-41 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 18-21 30956968-0 2019 Coexistence of BCR/ABL1-positive chronic myeloid leukemia and JAK2 V617F-mutated myelofibrosis successfully treated with dasatinib and ruxolitinib. Dasatinib 121-130 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 19-23 30705677-2 2018 ABL tyrosine kinase inhibitors (TKIs), such as imatinib, nilotinib, and dasatinib, are currently the front-line treatment options for CML. Dasatinib 72-81 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 0-3 30705677-13 2018 Our results highlight the dual effects of dasatinib in direct inhibition of ABL kinase and in immunomodulation through NKG2A down-regulation, contributing to accelerated molecular responses (MR) in CML. Dasatinib 42-51 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 76-79 30093398-1 2019 Dasatinib, a second-generation BCR-ABL1 tyrosine kinase inhibitor, is approved for the treatment of chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia, both as first-line therapy and after imatinib intolerance or resistance. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 35-39 30332954-2 2019 Bcr-Abl fusion protein has constitutively activated Abl tyrosine kinase activity which is responsible for the uncontrolled proliferation in CML The tyrosine kinase inhibitors (TKIs) such as Imatinib, Dasatinib, and Nilotinib are the current first-line treatments approved by the United States Food and Drug Administration (US FDA) for the treatment of the disease. Dasatinib 200-209 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 0-7 30971653-2 2019 The specific BCR-ABL inhibitors including imatinib, nilotinib, and dasatinib, are clinically utilized in the treatment with CML and ALL patients. Dasatinib 67-76 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 13-20 30587121-1 2018 BACKGROUND: Dasatinib (Sprycel) was developed as a tyrosine kinase inhibitor targeting Bcr-Abl and the family of Src kinases. Dasatinib 12-21 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 87-94 30616322-0 2018 [Study on mechanism for dasatinib inhibiting PDGFR/Bcr-Abl signaling pathway in hepatic stellate cells mediated hepatic fibrosis]. Dasatinib 24-33 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 51-58 30301525-1 2018 Chronic myeloid leukemia (CML) responds well to BCR-ABL tyrosine kinase inhibitors (TKI), such as imatinib and dasatinib. Dasatinib 111-120 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 48-55 30217442-4 2018 Treatment of CML-derived K562 cells with BCR-ABL tyrosine kinase inhibitors, including imatinib, dasatinib, nilotinib and ponatinib, prevented activation of eIF2alpha kinases, protein kinase-like endoplasmic reticulum kinase (PERK) and general control nonderepressible 2, and downstream ATF4 induction during metabolic stress. Dasatinib 97-106 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 41-48 30202081-3 2018 Recently, potent degraders against BCR-ABL have been developed by conjugating dasatinib to ligands for E3 ubiquitin ligases. Dasatinib 78-87 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 35-42 30202081-4 2018 Since the degraders contain the dasatinib moiety, they also inhibit BCR-ABL kinase activity, which complicates our understanding of the impact of BCR-ABL degradation by degraders in CML growth inhibition. Dasatinib 32-41 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 68-75 30024740-6 2018 Moreover, the inactivation of both Abl and Src by the inhibitor imatinib, dasatinib, and ponatinib was simultaneously traced, giving a whole picture of the competition behavior between the kinases for binding therapeutic molecules. Dasatinib 74-83 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 35-38 29902613-6 2018 RESULTS: Here, we report the discovery of a synergistic interaction between dasatinib (ABL and SRC family kinase inhibitor) and the mitogen-activated protein kinase kinase (MEK) inhibitor trametinib in KRAS-mutant cancer cells. Dasatinib 76-85 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 87-90 29937990-6 2018 Dasatinib (BMS-354825), a SRC/ABL inhibitor, effectively blocked SFK activation at nanomolar concentrations which correlated with a significant decrease in cell numbers of multiple lung cancer cell lines. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 30-33 29945329-1 2018 BACKGROUND: T315I mutation is the most common BCR-ABL mutation and confers resistance to all the first and second generation BCR-ABL tyrosine kinases, including nilotinib and dasatinib. Dasatinib 175-184 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 46-53 29945329-1 2018 BACKGROUND: T315I mutation is the most common BCR-ABL mutation and confers resistance to all the first and second generation BCR-ABL tyrosine kinases, including nilotinib and dasatinib. Dasatinib 175-184 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 125-132 29434033-4 2018 Further genomic profiling of longitudinally collected samples during treatment revealed the emergence of a mutation, PDGFRBC843G , which directly conferred resistance to all generations of ABL TKIs, including imatinib, dasatinib, nilotinib, and ponatinib. Dasatinib 219-228 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 189-192 29315500-2 2018 Dasatinib is a potent inhibitor of BCR-ABL, KIT, and SRC family kinases as well as imatinib-resistant cells. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 35-42 29541231-6 2018 The present data suggest that BCR-ABL gene amplification may be associated with imatinib resistance, which can be overcome with dasatinib. Dasatinib 128-137 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 30-37 29549929-9 2018 Importantly, combination of ropivacaine with imatinib or dasatinib (Bcr-Abl tyrosine kinase inhibitors) is significantly more effective in targeting CML cell lines as well as blast phase-CML CD34 cells than imatinib or dasatinib alone. Dasatinib 57-66 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 68-75 29549929-9 2018 Importantly, combination of ropivacaine with imatinib or dasatinib (Bcr-Abl tyrosine kinase inhibitors) is significantly more effective in targeting CML cell lines as well as blast phase-CML CD34 cells than imatinib or dasatinib alone. Dasatinib 219-228 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 68-75 29336809-2 2018 The screening method was established by using 5-carboxyfluorescein labeled peptide substrate of BCR-ABL (F-ABLS), a known BCR-ABL tyrosine kinase inhibitor dasatinib, as well as a small chemical library consisting of 37 natural products. Dasatinib 156-165 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 96-103 29035389-6 2018 The Src/Abl inhibitor dasatinib, a candidate anti-invasive drug, abrogated the invasive properties induced by MCC deficiency. Dasatinib 22-31 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 8-11 29464092-0 2018 mTOR inhibition enhances efficacy of dasatinib in ABL-rearranged Ph-like B-ALL. Dasatinib 37-46 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 50-53 29464092-5 2018 Here we show that combinations of the ABL-directed TKI dasatinib with mTOR kinase inhibitors (TOR-KIs) are more effective than TKI alone against patient-derived Ph-like B-ALL cells harboring rearrangements of ABL1 or ABL2. Dasatinib 55-64 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 38-41 29464092-5 2018 Here we show that combinations of the ABL-directed TKI dasatinib with mTOR kinase inhibitors (TOR-KIs) are more effective than TKI alone against patient-derived Ph-like B-ALL cells harboring rearrangements of ABL1 or ABL2. Dasatinib 55-64 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 209-213 29551130-6 2018 The first TK to be targeted, Bcr-Abl, led to the generation of several drugs including imatinib, dasatinib, and sunitinib that provided a rich understanding of this phenomenon. Dasatinib 97-106 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 29-36 28554234-0 2018 Molecular characterization and therapeutic reaction to dasatinib in a CML patient harboring a novel e8a2 BCR-ABL1 transcript with a somatic mutation in TP53BP2 and cadherin-10 genes. Dasatinib 55-64 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 109-113 30069624-3 2018 Dasatinib is a very potent inhibitor of BCR-ABL and an effective treatment for the BCR-ABL-driven diseases chronic myeloid leukemia (CML) and Philadelphia-chromosome-positive acute lymphoblastic leukemia (Ph+ ALL), characterized by the constitutively active tyrosine kinase, BCR-ABL. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 40-47 30069624-3 2018 Dasatinib is a very potent inhibitor of BCR-ABL and an effective treatment for the BCR-ABL-driven diseases chronic myeloid leukemia (CML) and Philadelphia-chromosome-positive acute lymphoblastic leukemia (Ph+ ALL), characterized by the constitutively active tyrosine kinase, BCR-ABL. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 83-90 30069624-3 2018 Dasatinib is a very potent inhibitor of BCR-ABL and an effective treatment for the BCR-ABL-driven diseases chronic myeloid leukemia (CML) and Philadelphia-chromosome-positive acute lymphoblastic leukemia (Ph+ ALL), characterized by the constitutively active tyrosine kinase, BCR-ABL. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 83-90 29256412-1 2017 The protein kinase inhibitor dasatinib, targeting BCR-ABL and Src family kinases, is used in chronic myeloid leukaemia and Philadelphia-chromosome positive acute lymphoblastic leukaemia. Dasatinib 29-38 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 50-57 29127384-1 2017 Dasatinib and radotinib are oral BCR-ABL tyrosine kinase inhibitors that were developed as drugs for the treatment of chronic myeloid leukemia. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 33-40 28821556-1 2017 Purpose: Dasatinib is a short-acting dual ABL/SRC family tyrosine kinase inhibitor (TKI), which is frequently used to treat chronic myeloid leukemia. Dasatinib 9-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 42-45 29067094-0 2017 Dasatinib and chemotherapy in a patient with early T-cell precursor acute lymphoblastic leukemia and NUP214-ABL1 fusion: A case report. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 108-112 29067094-1 2017 The present study aimed to evaluate the therapeutic efficacy of dasatinib in a patient with nucleoporin 214-tyrosine protein kinase ABL1 proto-oncogene 1 (NUP214-ABL1)-positive early T-cell precursor-acute lymphoblastic leukemia (ETP-ALL), as well as that of selinexor and dasatinib for NUP214-ABL1-positive ETP-ALL in vitro. Dasatinib 64-73 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 132-136 29067094-1 2017 The present study aimed to evaluate the therapeutic efficacy of dasatinib in a patient with nucleoporin 214-tyrosine protein kinase ABL1 proto-oncogene 1 (NUP214-ABL1)-positive early T-cell precursor-acute lymphoblastic leukemia (ETP-ALL), as well as that of selinexor and dasatinib for NUP214-ABL1-positive ETP-ALL in vitro. Dasatinib 64-73 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 162-166 29067094-1 2017 The present study aimed to evaluate the therapeutic efficacy of dasatinib in a patient with nucleoporin 214-tyrosine protein kinase ABL1 proto-oncogene 1 (NUP214-ABL1)-positive early T-cell precursor-acute lymphoblastic leukemia (ETP-ALL), as well as that of selinexor and dasatinib for NUP214-ABL1-positive ETP-ALL in vitro. Dasatinib 64-73 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 162-166 29067094-1 2017 The present study aimed to evaluate the therapeutic efficacy of dasatinib in a patient with nucleoporin 214-tyrosine protein kinase ABL1 proto-oncogene 1 (NUP214-ABL1)-positive early T-cell precursor-acute lymphoblastic leukemia (ETP-ALL), as well as that of selinexor and dasatinib for NUP214-ABL1-positive ETP-ALL in vitro. Dasatinib 273-282 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 132-136 29067094-1 2017 The present study aimed to evaluate the therapeutic efficacy of dasatinib in a patient with nucleoporin 214-tyrosine protein kinase ABL1 proto-oncogene 1 (NUP214-ABL1)-positive early T-cell precursor-acute lymphoblastic leukemia (ETP-ALL), as well as that of selinexor and dasatinib for NUP214-ABL1-positive ETP-ALL in vitro. Dasatinib 273-282 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 162-166 29067094-1 2017 The present study aimed to evaluate the therapeutic efficacy of dasatinib in a patient with nucleoporin 214-tyrosine protein kinase ABL1 proto-oncogene 1 (NUP214-ABL1)-positive early T-cell precursor-acute lymphoblastic leukemia (ETP-ALL), as well as that of selinexor and dasatinib for NUP214-ABL1-positive ETP-ALL in vitro. Dasatinib 273-282 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 162-166 29067094-12 2017 Dasatinib used in combination with traditional induction chemotherapy may reverse the high induction failure of ETP-ALL with NUP214-ABL1 fusion gene; however, further prospective studies are required to confirm this. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 132-136 29091939-2 2017 Dasatinib is a potent Src/Abl inhibitor and has demonstrated to have anti-proliferative and anti-invasive activity in many preclinical models. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 26-29 29296813-6 2017 In vitro screening using a panel of tyrosine kinase inhibitors against 14 different kinase alterations identified the ABL1-inhibitor, dasatinib, as a potent inhibitor of ABL-class fusions (ABL1, ABL2, CSF1R, PDGFRB), whereas the JAK1/JAK2 inhibitor ruxolitinib, was most effective against JAK-STAT-activating alterations (JAK1, JAK2, JAK3, IL7R, IL2RB), but not TYK2. Dasatinib 134-143 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 118-122 29296813-6 2017 In vitro screening using a panel of tyrosine kinase inhibitors against 14 different kinase alterations identified the ABL1-inhibitor, dasatinib, as a potent inhibitor of ABL-class fusions (ABL1, ABL2, CSF1R, PDGFRB), whereas the JAK1/JAK2 inhibitor ruxolitinib, was most effective against JAK-STAT-activating alterations (JAK1, JAK2, JAK3, IL7R, IL2RB), but not TYK2. Dasatinib 134-143 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 118-121 29296813-6 2017 In vitro screening using a panel of tyrosine kinase inhibitors against 14 different kinase alterations identified the ABL1-inhibitor, dasatinib, as a potent inhibitor of ABL-class fusions (ABL1, ABL2, CSF1R, PDGFRB), whereas the JAK1/JAK2 inhibitor ruxolitinib, was most effective against JAK-STAT-activating alterations (JAK1, JAK2, JAK3, IL7R, IL2RB), but not TYK2. Dasatinib 134-143 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 189-193 28556300-2 2017 Inhibitors of ABL tyrosine kinase, such as imatinib and dasatinib, exhibit remarkable therapeutic effects, although emergence of drug resistance hampers the therapy during long-term treatment. Dasatinib 56-65 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 14-17 28556300-6 2017 The resulting SNIPER(ABL)-39, in which dasatinib is conjugated to an IAP ligand LCL161 derivative by polyethylene glycol (PEG) x 3 linker, shows a potent activity to degrade the BCR-ABL protein. Dasatinib 39-48 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 21-24 28556300-6 2017 The resulting SNIPER(ABL)-39, in which dasatinib is conjugated to an IAP ligand LCL161 derivative by polyethylene glycol (PEG) x 3 linker, shows a potent activity to degrade the BCR-ABL protein. Dasatinib 39-48 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 178-185 28349229-2 2017 The Bcr-Abl inhibitor imatinib and other second-generation tyrosine kinase inhibitors such as dasatinib and nilotinib have remarkable efficacy in CML treatment. Dasatinib 94-103 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 4-11 28456613-6 2017 The key role of tyrosine kinases in this process is further substantiated by the rescue effect of the tyrosine kinase inhibitor genistein, and the more specific Src/Abl kinase inhibitor dasatinib: both reduced ROS-induced degradation of beta-catenin/E-cadherin in vitro and ameliorated skin damage in rodent models. Dasatinib 186-195 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 165-168 28599273-5 2017 Oral TKI dasatinib combined with potent SNG1153 inhibitor effectively eliminates infiltrated BCR-ABL+ blast cells and enhances survival of mice. Dasatinib 9-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 93-100 28749919-5 2017 In this review, we outline the age-related and geographic incidence of Ph-like ALL, the association with worse clinical outcomes, and early evidence for the use of ruxolitinib (a Janus kinase 2 inhibitor) and dasatinib (a tyrosine kinase inhibitor targeting ABL1). Dasatinib 209-218 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 258-262 28544567-3 2017 Herein we report the synthesis and evaluation of dedicated EPHA2 inhibitors based on the clinical BCR-ABL/SRC inhibitor dasatinib as a lead structure. Dasatinib 120-129 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 98-105 28674529-3 2017 Treatment of Abl tyrosine kinase-specific inhibitor, imatinib and dasatinib, also significantly decreased HCV RNA and protein levels in HCV-infected cells. Dasatinib 66-75 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 13-16 28674529-4 2017 We showed that both imatinib and dasatinib selectively inhibited HCV infection at the entry step of HCV life cycle, suggesting that Abl kinase activity may be necessary for HCV entry. Dasatinib 33-42 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 132-135 28622336-11 2017 The performance of the proposed T2-statistic is demonstrated using five published experimental datasets: the T-cell activation, the cAMP/PKA signaling, the myoblast differentiation, and the effect of dasatinib on the BCR-ABL pathway are proteomic datasets produced by mass spectrometry; and the protective effect of myocilin via the MAPK signaling pathway is a gene expression dataset of limited sample size. Dasatinib 200-209 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 217-224 28283735-2 2017 Dasatinib, a BCR-ABL1 tyrosine kinase inhibitor (TKI) approved for the treatment of chronic myelogenous leukemia, has been associated with PAH. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 13-20 27848186-0 2017 Dasatinib induces autophagy in mice with Bcr-Abl-positive leukemia. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 41-48 27848186-1 2017 Dasatinib, a second-generation tyrosine kinase inhibitor, is a highly effective treatment for Bcr-Abl-positive leukemia. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 94-101 27848186-5 2017 Here, we report that dasatinib induces autophagy in Bcr-Abl-positive leukemia cell lines and further show the induction of autophagy in an immunodeficient mouse model of human Bcr-Abl-positive leukemia with central nervous system (CNS) infiltration. Dasatinib 21-30 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 52-59 27848186-5 2017 Here, we report that dasatinib induces autophagy in Bcr-Abl-positive leukemia cell lines and further show the induction of autophagy in an immunodeficient mouse model of human Bcr-Abl-positive leukemia with central nervous system (CNS) infiltration. Dasatinib 21-30 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 176-183 28213007-3 2017 A recent report suggested that dasatinib (an ABL/Src kinase inhibitor) inhibits EMT induced by transforming growth factor (TGF)-beta in lung cancer cells (Wilson et al., 2014). Dasatinib 31-40 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 45-48 28245378-1 2017 OBJECTIVE: To investigate the effects of Btk inhibitor (PCI-32765) and BCR-ABL tyrosine kinase inhibitor (Dasatinib) on proliferation and apoptosis of acute lymphoblastic leukemia (ALL) cell lines (Sup-B15, RS4;11) and the possible mechanism. Dasatinib 106-115 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 71-78 28245378-8 2017 PCI-32765 and Dasatinib could decrease the expression and activity of BCR-ABL, Btk, Lyn, Src in Sup-B15 and RS4;11 cells. Dasatinib 14-23 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 70-77 27777238-8 2017 Similarly, superior efficacy of combined gedatolisib and dasatinib was observed in ABL/PDGFR-mutant models (P < .001). Dasatinib 57-66 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 83-86 28044939-1 2017 In a series of studies carried out over the last couple of years in various cell types, it was observed that the experimentally used Src family kinase inhibitors PP1 and PP2 and the clinically used Src/Abl inhibitors AZM475271 and dasatinib are potent inhibitors of TGF-beta mediated cellular responses such as Smad and p38 mitogen-activated protein kinase phosphorylation, Smad-dependent transcriptional activation, growth inhibition, epithelial-mesenchymal transition (EMT), and cell motility. Dasatinib 231-240 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 202-205 28743118-2 2017 Given the loss of major molecular response, we switched treatment to dasatinib 100 mg daily, observing a reduction in BCR-ABL transcript, a significant improvement of anemia, and a gradual disappearance of fibrosis. Dasatinib 69-78 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 118-125 27852118-1 2017 BACKGROUND: A previous meta-analysis demonstrated that 3 of the new-generation BCR-ABL tyrosine kinase inhibitors (TKIs) (dasatinib, nilotinib and ponatinib) are associated with an increased risk of vascular occlusive events in patients with Ph+ chronic myeloid leukemia compared with imatinib. Dasatinib 122-131 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 79-86 30167550-2 2016 Imatinib and dasatinib are 2 BCR-ABL tyrosine kinase inhibitors (TKI) used in the treatment of CML. Dasatinib 13-22 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 29-36 28191543-0 2016 The third-time chronic myeloid leukemia in lymphoblastic crisis with ABL1 kinase mutation induced by decitabine, dexamethason combined with nilotinib and dasatinib. Dasatinib 154-163 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 69-73 27636353-2 2016 Efforts to elucidate the role they play in these malignancies have led to important diagnostic and therapeutic triumphs, including the famous development of the tyrosine kinase inhibitor dasatinib targeting the BCR-ABL fusion. Dasatinib 187-196 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 211-218 27803756-1 2016 Dasatinib is a drug for treatment of oncogene fusion protein BCR-ABL-positive chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia resistant/intolerant to imatinib. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 61-68 26479578-6 2016 Baustinib, Nilotinib, Dasatinib, Ponatinib, Bafetinib, etc., which can able to combat against mutated domain of ABL tyrosine kinase protein. Dasatinib 22-31 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 112-115 27520370-2 2016 Here we show that niclosamide, a FDA-approved anthelmintic drug, enhances the sensitivity of BP-CML cells to dasatinib (2nd generation of BCR-ABL TKI) through inhibiting Erk/Mnk1/eIF4E signaling pathway. Dasatinib 109-118 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 138-145 27583255-4 2016 Then, several stop studies of first-generation (imatinib) and second-generation ABL TKIs (dasatinib, nilotinib), which induce earlier response than imatinib, have also been started. Dasatinib 90-99 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 80-83 27521332-5 2016 Dasatinib is a potent second-generation tyrosine kinase inhibitor designed to inhibit ABL and SRC kinases while also interfering with the c-Kit, platelet-derived growth factor receptor, and STAT5 pathways. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 86-89 27044711-1 2016 Chronic myeloid leukemia (CML) patients who relapse on imatinib due to acquired ABL1 kinase domain mutations are successfully treated with second-generation ABL1-tyrosine kinase inhibitors (ABL-TKIs) such as dasatinib, nilotinib or ponatinib. Dasatinib 208-217 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 80-84 27044711-1 2016 Chronic myeloid leukemia (CML) patients who relapse on imatinib due to acquired ABL1 kinase domain mutations are successfully treated with second-generation ABL1-tyrosine kinase inhibitors (ABL-TKIs) such as dasatinib, nilotinib or ponatinib. Dasatinib 208-217 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 157-161 27044711-3 2016 To identify these mechanisms of resistance and potential treatment options, we generated ABL-TKI-resistant K562 cells through prolonged sequential exposure to imatinib and dasatinib. Dasatinib 172-181 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 89-92 27347777-2 2016 We present here a chronic myeloid leukemia patient harboring the T315I and E255V BCR-ABL1 mutation successfully achieved deep molecular response with a combined treatment of dasatinib and IFN-alpha. Dasatinib 174-183 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 85-89 27078848-9 2016 Furthermore, CRKL tyrosine phosphorylation was inhibited by dasatinib (an inhibitor of ABL and SRC kinases), which in combination with the ALK inhibitor crizotinib displayed a synergistic inhibitory effect in vitro. Dasatinib 60-69 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 87-90 26582603-3 2016 The first-line treatment consists on BCR-ABL inhibitors such as Imatinib, Nilotinib and Dasatinib. Dasatinib 88-97 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 37-44 26507546-1 2016 PURPOSE: Dasatinib is a novel, oral, multi-targeted kinase inhibitor of breakpoint cluster region-abelson (BCR-ABL) and Src family kinases. Dasatinib 9-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 107-114 27656875-1 2016 Dasatinib is a potent inhibitor of the altered tyrosine kinase activity in disease states associated with BCR/ABL1. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 110-114 26802644-5 2016 We report two CP-CML patients achieving and maintaining major molecular responses while on very low doses of dasatinib, ultimately achieving undetectable levels of BCR-ABL fusion transcript in their peripheral blood. Dasatinib 109-118 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 164-171 26876246-0 2016 [Dasatinib treatment based on BCR- ABL mutation detection in imatinib- resistant patients with chronic myeloid leukemia]. Dasatinib 1-10 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 30-38 26876246-1 2016 OBJECTIVE: To evaluate the efficiency of dasatinib as the second- or third-line tyrosine kinase inhibitor (TKI)in imatinib-resistant patients with chronic myeloid leukemia (CML)based on BCR-ABL mutation detection. Dasatinib 41-50 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 186-193 26876246-5 2016 BCR- ABL mutation detection was performed once the patients failed on dasatinib. Dasatinib 70-79 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 0-8 26588899-2 2015 Here, we investigated the ability of the clinically utilised SRC/ABL inhibitor dasatinib to mimic the PP2/PP1 effect. Dasatinib 79-88 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 65-68 26284693-2 2015 Few cases of pulmonary arterial hypertension (PAH) have been reported in patients with leukemia treated with dasatinib, a second-generation BCR-ABL TKI. Dasatinib 109-118 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 140-147 26473951-4 2015 We found that KOSR protects CML cells from killing by BCR-ABL inhibitors--imatinib, dasatinib and nilotinib. Dasatinib 84-93 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 54-61 26430722-0 2015 Concomitant JAK2 V617F-positive polycythemia vera and BCR-ABL-positive chronic myelogenous leukemia treated with ruxolitinib and dasatinib. Dasatinib 129-138 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 54-61 25842192-2 2015 Dasatinib is a small-molecule inhibitor of the tyrosine kinases SRC and ABL that has been approved for the treatment of chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leukemia. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 72-75 25913326-4 2015 Although deletion or insertion of nucleotides in BCR-ABL1 has rarely been described, we identified a CML patient with an already described 35 nucleotides insertion (BCR-ABL1(35INS)) of controversial significance, that confers resistance to imatinib but sensitivity to dasatinib. Dasatinib 268-277 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 53-57 25996455-3 2015 In this work, molecular dynamics simulations of the Abl kinase complexes with cancer drugs (Imatinib and Dasatinib) were combined with structure-based network modeling to characterize dynamics of the residue interaction networks in these systems. Dasatinib 105-114 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 52-55 25996455-6 2015 In contrast, Dasatinib binding to the active kinase form may activate a broader ensemble of allosteric pathways that are less dependent on the phosphorylation status of Abl and provide a better balance between the efficiency and resilience of signaling routes. Dasatinib 13-22 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 169-172 25889792-4 2015 Interestingly, its expression on human monocyte-derived dendritic cells (moDC) is dramatically upregulated upon treatment with IL-10 but also by the BCR-ABL tyrosine kinase inhibitors (TKI) imatinib, nilotinib or dasatinib used for the treatment of chronic myeloid leukemia (CML). Dasatinib 213-222 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 149-156 25499760-2 2015 Despite major advances in the treatment of this highly aggressive disease with potent inhibitors of the BCR-ABL kinase such as dasatinib, patients in remission frequently relapse due to persistent minimal residual disease possibly supported, at least in part, by salutary cytokine-driven signaling within the hematopoietic microenvironment. Dasatinib 127-136 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 104-111 25526365-5 2015 Then, the dasatinib derivatives were synthesized and labeled with the fluorescent dye Alexa 488, and the binding and dissociation processes of Alexa 488-dasatinib and ABL1 were systematically investigated. Dasatinib 10-19 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 167-171 25526365-6 2015 The dissociation constant and the dissociation rate for the Alexa 488-dasatinib-ABL1 complex were determined. Dasatinib 70-79 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 80-84 25831762-0 2015 [Inhibitors for ABL, KIT and PDGFR tyrosine kinases--imatinib, nitotinib, and dasatinib]. Dasatinib 78-87 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 16-19 25351958-6 2015 Bosutinib and dasatinib were originally developed as inhibitors of the protein tyrosine kinases Bcr-Abl and Src but we show that, surprisingly, the effects of bosutinib and dasatinib on macrophage polarization are the result of the inhibition of the salt-inducible kinases. Dasatinib 14-23 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 96-111 25351958-6 2015 Bosutinib and dasatinib were originally developed as inhibitors of the protein tyrosine kinases Bcr-Abl and Src but we show that, surprisingly, the effects of bosutinib and dasatinib on macrophage polarization are the result of the inhibition of the salt-inducible kinases. Dasatinib 173-182 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 96-111 25179732-0 2015 Relapse of BCR-ABL1-like ALL mediated by the ABL1 kinase domain mutation T315I following initial response to dasatinib treatment. Dasatinib 109-118 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 15-19 25179732-0 2015 Relapse of BCR-ABL1-like ALL mediated by the ABL1 kinase domain mutation T315I following initial response to dasatinib treatment. Dasatinib 109-118 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 45-49 25025538-1 2015 Dasatinib, which is an inhibitor of BCR-ABL and SRC family tyrosine kinases, is used for the treatment of patients with Philadelphia chromosome (Ph) positive leukemia, especially for those who develop resistance or who are intolerant to imatinib. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 36-43 25331939-1 2014 Despite the clinical efficacy achieved with frontline therapies for BCR-ABL-positive disease, such as imatinib and second-generation ABL inhibitors like nilotinib or dasatinib that were originally designed to override insensitivity to imatinib, drug resistance still remains a challenge, especially for patients with advanced-stage chronic myeloid leukemia or Philadelphia chromosome-positive acute lymphoblastic leukemia. Dasatinib 166-175 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 68-75 25426931-1 2014 ABL tyrosine kinase inhibitors (TKI) like Imatinib, Dasatinib and Nilotinib are the gold standard in conventional treatment of CML. Dasatinib 52-61 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 0-3 25584281-1 2014 Dasatinib is a second-generation multi-target tyrosine kinase inhibitor (TKI) that has activity against many imatinib-resistant BCR-ABL mutant forms, Src, and c-Kit tyrosine kinases. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 128-135 25284075-0 2014 Reduced miR-3127-5p expression promotes NSCLC proliferation/invasion and contributes to dasatinib sensitivity via the c-Abl/Ras/ERK pathway. Dasatinib 88-97 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 118-123 25284075-5 2014 Overexpression of miR-3127-5p in A549 or H292 cells resulted in enhanced resistance to dasatinib, an Abl/src tyrosine kinase inhibitor. Dasatinib 87-96 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 101-104 25173530-5 2014 The effectiveness of an oral dual-specific (Src and Abl) multikinase inhibitors-dasatinib-was observed in different cell lines and in some NSCLC patients with identified DDR2 mutation. Dasatinib 80-89 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 52-55 25193862-5 2014 The mesenchymal cells were more resistant to most tested agents; however, a small number of agents showed selective growth inhibitory activity against the mesenchymal cells, with the most potent being the Abl/Src inhibitor, dasatinib. Dasatinib 224-233 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 205-208 25207766-8 2014 Cell lines and human leukemic cells expressing ABL1, ABL2, CSF1R, and PDGFRB fusions were sensitive in vitro to dasatinib, EPOR and JAK2 rearrangements were sensitive to ruxolitinib, and the ETV6-NTRK3 fusion was sensitive to crizotinib. Dasatinib 112-121 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 47-51 25198091-9 2014 In the intracellular context, EC50 for BCR-ABL inhibition was in subnanomolar range for dasatinib and in submicromolar one for imatinib. Dasatinib 88-97 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 39-46 25023728-8 2014 Addition of the Src/c-Abl inhibitor, dasatinib, completely blocks this feedback activation, confirming convergence between Src and the mTOR pathway. Dasatinib 37-46 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 20-25 24882272-4 2014 Here, we investigated whether the BCR-ABL/SRC inhibitor dasatinib would modulate the major effector functions of DCs, especially their migration, a prerequisite to interaction with lymphocytes in secondary lymphoid organs. Dasatinib 56-65 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 34-41 25114223-5 2014 This approach identified a number of kinase inhibitors that robustly up-regulate IL-10 production including the Food and Drug Administration (FDA)-approved drugs dasatinib, bosutinib, and saracatinib that target ABL, SRC-family, and numerous other kinases. Dasatinib 162-171 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 212-215 24143950-3 2014 RESULTS: Therapeutic options for front-line treatment have increased with the approval of two second-generation BCR-ABL inhibitors, dasatinib and nilotinib. Dasatinib 132-141 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 112-119 25068103-4 2014 We herein report a case of T-PLL with a novel SEPT9-ABL1 fusion gene which induced strong resistance to tyrosine kinase inhibitors such as imatinib and dasatinib. Dasatinib 152-161 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 52-56 24975338-0 2014 [Successful treatment with dasatinib for polycythemia vera patient emerging BCR-ABL positive clone during 13 years of treatment]. Dasatinib 27-36 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 76-83 24569990-7 2014 Expression of "gate-keeper" mutants of c-Abl or c-Src that are active in the presence of dasatinib restored phosphorylation of PKCdelta at Tyr-155 and Tyr-64, respectively. Dasatinib 89-98 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 39-44 24569263-10 2014 Imatinib-resistant/-intolerant patients with CML-CP can experience long-term benefit with dasatinib therapy, particularly if achieving BCR-ABL <=10% at 3 months. Dasatinib 90-99 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 135-142 24847647-2 2014 Second generation Bcr-Abl inhibitors, such as Nilotinib and Dasatinib, are able to overcome most Imatinib- resistant mutants, with the exception of the T315I substitution. Dasatinib 60-69 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 18-25 24258348-4 2014 To overcome this resistance, four second-generation ATP competitive ABL TKIs, dasatinib, nilotinib, bosutinib and bafetinib, have been developed. Dasatinib 78-87 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 68-71 24311723-5 2014 At 3 and 6 months, the proportion of patients with BCR-ABL transcript levels <=10% was higher in the dasatinib arm. Dasatinib 104-113 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 51-58 25006277-2 2014 Shortly thereafter, more potent BCR-ABL inhibitors (dasatinib and nilotinib) were introduced for use in patients resistant to or intolerant of imatinib. Dasatinib 52-61 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 32-39 23989453-7 2014 Strikingly, cotreatment with DHA and dasatinib in vivo strongly reduced primary leukemia burden and improved long-term survival in a murine model that faithfully captures the BCR-ABL-KI-resistant phenotype of human Ph+ ALL. Dasatinib 37-46 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 175-182 25501110-1 2014 Dasatinib is a BCR-ABL kinase inhibitor with improved potency compared with imatinib, for which efficacy and safety in imatinib-resistant and imatinib-intolerant patients with chronic myelogenous leukemia (CML) have been established. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 15-22 25501110-8 2014 A lower level of BCR-ABL transcript at 1 or 3 months after the initiation of dasatinib treatment was more strongly correlated with the BCR-ABL transcript level at 12 and 18 months (p < 0.001) than a higher level of BCR-ABL. Dasatinib 77-86 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 17-24 25501110-8 2014 A lower level of BCR-ABL transcript at 1 or 3 months after the initiation of dasatinib treatment was more strongly correlated with the BCR-ABL transcript level at 12 and 18 months (p < 0.001) than a higher level of BCR-ABL. Dasatinib 77-86 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 135-142 25501110-8 2014 A lower level of BCR-ABL transcript at 1 or 3 months after the initiation of dasatinib treatment was more strongly correlated with the BCR-ABL transcript level at 12 and 18 months (p < 0.001) than a higher level of BCR-ABL. Dasatinib 77-86 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 135-142 24734217-1 2014 Dasatinib (DAS) is a potent inhibitor of the BCR-ABL, SRC, c-KIT, PDGFR, and ephrin tyrosine kinases that has demonstrated only modest clinical efficacy in melanoma patients. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 45-52 24756784-1 2014 Dasatinib is an orally available short-acting dual ABL/SRC tyrosine kinase inhibitor (TKI). Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 51-54 24756784-5 2014 Dasatinib inhibits BCR-ABL with greater potency compared with other BCR-ABL inhibitors and is active in CML resistant or intolerant to imatinib. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 19-26 24756784-5 2014 Dasatinib inhibits BCR-ABL with greater potency compared with other BCR-ABL inhibitors and is active in CML resistant or intolerant to imatinib. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 68-75 24095296-2 2013 Three BCR-ABL inhibitors, imatinib, nilotinib, and dasatinib, have been approved by the US Food and Drug Administration for first-line treatment of patients with newly diagnosed CML in chronic phase (CML-CP). Dasatinib 51-60 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 6-13 23701117-5 2013 BMS-354825 (dasatinib) and SKI-606 (bosutinib), second and third generation clinical SFK/ABL inhibitors, were found to be potent cytotoxic agents against tumorigenic cells with low toxicity to normal pediatric stem cells. Dasatinib 12-21 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 89-92 23942795-1 2013 PURPOSE: Dasatinib is a dual Abl/Src tyrosine kinase inhibitor (TKI) designed as a prototypic short-acting BCR-ABL-targeted TKI that inhibits BCR-ABL with greater potency compared with imatinib, nilotinib, bosutinib, and ponatinib and has been shown to have potential immunomodulatory effects. Dasatinib 9-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 29-32 23942795-1 2013 PURPOSE: Dasatinib is a dual Abl/Src tyrosine kinase inhibitor (TKI) designed as a prototypic short-acting BCR-ABL-targeted TKI that inhibits BCR-ABL with greater potency compared with imatinib, nilotinib, bosutinib, and ponatinib and has been shown to have potential immunomodulatory effects. Dasatinib 9-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 107-114 23942795-1 2013 PURPOSE: Dasatinib is a dual Abl/Src tyrosine kinase inhibitor (TKI) designed as a prototypic short-acting BCR-ABL-targeted TKI that inhibits BCR-ABL with greater potency compared with imatinib, nilotinib, bosutinib, and ponatinib and has been shown to have potential immunomodulatory effects. Dasatinib 9-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 142-149 23942795-5 2013 RESULTS: Dasatinib demonstrates efficacy against most BCR-ABL mutations arising during imatinib therapy and is effective in treating patients with imatinib resistance due to other mechanisms. Dasatinib 9-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 54-61 24236021-2 2013 The inhibitors such as imatinib, dasatinib and nilotinib are effective drugs but are resistant to some BCR-ABL mutations. Dasatinib 33-42 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 103-110 24155950-8 2013 These results open novel possibilities for the treatment of Bcr-Abl-positive leukemias, especially in the imatinib, dasatinib and nilotinib-resistant CML cases. Dasatinib 116-125 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 60-67 24130846-4 2013 Here, we applied an integrated experimental and computational approach that allowed us to estimate the differential impact of the bcr-abl inhibitors nilotinib, dasatinib, Bosutinib and Bafetinib. Dasatinib 160-169 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 130-137 24729782-6 2013 The Src kinase inhibitor PP2 was active only in cells grown on ripples, while the Abl inhibitors dasatinib and imatinib suppressed beta-catenin translocation on both structures. Dasatinib 97-106 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 82-85 23383600-4 2013 Following approval of second-generation BCR-ABL inhibitors in the first-line setting (nilotinib, dasatinib), which have significantly faster and deeper response rates than imatinib, molecular-based surrogate markers at earlier time points of 3 and 6 months are also being explored, although longer follow-up is needed. Dasatinib 97-106 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 40-47 23816609-0 2013 Through the open door: Preferential binding of dasatinib to the active form of BCR-ABL unveiled by in silico experiments. Dasatinib 47-56 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 79-86 23816609-1 2013 Dasatinib is a second-generation BCR-ABL inhibitor approved for the treatment of patients with chronic myeloid leukemia, both in the frontline and in the imatinib-resistant/intolerant settings. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 33-40 23816609-2 2013 The high affinity of dasatinib for the protein is currently assumed to result from its ability to bind both the active and inactive conformations of the BCR-ABL kinase. Dasatinib 21-30 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 153-160 23816609-3 2013 In the present work, using state of the art molecular simulation techniques we prove that dasatinib exhibits a highly selective preference for the active (open) BCR-ABL conformation. Dasatinib 90-99 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 161-168 23816609-4 2013 By using three different BCR-ABL conformations (active, inactive, and intermediate inactive) we show that, from a thermodynamic standpoint, the affinity of dasatinib for BCR-ABL drastically decreases in the order: active > alternative inactive > inactive, as a result of differential contributions from the single residues lining the kinase binding pocket and the concomitant stabilization/destabilization of the kinase hydrophobic spine. Dasatinib 156-165 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 25-32 23816609-4 2013 By using three different BCR-ABL conformations (active, inactive, and intermediate inactive) we show that, from a thermodynamic standpoint, the affinity of dasatinib for BCR-ABL drastically decreases in the order: active > alternative inactive > inactive, as a result of differential contributions from the single residues lining the kinase binding pocket and the concomitant stabilization/destabilization of the kinase hydrophobic spine. Dasatinib 156-165 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 170-177 23816609-5 2013 Molecule-pulling experiments also corroborate this trend as significantly lower forces and smaller times are required to extract dasatinib from its inactive BCR-ABL complexes with respect to the active complex counterparts. Dasatinib 129-138 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 157-164 24007855-0 2013 Impressive thrombocytosis evolving in a patient with a BCR-ABL positive CML in major molecular response during dasatinib treatment unmasks an additional JAK2V617F. Dasatinib 111-120 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 55-62 23906052-2 2013 These studies have led to the rapid development of many BCR-ABL specific tyrosine kinase inhibitors (TKIs), such as Imatinib, Nilotinib and Dasatinib, which have improved 10-years survival to more than 80%. Dasatinib 140-149 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 56-63 23433665-10 2013 Nine out of the 15 patients with ABL mutation responded to a treatment switch to nilotinib (n=4), dasatinib (n=2), interferon (n=1) or hematopoietic stem cell transplantation (n=2). Dasatinib 98-107 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 33-36 23630094-5 2013 The ABL1 gene at 9q34 was targeted by these rearrangements leading to its overexpression in L-1236 cells, correlating with pharmacological resistance to treatment with the kinase inhibitor dasatinib. Dasatinib 189-198 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 4-8 23466625-3 2013 We and others have shown that the BCR-ABL/SRC kinase inhibitor dasatinib may enhance or suppress T cells in vitro. Dasatinib 63-72 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 34-41 23715577-1 2013 PURPOSE: Dasatinib is a potent BCR-ABL inhibitor with proven efficacy in adults with newly diagnosed chronic myeloid leukemia (CML) in chronic phase (CP) and in imatinib-resistant/intolerant disease. Dasatinib 9-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 31-38 23576564-2 2013 However, clinical responses seen in patients treated with the ABL TKI dasatinib despite its much shorter plasma half-life and the apparent rapid restoration of BCR-ABL signaling activity following once-daily dosing suggested acute, potent inhibition of kinase activity may be sufficient to irrevocably commit CML cells to apoptosis. Dasatinib 70-79 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 62-65 23576564-2 2013 However, clinical responses seen in patients treated with the ABL TKI dasatinib despite its much shorter plasma half-life and the apparent rapid restoration of BCR-ABL signaling activity following once-daily dosing suggested acute, potent inhibition of kinase activity may be sufficient to irrevocably commit CML cells to apoptosis. Dasatinib 70-79 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 160-167 23065516-3 2013 This study compares intracellular concentration of dasatinib and Bcr-Abl kinase inhibition in CML-CD34(+) progenitors and mononuclear cells induced by dasatinib. Dasatinib 151-160 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 65-72 24385789-0 2013 Dasatinib May Override F317L BCR-ABL Kinase Domain Mutation in Patients with Chronic Myeloid Leukemia. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 29-36 23815902-0 2013 [Efficacy of dasatinib in treatment of imatinib-resistant BCR/ABL positive leukemia]. Dasatinib 13-22 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 58-65 23815902-1 2013 This study was aimed to evaluate the efficacy and safety of dasatinib in BCR/ABL positive leukemia patients with primary or secondary resistance to imatinib. Dasatinib 60-69 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 73-80 23815902-4 2013 The results showed that the median duration of dasatinib therapy was 8 (1-66) months in the 27 imatinib-resistant BCR/ABL positive leukemia cases, with a median follow-up of 54 (3-75) months. Dasatinib 47-56 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 114-121 23815902-10 2013 It is concluded that dasatinib is an effective drug in imatinib-resistant BCR/ABL positive leukemia patients, the better curative effect and better tolerance has been observed in patients who received dasatinib in stable disease. Dasatinib 21-30 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 74-81 23420553-0 2013 Apoptosis in chronic myeloid leukemia cells transiently treated with imatinib or dasatinib is caused by residual BCR-ABL kinase inhibition. Dasatinib 81-90 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 113-120 23065514-0 2013 The quantitative level of T315I mutated BCR-ABL predicts for major molecular response to second-line nilotinib or dasatinib treatment in patients with chronic myeloid leukemia. Dasatinib 114-123 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 40-47 23299860-0 2013 Molecular subtype and response to dasatinib, an Src/Abl small molecule kinase inhibitor, in hepatocellular carcinoma cell lines in vitro. Dasatinib 34-43 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 52-55 23299860-9 2013 Next, we evaluated whether molecular subgroup would have predictive value for response to the Src/Abl inhibitor dasatinib. Dasatinib 112-121 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 98-101 23247657-0 2013 The synthesis of Bcr-Abl inhibiting anticancer pharmaceutical agents imatinib, nilotinib and dasatinib. Dasatinib 93-102 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 17-24 23247657-1 2013 Imatinib (1), nilotinib (2) and dasatinib (3) are Bcr-Abl tyrosine kinase inhibitors approved for the treatment of chronic myelogenous leukemia (CML). Dasatinib 32-41 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 50-57 23372106-2 2013 Five currently available BCR-ABL inhibitors form the mainstay of CML treatment, including first-generation imatinib and more potent second-generation BCR-ABL inhibitors dasatinib and nilotinib, with bosutinib and ponatinib having been recently approved for market inclusion. Dasatinib 169-178 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 25-32 23372106-2 2013 Five currently available BCR-ABL inhibitors form the mainstay of CML treatment, including first-generation imatinib and more potent second-generation BCR-ABL inhibitors dasatinib and nilotinib, with bosutinib and ponatinib having been recently approved for market inclusion. Dasatinib 169-178 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 150-157 23233201-3 2013 The BCR/ABL fusion tyrosine kinase is expressed in chronic myeloid leukemia and Philadelphia-positive (Ph+) acute lymphoblastic leukemia cells, and its inhibition by the clinically used tyrosine kinase inhibitors imatinib or dasatinib induces apoptosis of these cells. Dasatinib 249-258 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 4-11 23233201-5 2013 Studies using imatinib and dasatinib as well as transient expression experiments in 293T cells revealed that PECAM-1 was phosphorylated directly by BCR/ABL, which was enhanced by the imatinib-resistant E255K and T315I mutations, or partly by the Src family tyrosine kinases, including Lyn, which were activated dependently or independently on BCR/ABL. Dasatinib 27-36 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 172-179 22392508-1 2013 PURPOSE: Dasatinib is an oral tyrosine kinase inhibitor (TKI) of BCR-ABL and SRC family and ixabepilone is an epothilone B analog. Dasatinib 9-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 65-72 23053188-0 2013 Impact of BCR-ABL mutations on response to dasatinib after imatinib failure in elderly patients with chronic-phase chronic myeloid leukemia. Dasatinib 43-52 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 10-17 23053188-4 2013 Our data suggest that, in elderly patients, detection of BCR-ABL mutations negatively affects response to dasatinib. Dasatinib 106-115 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 57-64 24240798-3 2013 Dasatinib was administered to inhibit Bcr-Abl and Lyn kinase. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 38-45 24240798-5 2013 To our knowledge, this is the first report to describe the occurrence of a gradual increase in the Bcr-Abl transcript level prior to the diagnosis of Ph-positive CML in an individual with CLL who was successfully treated with dasatinib as the first-line therapy. Dasatinib 226-235 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 99-106 23569389-1 2013 Dasatinib is a dual tyrosine kinase inhibitor active against ABL and Src family kinases, and is approved for the treatment of chronic myeloid leukemia (CML) patients in chronic, accelerated, or blast phase with resistance or intolerance to imatinib therapy, for newly diagnosed chronic phase patients, and for adults with Philadelphia chromosome-positive acute lymphoblastic leukemia who have become resistant to or intolerant of other treatments. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 61-64 24072218-2 2013 METHODS: Dasatinib is an oral multitarget tyrosine kinase inhibitor that targets BCR-ABL, c-Src, c-KIT, platelet-derived growth factor receptor beta, and EphA2. Dasatinib 9-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 81-88 23409026-14 2013 After the recent approval of nilotinib, dasatinib, bosutinib and ponatinib for treatment of chronic myeloid leukemia along with imatinib, all of which vary in their effectiveness against mutated BCR-ABL forms, detection of pre-existing BCR-ABL mutations can help in selection of appropriate first-line drug therapy. Dasatinib 40-49 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 195-202 23409026-14 2013 After the recent approval of nilotinib, dasatinib, bosutinib and ponatinib for treatment of chronic myeloid leukemia along with imatinib, all of which vary in their effectiveness against mutated BCR-ABL forms, detection of pre-existing BCR-ABL mutations can help in selection of appropriate first-line drug therapy. Dasatinib 40-49 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 236-243 24137941-6 2013 Among the BCR-ABL TK inhibitors (TKI) registered in the Russian Federation and recommended for the treatment of chronic myeloid leukemia, there are 3 medications: imatinib, nilotinib, and dasatinib. Dasatinib 188-197 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 10-17 23138519-1 2012 Dasatinib is a multi-kinase inhibitor that potently inhibits Bcr-Abl, Src family and platelet-derived growth factor receptor kinases. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 61-68 23138519-3 2012 Clinical trials utilizing a combination of dasatinib and methotrexate in patients with Philadelphia chromosome positive and/or Bcr-Abl positive acute lymphoblastic leukemia are currently ongoing. Dasatinib 43-52 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 127-134 23238683-2 2012 Indeed, inhibition of BCR-ABL by imatinib, dasatinib or nilotinib triggers durable responses in most patients suffering from this disease. Dasatinib 43-52 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 22-29 23090888-9 2012 Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacological profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutational status. Dasatinib 52-61 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 211-218 22992064-1 2012 INTRODUCTION: Dasatinib is a dual Abl/Src tyrosine kinase inhibitor (TKI), which was developed to treat patients with chronic myelogenous leukemia (CML), who had failed or were intolerant to therapy with imatinib. Dasatinib 14-23 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 34-37 22874537-3 2012 Here we show that the BCR-ABL/Src kinase inhibitor dasatinib decreases PRH phosphorylation and increases PRH-dependent repression of Vegf and Vegfr-1. Dasatinib 51-60 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 22-29 23010482-11 2012 Dasatinib suppressed phosphorylation of c-Src in both cell lines, but decreased repair of radiation-induced DNA damage in HN-5 cells only as evidenced by suppression of c-Abl and Nbs-1 activity, inhibition of the association between c-Src and EGFR or Her-2, prolongation of nuclear gamma-H2AX and 53BP1 foci and inhibition of EGFR nuclear localization and its association with DNA-PKcs. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 169-174 22554713-2 2012 Nilotinib and dasatinib strongly reduced telomerase activity in BCR-ABL-positive (K562) and BCR-ABL-negative (HL60) cells, demonstrating that their effect on telomerase activity is uncoupled from their effect on BCR-ABL. Dasatinib 14-23 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 64-71 22554713-2 2012 Nilotinib and dasatinib strongly reduced telomerase activity in BCR-ABL-positive (K562) and BCR-ABL-negative (HL60) cells, demonstrating that their effect on telomerase activity is uncoupled from their effect on BCR-ABL. Dasatinib 14-23 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 92-99 22554713-2 2012 Nilotinib and dasatinib strongly reduced telomerase activity in BCR-ABL-positive (K562) and BCR-ABL-negative (HL60) cells, demonstrating that their effect on telomerase activity is uncoupled from their effect on BCR-ABL. Dasatinib 14-23 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 92-99 22985168-3 2012 The ABL-kinase inhibitors (AKIs) Imatinib, Nilotinib or Dasatinib, which target the ATP-binding site, are effective in Ph + leukemia. Dasatinib 56-65 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 4-7 22985168-8 2012 Interestingly, the combination of Dasatinib and GNF-2 overcame resistance of BCR/ABL-T315I in all models used in a synergistic manner. Dasatinib 34-43 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 77-84 22419518-2 2012 NK large granular lymphocyte expansions associated with improved survival have been described under monotherapy with the Bcr-Abl/Src inhibitor dasatinib, which inhibits NK cell functions in vitro. Dasatinib 143-152 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 121-128 22689211-0 2012 Complete morphologic and molecular remission after introduction of dasatinib in the treatment of a pediatric patient with t-cell acute lymphoblastic leukemia and ABL1 amplification. Dasatinib 67-76 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 162-166 22689211-3 2012 Dasatinib, a second-generation tyrosine kinase inhibitor, directly targets the BCR-ABL gene. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 79-86 22689211-4 2012 We describe a pediatric case of T-cell ALL with amplification of the ABL1 gene in which remission was achieved only after the addition of dasatinib to conventional chemotherapy. Dasatinib 138-147 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 69-73 22591714-9 2012 Finally, we showed that MKN74 cells with CRKL amplification were responsive to the dual Src/BCR-ABL kinase inhibitor BMS354825, likely via the inhibition of CRKL phosphorylation, and that the proliferation of MKN74 cells was suppressed by treatment with a CRKL-targeting peptide. Dasatinib 117-126 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 92-99 22538170-1 2012 Dasatinib, a multitargeted inhibitor of BCR-ABL and SRC kinases, exhibits antitumor activity and extends the survival of patients with chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leukemia (ALL). Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 40-47 22428569-7 2012 Myeloma resistance to dexamethasone mediated by HS5 cells and osteoclasts was reversed by treatment with the Src/c-Abl inhibitor dasatinib but not with bortezomib. Dasatinib 129-138 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 113-118 22587422-4 2012 Despite the potent inhibition of BCR-ABL kinase by dasatinib, little is known about the relationship between dasatinib pharmacokinetics and the emergence of kinase domain mutations in vivo. Dasatinib 51-60 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 33-40 22587422-10 2012 Notably, these data also suggest that newly acquired BCR-ABL mutations may be inhibited by an increased exposure of dasatinib. Dasatinib 116-125 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 53-60 25031941-3 2012 The tyrosine kinase inhibitors imatinib, nilotinib, and dasatinib block the BCR-ABL protein and prevent activation of the transformation pathways. Dasatinib 56-65 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 76-83 22344285-7 2012 Our results indicate that whilst both BCR-ABL and c-ABL shuttle from the cytoplasm to the nucleus following dasatinib treatment, the temporal dynamics are not synchronized. Dasatinib 108-117 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 38-45 22344285-7 2012 Our results indicate that whilst both BCR-ABL and c-ABL shuttle from the cytoplasm to the nucleus following dasatinib treatment, the temporal dynamics are not synchronized. Dasatinib 108-117 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 50-55 22262776-5 2012 Specifically, GSK3beta activity and nuclear import were increased by imatinib mesylate (IM), a selective ABL inhibitor, but prevented by dasatinib that targets both BCR-ABL- and cytokine-dependent MAPK/p60-SRC activity. Dasatinib 137-146 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 165-172 22160483-1 2012 Dasatinib is a highly potent BCR-ABL inhibitor with established efficacy and safety in imatinib-resistant/-intolerant patients with chronic myeloid leukemia (CML). Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 29-36 22160483-5 2012 Cumulative response rates by 24 months in dasatinib and imatinib arms were: CCyR in 86% versus 82%, MMR in 64% versus 46%, and BCR-ABL reduction to <= 0.0032% (4.5-log reduction) in 17% versus 8%. Dasatinib 42-51 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 127-134 22233429-1 2012 Dasatinib (Sprycel ) is an orally administered small molecule inhibitor of multiple tyrosine kinases, including BCR-ABL and SRC family kinases, which is indicated for the treatment of adults with newly diagnosed chronic-phase chronic myeloid leukemia (CML), CML (chronic-, accelerated- or blast-phase) with resistance or intolerance to prior therapy, including imatinib, or Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) with resistance or intolerance to prior therapy. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 112-119 22233429-2 2012 Dasatinib is 325-fold more active than imatinib in inhibiting wild-type BCR-ABL kinase in vitro and is active against a wide variety of imatinib-resistant BCR-ABL mutants, except for T315I. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 73-80 22233429-2 2012 Dasatinib is 325-fold more active than imatinib in inhibiting wild-type BCR-ABL kinase in vitro and is active against a wide variety of imatinib-resistant BCR-ABL mutants, except for T315I. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 156-163 22233429-12 2012 Dasatinib was generally equally effective in patients with or without BCR-ABL mutations at baseline. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 70-77 21874302-4 2012 We here report that exposure of developing human monocyte-derived dendritic cells to the BCR-ABL inhibitors imatinib, dasatinib, and nilotinib results in profound upregulation of the transmembrane glycoprotein osteoactivin that has recently been characterized as a negative regulator of T-cell activation. Dasatinib 118-127 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 89-96 22285209-3 2012 Dasatinib has a half-maximal inhibitory concentration 325 times lower than imatinib for BCR-ABL substrate phosphorylation in vitro and is less susceptible to most known molecular mechanisms of BCR-ABL imatinib resistance. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 193-200 22262141-2 2012 This mutation confers resistance not only to imatinib, but also to second-generation BCR-ABL tyrosine kinases, such as nilotinib and dasatinib. Dasatinib 133-142 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 85-92 22089930-8 2012 RESULTS: The ABL-inhibitors imatinib and nilotinib activate MAPKs in CD34+ chronic myelogenous leukemia progenitor cells, whereas treatment with the SRC/ABL-inhibitor dasatinib does not affect MAPK-activation at clinically relevant concentrations. Dasatinib 167-176 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 153-156 21844872-5 2012 Recent randomized phase 3 trials have shown that first-line treatment with dasatinib or nilotinib-more potent BCR-ABL inhibitors-results in significantly higher rates and more rapid achievement of CCyR and MMR in comparison with standard-dose imatinib. Dasatinib 75-84 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 110-117 21717440-4 2012 Various strategies aimed at improving cytogenetic response have been explored, such as escalation of imatinib and switching to the newer breakpoint cluster region/v-abl Abelson murine leukemia viral oncogene (BCR-ABL) inhibitors dasatinib and nilotinib. Dasatinib 229-238 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 209-216 21751967-0 2012 Inhibition of cell growth and up-regulation of MAD2 in human oesophageal squamous cell carcinoma after treatment with the Src/Abl inhibitor dasatinib. Dasatinib 140-149 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 126-129 22956142-5 2012 Using Imatinib and BCR/ABL as a paradigm for a drug-target pair, we reported a retroviral vector-based screening strategy to identify the spectrum of resistance-conferring mutations, which has helped in designing the next-generation BCR/ABL inhibitors such as Nilotinib, Dasatinib, and Ponatinib. Dasatinib 271-280 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 19-26 22956142-5 2012 Using Imatinib and BCR/ABL as a paradigm for a drug-target pair, we reported a retroviral vector-based screening strategy to identify the spectrum of resistance-conferring mutations, which has helped in designing the next-generation BCR/ABL inhibitors such as Nilotinib, Dasatinib, and Ponatinib. Dasatinib 271-280 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 233-240 22846973-1 2012 BACKGROUND: With sorafenib displaying the highest affinities for Flt3, VEGFR (vascular endothelial growth factor receptor) and Raf and dasatinib for Abl and Src kinases, the profiles of kinases targeted by these inhibitors differ strongly. Dasatinib 135-144 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 149-152 23049975-9 2012 CONCLUSIONS/SIGNIFICANCE: The present results suggest that c-Abl is a potential therapeutic target for ALS and that the c-Abl inhibitor dasatinib has neuroprotective properties in vitro and in vivo. Dasatinib 136-145 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 59-64 23049975-9 2012 CONCLUSIONS/SIGNIFICANCE: The present results suggest that c-Abl is a potential therapeutic target for ALS and that the c-Abl inhibitor dasatinib has neuroprotective properties in vitro and in vivo. Dasatinib 136-145 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 120-125 22815843-3 2012 Here, we report a novel mechanism of prolonged intracellular TKI activity upon HD-TKI pulse-exposure (imatinib, dasatinib) in BCR-ABL-positive cells. Dasatinib 112-121 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 126-133 22493660-2 2012 The Abl inhibitors imatinib, nilotinib and dasatinib are currently used to treat CML, but resistance to these inhibitors is a significant clinical problem. Dasatinib 43-52 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 4-7 21931113-1 2011 Dasatinib is a potent BCR-ABL inhibitor effective in chronic myeloid leukemia and Ph(+) acute lymphoblastic leukemia (ALL) resistant/intolerant to imatinib. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 22-29 21908430-2 2011 The additional approved ABL tyrosine kinase inhibitors (TKIs) nilotinib and dasatinib, along with investigational TKIs such as ponatinib (AP24534) and DCC-2036, support the possibility that mutation-mediated resistance in chronic myeloid leukemia can be fully controlled; however, the molecular events underlying resistance in patients lacking BCR-ABL point mutations are largely unknown. Dasatinib 76-85 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 344-351 21990409-1 2011 PURPOSE: BCR-ABL1 mutation analysis is recommended to facilitate selection of appropriate therapy for patients with chronic myeloid leukemia after treatment with imatinib has failed, since some frequently occurring mutations confer clinical resistance to nilotinib and/or dasatinib. Dasatinib 272-281 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 13-17 21718141-6 2011 However, when a dasatinib-resistant K562 culture was generated we observed gradually increasing BCR-ABL expression which peaked prior to identification of the T315I mutation. Dasatinib 16-25 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 96-103 21902298-1 2011 Dasatinib (Sprycel ) is an orally administered small molecule inhibitor of multiple tyrosine kinases, including BCR-ABL and SRC family kinases, which is indicated for the treatment of adults with newly diagnosed chronic-phase chronic myeloid leukaemia (CML), CML (chronic-, accelerated- or blast-phase) with resistance or intolerance to prior therapy, including imatinib, or Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukaemia (ALL) with resistance or intolerance to prior therapy. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 112-119 21902298-2 2011 Dasatinib is 325-fold more active than imatinib in inhibiting wild-type ABL kinase in vitro and is active against a wide variety of imatinib-resistant BCR-ABL mutants, except for T315I. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 152-159 21902298-12 2011 Dasatinib was generally equally effective in patients with or without BCR-ABL mutations at baseline. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 70-77 21670084-2 2011 Among the most sensitive dasatinib targets are ABL, the SRC family kinases (SRC, LCK, HCK, FYN, YES, FGR, BLK, LYN, and FRK), and the receptor tyrosine kinases c-KIT, platelet-derived growth factor receptor (PDGFR) alpha and beta, discoidin domain receptor 1 (DDR1), c-FMS, and ephrin receptors. Dasatinib 25-34 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 47-50 21660654-4 2011 Small-molecule tyrosine kinase inhibitors, such as imatinib and dasatinib, directly inhibit the BCR-ABL kinase, offering a targeted approach as a therapeutic option. Dasatinib 64-73 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 96-103 21863287-7 2011 Tyrosine kinase inhibitors, imatinib and dasatinib, coadministered with dexamethasone achieved transient clinical effects in the present RCSD1-ABL1-positive ALL. Dasatinib 41-50 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 143-147 21633166-7 2011 M and MSL subtypes were enriched in GE for epithelial-mesenchymal transition, and growth factor pathways and cell models responded to NVP-BEZ235 (a PI3K/mTOR inhibitor) and dasatinib (an abl/src inhibitor). Dasatinib 173-182 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 187-190 21654685-8 2011 Treatment with the Src/Abl inhibitor, dasatinib, reduced HOXC11-SRC-1 interaction and prevented recruitment of HOXC11 to the S100beta promoter. Dasatinib 38-47 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 23-26 21528941-1 2011 Dasatinib is an oral dual tyrosine kinase inhibitor active against ABL1 and SRC family kinases. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 67-71 22035738-6 2011 Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacological profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutational status. Dasatinib 52-61 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 211-218 21454413-6 2011 Similarly, the treatment of primary MALT lymphoma cells with the ABL inhibitors imatinib and dasatinib prevented tumor cell growth. Dasatinib 93-102 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 65-68 21385851-1 2011 Dasatinib is a novel, potent, ATP-competitive inhibitor of Bcr-Abl, cKIT, and Src family kinases that exhibits efficacy in patients with imatinib-resistant chronic myelogenous leukemia. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 59-66 21505103-2 2011 The BCR-ABL(T315I) mutant is highly resistant to imatinib, nilotinib, and dasatinib, and is frequently detected in relapsed patients. Dasatinib 74-83 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 4-11 21463117-1 2011 Dasatinib is a kinase inhibitor that inhibits BCR-ABL, Src family kinases, c-Kit, and platelet-derived growth factor receptor kinase. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 46-53 21463117-3 2011 Potential targets for dasatinib in chronic lymphocytic leukemia (CLL) include Lyn (a Src family kinase), ABL, and the associated CD40 pathway. Dasatinib 22-31 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 105-108 21575924-8 2011 Patients who relapse during treatment with dasatinib frequently carry the T315I mutation of BCR-ABL. Dasatinib 43-52 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 92-99 21226671-1 2011 Dasatinib (BMS-354825, Sprycel ) is an oral, multitargeted inhibitor of receptor tyrosine kinases (RTKs), including BCR-ABL fusion protein, stem cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGFR), and Src family kinases (SFKs). Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 116-123 21226671-2 2011 Several early- and late-phase clinical trials for chronic myelogeneous leukaemia (CML) have demonstrated the direct inhibition of BCR-ABL fusion protein and SFKs, which led to dasatinib approval by the Food and Drug Administration (FDA) and the European Union for the treatment of imatinib-resistant or -intolerant CML, and Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL). Dasatinib 176-185 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 130-137 20942869-0 2011 An investigation of reversal of imatinib resistance in the Bcr-Abl positive imatinib-resistant cell line K562r by dasatinib, nilotinib, rapamycin and bortezomib. Dasatinib 114-123 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 59-66 20942869-8 2011 CONCLUSION: K562r due to duplication of autophosphorylation of wild-type Bcr-Abl induced by imatinib was still partially resistant to dasatinib and nilotinib, but this was overcome by incremental dosing. Dasatinib 134-143 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 73-80 20945321-9 2011 Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacologic profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutation status. Dasatinib 52-61 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 209-216 21263099-1 2011 UNLABELLED: PURPOSE Dasatinib is an orally available tyrosine kinase inhibitor with low nanomolar activity against SRC family kinases, BCR-ABL, c-KIT, EPHA2, and the PDGF-beta receptor. Dasatinib 20-29 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 135-142 21148814-3 2011 The dual Src/Abl inhibitors BMS354825 and SKI-606 blocked Chk1-inhibitor-induced extracellular signal-regulated kinase 1/2 (ERK1/2) activation, markedly increasing apoptosis in association with BimEL up-regulation, p34(cdc2) activation, and DNA damage in MM cell lines and primary CD138(+) MM samples. Dasatinib 28-37 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 13-16 21264552-1 2011 BCR-ABL kinase domain mutations were sequentially analyzed in a patient with chronic myeloid leukemia (CML) who exhibited repeated B-lymphoid blast crisis (CML-BC) during treatment with imatinib and dasatinib. Dasatinib 199-208 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 0-7 21264552-3 2011 The in vitro analysis using K294RGG mutant BCR-ABL-expressing 32D cells revealed that K294RGG mutation was imatinib resistant but dasatinib sensitive. Dasatinib 130-139 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 43-50 21264552-6 2011 However, after the dasatinib treatment, wild-type BCR-ABL clone disappeared and T315I or F317L mutation was acquired in G250E and Y253H mutant clones on the same allele without the emergence of each sole mutant clone. Dasatinib 19-28 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 50-57 21098337-2 2011 The recognition that some patients experience relapse due to resistance-conferring point mutations within BCR-ABL sparked the development of the second-generation ABL kinase inhibitors nilotinib and dasatinib. Dasatinib 199-208 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 106-113 21220945-1 2011 Therapies that target BCR-ABL in chronic myeloid leukemia, including imatinib, dasatinib and nilotinib, have dramatically improved patient outcome. Dasatinib 79-88 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 22-29 21220945-4 2011 In vitro, dasatinib and nilotinib inhibit most imatinib-resistant BCR-ABL mutations, except for T315I. Dasatinib 10-19 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 66-73 20807497-5 2011 This dual detection technique was used to evaluate the inhibition of c-Abl kinase by imatinib and dasatinib. Dasatinib 98-107 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 69-74 20473616-1 2011 Dasatinib is a highly potent Bcr-Abl inhibitor that is approved for the treatment of imatinib-resistant or -intolerant chronic myeloid leukemia (CML). Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 29-36 20952511-7 2011 Nilotinib and dasatinib (second-generation BCR-ABL inhibitors), at concentrations comparable to those used in therapy, increase the CKI but do not affect p27(Kip)1 level. Dasatinib 14-23 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 43-50 21792346-2 2011 The current second generation of FDA-approved ABL tyrosine kinase inhibitors, dasatinib and nilotinib, are more potent inhibitors of BCR-ABL1 kinase in vitro. Dasatinib 78-87 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 46-49 21792346-2 2011 The current second generation of FDA-approved ABL tyrosine kinase inhibitors, dasatinib and nilotinib, are more potent inhibitors of BCR-ABL1 kinase in vitro. Dasatinib 78-87 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 137-141 22087818-1 2011 In chronic myeloid leukemia (CML), BCR-ABL-mediated oncogenic signaling can be successfully targeted with the BCRABL- inhibitors imatinib, nilotinib, and dasatinib leading to complete cytogenetic (Philadelphia chromosome not detectable upon cytogenetic testing of bone marrow) and even complete molecular (BCR-ABL not detectable by PCR in peripheral blood) responses. Dasatinib 154-163 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 35-42 22087818-1 2011 In chronic myeloid leukemia (CML), BCR-ABL-mediated oncogenic signaling can be successfully targeted with the BCRABL- inhibitors imatinib, nilotinib, and dasatinib leading to complete cytogenetic (Philadelphia chromosome not detectable upon cytogenetic testing of bone marrow) and even complete molecular (BCR-ABL not detectable by PCR in peripheral blood) responses. Dasatinib 154-163 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 306-313 20962097-6 2011 While inhibitors of both Src and Abl family kinases, such as dasatinib (BMS-354825; Sprycel), are effective in limiting dissemination of VacV, VarV, and MPX in vitro, members of this class of drugs appear to have immunosuppressive effects in vivo that preclude their use as anti-infectives. Dasatinib 61-70 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 33-36 21632458-4 2011 A number of such studies have been published, and now that two inhibitors-dasatinib and nilotinib-are available for the treatment of imatinib-resistant cases, it is tempting for clinicians to reason on the IC50 values to guess, case by case, which one will work best in patients harboring specific Bcr-Abl KD mutations. Dasatinib 74-83 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 298-305 21108851-2 2010 Dasatinib and nilotinib, two newer drugs with higher potency than imatinib against BCR-ABL and activity against most imatinib-resistant BCR-ABL mutations, have each shown superior efficacy compared with imatinib for first-line treatment of chronic-phase CML in randomized phase 3 trials. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 83-90 21108851-2 2010 Dasatinib and nilotinib, two newer drugs with higher potency than imatinib against BCR-ABL and activity against most imatinib-resistant BCR-ABL mutations, have each shown superior efficacy compared with imatinib for first-line treatment of chronic-phase CML in randomized phase 3 trials. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 136-143 20629079-1 2010 BACKGROUND: Dasatinib, an inhibitor of Src/Abl family kinases, can inhibit tumor growth of several solid tumors. Dasatinib 12-21 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 43-46 20143399-0 2010 The BCR/ABL-inhibitors imatinib, nilotinib and dasatinib differentially affect NK cell reactivity. Dasatinib 47-56 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 8-11 20143399-1 2010 In chronic myeloid leukemia (CML), BCR/ABL-mediated oncogenic signaling can be targeted with the BCR/ABL-inhibitors Imatinib, Nilotinib and Dasatinib. Dasatinib 140-149 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 39-42 20143399-1 2010 In chronic myeloid leukemia (CML), BCR/ABL-mediated oncogenic signaling can be targeted with the BCR/ABL-inhibitors Imatinib, Nilotinib and Dasatinib. Dasatinib 140-149 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 101-104 20860375-5 2010 To validate the assay, the activity of two small-molecule kinase inhibitors, imatinib and dasatinib, which target the oncogenic mutant tyrosine kinase Bcr-Abl to treat chronic myeloid leukemia (CML), was tested. Dasatinib 90-99 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 151-158 20597967-8 2010 For such patients, novel multikinase inhibitors such as nilotinib, dasatinib, bosutinib or bafetinib, which block the kinase activity of various BCR/ABL1 mutants, have been developed and reportedly exert antileukaemic effects in drug-resistant cells. Dasatinib 67-76 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 149-153 20537386-6 2010 The second-generation BCR-ABL TKIs nilotinib (Tasigna) and dasatinib (Sprycel), showed significant activity in clinical trials in patients intolerant or resistant to imatinib therapy, except in those patients with the T315I BCR-ABL mutation. Dasatinib 59-68 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 22-29 20537386-6 2010 The second-generation BCR-ABL TKIs nilotinib (Tasigna) and dasatinib (Sprycel), showed significant activity in clinical trials in patients intolerant or resistant to imatinib therapy, except in those patients with the T315I BCR-ABL mutation. Dasatinib 59-68 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 224-231 20875551-8 2010 Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacological profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutational status. Dasatinib 52-61 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 211-218 20922699-12 2010 Inhibitors of the BCR-Abl tyrosine kinase domain on the Philadelphia chromosome (imatinib, nilotinib and dasatinib) may cause acute renal failure. Dasatinib 105-114 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 18-25 20447687-0 2010 A T315I mutation in e19a2 BCR/ABL1 chronic myeloid leukemia responding to dasatinib. Dasatinib 74-83 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 30-34 20615173-4 2010 Dasatinib is an oral kinase inhibitor of BCR-ABL that has been developed for treating CML patients across all phases of disease who are resistant or intolerant to imatinib. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 41-48 20557276-5 2010 Dasatinib, the first dual Src/Abl inhibitor approved by the US FDA in 2006 for the treatment of imatinib-resistant CML, is currently being tested in several clinical trials for the treatment of different solid tumors. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 30-33 20225261-2 2010 While designed to inhibit Abl and Src kinases, dasatinib shows multitarget effects, including inhibition of the macrophage colony-stimulating factor (M-CSF) receptor c-fms. Dasatinib 47-56 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 26-29 20139893-1 2010 Abl tyrosine kinase inhibitors (TKIs) such as imatinib and dasatinib are ineffective against Bcr-Abl(+) leukemic stem cells. Dasatinib 59-68 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 0-3 20375898-1 2010 PURPOSE OF REVIEW: Dasatinib is a novel tyrosine-kinase inhibitor approved for treatment of BCR-ABL positive chronic myeloid leukemia (CML) and Philadelphia chromosome positive acute lymphoblastic leukemia (ALL) after imatinib failure. Dasatinib 19-28 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 92-99 20585556-7 2010 HIV-1 Env-dependent cell-cell fusion, virus-cell fusion and infection were also inhibited by Abl kinase inhibitors, imatinib, nilotinib, and dasatinib. Dasatinib 141-150 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 93-96 20305692-1 2010 The use of c-abl-specific inhibitors such as Imatinib (IM) or Dasatinib has revolutionized the treatment of chronic myeloid leukemia (CML). Dasatinib 62-71 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 11-16 20222756-3 2010 Imatinib and dasatinib both target the tyrosine kinase activity of the BCR/ABL oncogenic fusion protein. Dasatinib 13-22 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 71-78 20222756-10 2010 Data suggest dasatinib 100 mg once daily achieves oncogenic shock and chronic inhibition of BCR/ABL activity, suggesting that in the future, pulse therapy with TKIs may be an option in some specific patients with CML. Dasatinib 13-22 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 92-99 20529808-9 2010 Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacologic profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutational status. Dasatinib 52-61 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 209-216 19768693-1 2010 We analysed the dynamic change of imatinib-resistant mutations in BCR-ABL kinase domain focusing on T315I mutation during dasatinib or nilotinib therapy. Dasatinib 122-131 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 70-73 20406945-1 2010 Dasatinib is an orally administered multitargeted kinase inhibitor that targets Src family tyrosine kinases, Abl, c-Kit, and PDGFR. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 109-112 20111071-0 2010 Development of resistance to dasatinib in Bcr/Abl-positive acute lymphoblastic leukemia. Dasatinib 29-38 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 46-49 20111071-1 2010 Dasatinib is a potent dual Abl/Src inhibitor approved for treatment of Philadelphia chromosome-positive (Ph-positive) leukemias. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 27-30 20111071-4 2010 Here, the effect of dasatinib on treatment of Bcr/Abl-positive acute lymphoblastic leukemia (ALL) cells was evaluated in the presence of stromal support. Dasatinib 20-29 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 50-53 20111071-5 2010 Dasatinib eradicated Bcr/Abl ALL cells, caused significant apoptosis and eliminated tyrosine phosphorylation on Bcr/Abl, Src, Crkl and Stat-5. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 25-28 20111071-5 2010 Dasatinib eradicated Bcr/Abl ALL cells, caused significant apoptosis and eliminated tyrosine phosphorylation on Bcr/Abl, Src, Crkl and Stat-5. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 116-119 20108303-1 2010 BACKGROUND: The recently developed the Src and Abelson (Abl) kinase inhibitor dasatinib has antitumor effects in epithelial and mesenchymal tumors. Dasatinib 78-87 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 47-54 20108303-1 2010 BACKGROUND: The recently developed the Src and Abelson (Abl) kinase inhibitor dasatinib has antitumor effects in epithelial and mesenchymal tumors. Dasatinib 78-87 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 56-59 20197479-4 2010 These strategies include upfront treatment with next-generation tyrosine kinase inhibitors, such as dasatinib, nilotinib, or bosutinib, which also target BCR-ABL but with increased in vitro potency compared with imatinib, and possibly a reduced potential for resistance. Dasatinib 100-109 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 154-161 20113198-1 2010 IMPORTANCE OF THE FIELD: Dasatinib is an oral, potent adenosine triphosphate-competitive inhibitor of multiple tyrosine kinases including BCR-ABL, c-KIT, platelet-derived growth factor receptor, and Src family kinases (SFKs). Dasatinib 25-34 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 138-145 20038231-5 2010 Dasatinib is a dual BCR-ABL/Src-family kinase (SFK) inhibitor approved for patients with imatinib-resistant and -intolerant CML in any phase and Ph+ ALL. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 20-27 20145167-1 2010 PURPOSE: Dasatinib is a dual Src/Abl inhibitor recently approved for Bcr-Abl+ leukemias with resistance or intolerance to prior therapy. Dasatinib 9-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 33-36 20145167-1 2010 PURPOSE: Dasatinib is a dual Src/Abl inhibitor recently approved for Bcr-Abl+ leukemias with resistance or intolerance to prior therapy. Dasatinib 9-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 69-76 20139391-0 2010 Potent, transient inhibition of BCR-ABL with dasatinib 100 mg daily achieves rapid and durable cytogenetic responses and high transformation-free survival rates in chronic phase chronic myeloid leukemia patients with resistance, suboptimal response or intolerance to imatinib. Dasatinib 45-54 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 32-39 20139391-1 2010 BACKGROUND: Dasatinib 100 mg once daily achieves intermittent BCR-ABL kinase inhibition and is approved for chronic-phase chronic myeloid leukemia patients resistant or intolerant to imatinib. Dasatinib 12-21 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 62-69 20001232-9 2010 The dual BCR-ABL/SRC family kinase inhibitor, dasatinib, has shown promising activity in the treatment of Ph+ ALL after imatinib failure and has recently been approved in this indication. Dasatinib 46-55 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 9-16 19924787-1 2010 BACKGROUND: Dasatinib, a highly potent BCR-ABL inhibitor, is an effective treatment for patients with chronic myeloid leukemia in chronic phase (CML CP) after resistance, suboptimal response, or intolerance to prior imatinib. Dasatinib 12-21 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 39-46 20460883-3 2010 This report presents the case of a patient with a post-transplant persistent positive BCR/ABL value, who was treated with imatinib and dasatinib before a second allo-HSCT. Dasatinib 135-144 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 86-93 20047099-0 2010 Successful prior treatment with dasatinib followed by stem cell transplantation in a patient with CML in blastic crisis with a BCR-ABL mutation. Dasatinib 32-41 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 127-134 20047099-2 2010 Before dasatinib therapy, the patient was found to have a F359V BCR-ABL mutation. Dasatinib 7-16 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 64-71 19798095-4 2010 Only a few BCR-ABL mutations seem to be less responsive to either nilotinib or dasatinib and it is recommended to choose the second-line TKI that has shown clinical activity against the specific mutation in these cases. Dasatinib 79-88 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 11-18 20072833-2 2010 It potently inhibits BCR-ABL and SRC-family kinases (SRC, LCK, YES, FYN), but also c-KIT, PDGFR-alpha and beta, and ephrin receptor kinase.Dasatinib is about 300 times more potent than imatinib in cells expressing unmutated BCR-ABL in vitro. Dasatinib 139-148 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 21-28 20072833-2 2010 It potently inhibits BCR-ABL and SRC-family kinases (SRC, LCK, YES, FYN), but also c-KIT, PDGFR-alpha and beta, and ephrin receptor kinase.Dasatinib is about 300 times more potent than imatinib in cells expressing unmutated BCR-ABL in vitro. Dasatinib 139-148 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 224-231 20072833-3 2010 The drug has demonstrated activity against clinically relevant mutations, including those associated with poor prognosis during ongoing imatinib therapy.Dasatinib is approved for the treatment of patients with BCR-ABL-positive chronic myeloid leukemia (CML), resistant or intolerant to imatinib in chronic, accelerated, and blast phase. Dasatinib 153-162 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 210-217 20072840-8 2010 However, this particular mutation is predicted to play an even more important clinical role in the future, since in addition to Imatinib, it also confers resistance to second-generation Bcr-Abl inhibitors such as Nilotinib, Dasatinib, and Bosutinib. Dasatinib 224-233 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 186-193 19880502-1 2009 Preclinical studies of BCR-ABL mutation sensitivity to nilotinib or dasatinib suggested that the majority would be sensitive. Dasatinib 68-77 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 23-30 19779040-0 2009 Dasatinib treatment of chronic-phase chronic myeloid leukemia: analysis of responses according to preexisting BCR-ABL mutations. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 110-117 19779040-1 2009 Dasatinib is a BCR-ABL inhibitor with 325-fold higher potency than imatinib against unmutated BCR-ABL in vitro. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 15-22 19779040-1 2009 Dasatinib is a BCR-ABL inhibitor with 325-fold higher potency than imatinib against unmutated BCR-ABL in vitro. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 94-101 19779040-3 2009 Here, dasatinib efficacy was analyzed in patients recruited to phase 2/3 trials with chronic-phase chronic myeloid leukemia with or without BCR-ABL mutations after prior imatinib. Dasatinib 6-15 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 140-147 19779040-9 2009 Overall, dasatinib has durable efficacy in patients with or without BCR-ABL mutations. Dasatinib 9-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 68-75 19672773-1 2009 Dasatinib, a dual Src/Abl tyrosine kinase inhibitor, has significant antileukemic effects against various imatinib mesylate-resistant BCR/ABL mutants. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 22-25 19672773-1 2009 Dasatinib, a dual Src/Abl tyrosine kinase inhibitor, has significant antileukemic effects against various imatinib mesylate-resistant BCR/ABL mutants. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 134-141 19672773-2 2009 Despite well-documented inhibitory effects of dasatinib on BCR/ABL kinase, the exact downstream cellular events leading to generation of its potent antileukemic effects remain to be defined. Dasatinib 46-55 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 63-66 19672773-3 2009 We provide evidence that p38 Map kinase (MAPK) pathway is activated leading to increased upregulation of mixed lineage kinase 3, MKK3/6, MSK1, and Mapkapk2, upon treatment of BCR/ABL expressing cells with dasatinib, including cells expressing various imatinib-resistant mutants, except for T315I. Dasatinib 205-214 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 175-182 19672773-6 2009 Altogether, our findings suggest a critical role for p38 MAPK pathway in the generation of antileukemic effects of dasatinib, and raise the possibility that development of novel means to enhance p38 MAPK activation in BCR/ABL expressing cells may be an approach to promote antileukemic responses and, possibly, reverse T315I mutation-mediated resistance. Dasatinib 115-124 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 218-225 20017607-5 2009 Dasatinib is a dual Abl/Src kinase TKI that is structurally unrelated to imatinib and is approved for therapy of all phases of CML in patients who are resistant or intolerant to imatinib. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 20-23 19651622-8 2009 In contrast to MAPK inhibitors, dasatinib, a clinical drug directed against BCR-ABL, which is the cause of chronic myelogenous leukemia, affected nearly 1,000 phosphopeptides. Dasatinib 32-41 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 76-83 19844167-5 2009 We found such genetic lesions to predict activity of geldanamycin-derived Hsp90 inhibitors as well as of the clinically approved SRC/ABL-inhibitor dasatinib. Dasatinib 147-156 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 133-136 19878872-1 2009 Inhibition of BCR-ABL by imatinib induces durable responses in many patients with chronic myeloid leukemia (CML), but resistance attributable to kinase domain mutations can lead to relapse and a switch to second-line therapy with nilotinib or dasatinib. Dasatinib 243-252 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 14-21 19706883-0 2009 Acute dasatinib exposure commits Bcr-Abl-dependent cells to apoptosis. Dasatinib 6-15 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 33-40 19706883-2 2009 Surprisingly, the second-generation Bcr-Abl inhibitor, dasatinib, was reported to be clinically effective with once-daily dosing, despite a short (3- to 5-hour) plasma half-life. Dasatinib 55-64 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 36-43 19706883-4 2009 Such acute treatments with clinically achievable dasatinib concentrations also irreversibly committed Bcr-Abl+ CML cell lines to apoptotic cell death. Dasatinib 49-58 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 102-109 19793709-4 2009 Resistance to imatinib has driven the development of second-line therapies, such as dasatinib, a dual BCR-ABL/SFK inhibitor more potent than imatinib at targeting BCR-ABL. Dasatinib 84-93 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 102-109 19793709-4 2009 Resistance to imatinib has driven the development of second-line therapies, such as dasatinib, a dual BCR-ABL/SFK inhibitor more potent than imatinib at targeting BCR-ABL. Dasatinib 84-93 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 163-170 19794096-0 2009 A novel dasatinib-sensitive RCSD1-ABL1 fusion transcript in chemotherapy-refractory adult pre-B lymphoblastic leukemia with t(1;9)(q24;q34). Dasatinib 8-17 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 34-38 19608684-0 2009 A co-operative evaluation of different methods of detecting BCR-ABL kinase domain mutations in patients with chronic myeloid leukemia on second-line dasatinib or nilotinib therapy after failure of imatinib. Dasatinib 149-158 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 60-67 19641527-1 2009 Dasatinib is a highly potent BCR-ABL inhibitor that has shown durable efficacy in patients with chronic phase (CP) chronic myeloid leukemia (CML) after resistance, suboptimal response, or intolerance to prior imatinib. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 29-36 19494352-1 2009 Dasatinib is an oral potent adenosine triphosphate (ATP)-competitive inhibitor of BCR-ABL, cKIT, platelet-derived growth factor receptor, and SRC family kinases (SFKs), which has demonstrated high efficiency in patients with imatinib-resistant chronic myelogenous leukemia. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 82-89 19295545-1 2009 Dasatinib, a broad-spectrum tyrosine kinase inhibitor (TKI), predominantly targets BCR-ABL and SRC oncoproteins and also inhibits off-target kinases, which may result in unexpected drug responses. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 83-90 19487385-2 2009 Dasatinib, a potent inhibitor of BCR-ABL and SRC-family kinases, has efficacy in patients with CML-AP who have experienced treatment failure with imatinib. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 33-40 19402171-3 2009 Dasatinib is a 325-fold more potent inhibitor of Bcr-Abl than imatinib and has been associated with high rates of durable responses in patients with CML in chronic phase (CP) after imatinib failure. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 49-56 19369231-1 2009 Dasatinib is the most potent BCR-ABL inhibitor, with 325-fold higher potency than imatinib against unmutated BCR-ABL in vitro. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 29-36 19369231-1 2009 Dasatinib is the most potent BCR-ABL inhibitor, with 325-fold higher potency than imatinib against unmutated BCR-ABL in vitro. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 109-116 19502190-3 2009 Dasatinib is the first and only dual BCR-ABL/SRC family kinase inhibitor approved by the U.S. Food and Drug Administration for the treatment of patients with CML in any phase or Philadelphia chromosome-positive acute lymphoblastic leukemia who are resistant to or intolerant of imatinib. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 37-44 19502192-1 2009 Dasatinib, an oral inhibitor of multiple tyrosine kinases, including BCR-ABL, Src, and platelet-derived growth factor receptor, was approved for patients with imatinib-resistant or -intolerant chronic myeloid leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL). Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 69-76 19282395-1 2009 Dasatinib was approved in 2006 for the treatment of imatinib-resistant chronic myelogenous leukemia and functions primarily through the inhibition of BCR-ABL and Src kinase. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 150-157 19455391-2 2009 Dasatinib is 325-fold more potent than imatinib in inhibiting BCR-ABL in vitro and is indicated for the treatment of chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leukemia resistant or intolerant to imatinib. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 62-69 19395585-1 2009 Dasatinib is a tyrosine kinase inhibitor (including BCR-ABL and the SRC family) that is effective in patients with chronic myeloid leukemia. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 52-59 19013641-2 2009 Dasatinib is a tyrosine kinase inhibitor with activity against BCR-ABL, platelet-derived growth factor receptors (PDGFRs), c- KIT, fibroblast growth factor receptors (FGFRs), SRC family kinases (SFKs), and EPHA receptors, all of which have been implicated in the pathogenesis of Ph- leukemias and myeloid disorders. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 63-70 18978822-0 2009 Dasatinib-induced restoration of donor chimerism in BCR-ABL1-positive ALL after failure of imatinib therapy and allo-SCT. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 56-60 19195046-1 2009 Dasatinib is a highly potent Bcr-Abl inhibitor that is approved for the treatment of imatinib-resistant or -intolerant chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leukemia. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 29-36 19363859-0 2009 Hair depigmentation during chemotherapy with dasatinib, a dual Bcr-Abl/Src family tyrosine kinase inhibitor. Dasatinib 45-54 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 63-70 19363859-2 2009 This article reports the case of a patient who experienced depigmentation of her eyelashes, eyebrows, and temporal scalp hair six-to-eight weeks after initiating treatment with dasatinib (BMS-354825 or Sprycel), a novel dual Bcr-Abl/Src family tyrosine kinase inhibitor for chronic myeloid leukemia (CML). Dasatinib 177-186 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 225-232 19536317-7 2009 Dasatinib is well tolerated and has broad efficacy, resulting in durable responses in patients with any BCR-ABL mutation except for T3151 and mutations in codon 317 - most commonly F317L - including mutations that were highly resistant to imatinib, such as L248, Y253, E255, F359, and H396. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 104-111 19275507-1 2009 Dasatinib, a tyrosine kinase inhibitor of BCR-ABL, was originally approved for the second-line treatment of any-phase chronic myelogenous leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia at a dosage of 70 mg twice daily. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 42-49 19236716-2 2009 Dasatinib is a tyrosine kinase inhibitor that has 325-fold greater in vitro activity against native BCR-ABL (breakpoint cluster region-Abelson leukemia virus) compared with imatinib and can overcome primary (intrinsic) and secondary (acquired) imatinib resistance. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 100-107 19236722-3 2009 RESULTS: We examined the inhibition of NQO2 activity by the Abl kinase inhibitors imatinib, nilotinib, and dasatinib, and obtained IC50 values of 80 nM, 380 nM, and >100 microM, respectively. Dasatinib 107-116 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 60-63 20616897-5 2009 Dasatinib is a multi-target kinase inhibitor which has increased potency and is able to inhibit most Bcr-Abl mutant cell lines. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 101-108 19100678-0 2009 Combined BCR-ABL inhibition with lentiviral-delivered shRNA and dasatinib augments induction of apoptosis in Philadelphia-positive cells. Dasatinib 64-73 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 9-16 19100678-1 2009 OBJECTIVE: This study investigated two approaches, short hairpin RNA (shRNA) and the potent ABL inhibitor, dasatinib, alone and together, to achieve complete inhibition of BCR-ABL activity in Philadelphia-positive (Ph(+)) cells. Dasatinib 107-116 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 92-95 19100678-1 2009 OBJECTIVE: This study investigated two approaches, short hairpin RNA (shRNA) and the potent ABL inhibitor, dasatinib, alone and together, to achieve complete inhibition of BCR-ABL activity in Philadelphia-positive (Ph(+)) cells. Dasatinib 107-116 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 172-179 19100678-11 2009 CONCLUSION: These results confirm that by lowering BCR-ABL levels with shRNA, complete inhibition of oncoprotein activity can be achieved with a lower concentration of dasatinib, thus providing a rationale for combining these approaches in the setting of high target expression, such as found in advanced phase disease and in the stem cell compartment. Dasatinib 168-177 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 51-58 19190119-2 2009 BMS-354825 (dasatinib) is an ATP-competitive small-molecule inhibitor effective in treating drug-resistant tumors with mutant BCR-ABL, KIT, and epidermal growth factor receptor by blocking tyrosine phosphorylation sites that are critical in tumorigenesis. Dasatinib 12-21 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 126-133 19296866-11 2009 Newer compounds, such as dasatinib, which targets the ABL active state, have been developed to increase potency and have proved effective for some, but not all, drug-resistant mutations. Dasatinib 25-34 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 54-57 18984583-4 2009 Here we report the crystal structure of the non-liganded form of Lyn kinase domain, as well as in complex with three different inhibitors: the ATP analogue AMP-PNP; the pan Src kinase inhibitor PP2; and the BCR-Abl/Src-family inhibitor Dasatinib. Dasatinib 236-245 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 207-214 20008223-4 2009 Second generation TKIs, eg, dasatinib and nilotinib, show activity against most of the bcr-abl tyrosine kinase domain (TKD) mutations involved in acquired imatinib resistance, but clinical benefit is generally short-lived. Dasatinib 28-37 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 87-94 19061839-1 2008 The BCR-ABL inhibitor dasatinib achieves clinical remissions in chronic myeloid leukemia (CML) patients using a dosing schedule that achieves potent but transient BCR-ABL inhibition. Dasatinib 22-31 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 4-11 19061839-1 2008 The BCR-ABL inhibitor dasatinib achieves clinical remissions in chronic myeloid leukemia (CML) patients using a dosing schedule that achieves potent but transient BCR-ABL inhibition. Dasatinib 22-31 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 163-170 19061839-2 2008 In vitro, transient potent BCR-ABL inhibition with either dasatinib or imatinib is cytotoxic to CML cell lines, as is transient potent EGFR inhibition with erlotinib in a lung cancer cell line. Dasatinib 58-67 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 27-34 19061839-5 2008 In CML patients receiving dasatinib once daily, response correlates with the magnitude of BCR-ABL kinase inhibition, thereby demonstrating the potential clinical utility of intermittent potent kinase inhibitor therapy. Dasatinib 26-35 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 90-97 18938156-1 2008 Imatinib, nilotinib and dasatinib are protein kinase inhibitors which target the tyrosine kinase activity of the Breakpoint Cluster Region-Abelson kinase (BCR-ABL) and are used to treat chronic myelogenous leukemia. Dasatinib 24-33 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 113-153 18938156-1 2008 Imatinib, nilotinib and dasatinib are protein kinase inhibitors which target the tyrosine kinase activity of the Breakpoint Cluster Region-Abelson kinase (BCR-ABL) and are used to treat chronic myelogenous leukemia. Dasatinib 24-33 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 155-162 19062342-1 2008 The dual c-abl/Src kinase inhibitor, dasatinib, utilized to treat chronic myeloid leukaemia (CML) when used at clinically attainable sublethal concentrations, synergistically sensitized primary chronic lymphocytic leukaemia (CLL) lymphocytes to chlorambucil and fludarabine. Dasatinib 37-46 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 9-14 19062342-3 2008 Dasatinib resistance and poorer dasatinib-mediated sensitization to chlorambucil and fludarabine was associated with higher expression of c-abl protein levels. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 138-143 19062342-3 2008 Dasatinib resistance and poorer dasatinib-mediated sensitization to chlorambucil and fludarabine was associated with higher expression of c-abl protein levels. Dasatinib 32-41 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 138-143 19047139-4 2008 Dasatinib (BMS-354825) is a potent dual Abl/Src kinase inhibitor approved for clinical use in CML patients. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 40-43 19047139-7 2008 Dasatinib showed potent Src inhibitory activity in CML progenitors, inhibiting both Bcr-Abl-dependent and -independent Src activity. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 88-91 19047139-12 2008 Our results indicate that Dasatinib, in addition to potent anti-Bcr-Abl kinase activity, effectively inhibits Src kinase activity and downstream signaling pathways in CML progenitors but does not induce a strong proapoptotic response. Dasatinib 26-35 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 68-71 19047160-9 2008 In contrast, dasatinib, a dual Bcr-Abl and Src kinase inhibitor, inhibited the phosphorylation of both BCR-ABL and Lyn, and induced apoptosis of the Bcr-Abl cell line overexpressing p53/56 Lyn. Dasatinib 13-22 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 31-38 19047160-9 2008 In contrast, dasatinib, a dual Bcr-Abl and Src kinase inhibitor, inhibited the phosphorylation of both BCR-ABL and Lyn, and induced apoptosis of the Bcr-Abl cell line overexpressing p53/56 Lyn. Dasatinib 13-22 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 103-110 19047160-9 2008 In contrast, dasatinib, a dual Bcr-Abl and Src kinase inhibitor, inhibited the phosphorylation of both BCR-ABL and Lyn, and induced apoptosis of the Bcr-Abl cell line overexpressing p53/56 Lyn. Dasatinib 13-22 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 149-156 18754032-1 2008 Dasatinib is an inhibitor of BCR-ABL and SRC-family kinases for patients with imatinib-resistant or -intolerant chronic myelogenous leukemia (CML). Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 29-36 18992904-2 2008 The cytotoxic activities of all compounds were investigated on K562R (imatinib-resistant) human chronic myeloid leukaemia and DA1-3b/M2(BCR-ABL) (dasatinib-resistant) mouse leukemia cell line. Dasatinib 146-155 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 136-143 19010823-3 2008 Dasatinib (BMS-354825) is a dual Src/Abl kinase inhibitor with potent antiproliferative activity against hematologic malignancies harboring activated BCR-ABL. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 150-157 18669873-8 2008 Compared with imatinib, dasatinib achieved superior intracellular levels and BCR-ABL suppression even in cells with low or blocked hOCT1. Dasatinib 24-33 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 77-84 20641266-5 2004 Dasatinib is a dual inhibitor of Src/Abl and c-Kit that was recently approved for treatment of imatinib-refractory CML and Ph+ acute lymphoblastic leukemia (ALL) (5, 6). Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 37-40 18797457-3 2008 Dasatinib, which is a multi-targeted kinase inhibitor mainly developed for Bcr-Abl and Src family kinases, has recently been shown to have significant activity against EphA2. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 75-82 18829496-2 2008 EXPERIMENTAL DESIGN: We used TF-1 BCR/ABL cells, by introducing the BCR/ABL gene into a leukemia cell line, TF-1 and K562, and established dasatinib- (BMS-R) and imatinib-resistant (IM-R) cells. Dasatinib 139-148 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 34-41 18829496-2 2008 EXPERIMENTAL DESIGN: We used TF-1 BCR/ABL cells, by introducing the BCR/ABL gene into a leukemia cell line, TF-1 and K562, and established dasatinib- (BMS-R) and imatinib-resistant (IM-R) cells. Dasatinib 139-148 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 68-75 18829496-4 2008 RESULTS: The IC(50) of dasatinib was 0.75 nmol/L (TF-1 BCR/ABL), 1 nmol/L (K562), 7.5 nmol/L (TF-1 BCR/ABL IM-R), 10 nmol/L (K562 IM-R), 15 micromol/L (TF-1 BCR/ABL BMS-R), and 25 micromol/L (K562 BMS-R). Dasatinib 23-32 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 50-62 18829496-4 2008 RESULTS: The IC(50) of dasatinib was 0.75 nmol/L (TF-1 BCR/ABL), 1 nmol/L (K562), 7.5 nmol/L (TF-1 BCR/ABL IM-R), 10 nmol/L (K562 IM-R), 15 micromol/L (TF-1 BCR/ABL BMS-R), and 25 micromol/L (K562 BMS-R). Dasatinib 23-32 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 55-62 18829496-4 2008 RESULTS: The IC(50) of dasatinib was 0.75 nmol/L (TF-1 BCR/ABL), 1 nmol/L (K562), 7.5 nmol/L (TF-1 BCR/ABL IM-R), 10 nmol/L (K562 IM-R), 15 micromol/L (TF-1 BCR/ABL BMS-R), and 25 micromol/L (K562 BMS-R). Dasatinib 23-32 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 94-106 18829496-7 2008 We found that protein levels of BCR/ABL were reduced in dasatinib-resistant cell lines. Dasatinib 56-65 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 32-39 19383348-1 2008 We have identified differentially regulated genes in chronic myeloid leukemia (CML) cells upon short treatment with the broad-spectrum Bcr-Abl inhibitor dasatinib. Dasatinib 153-162 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 135-142 19383348-2 2008 The highly specific Bcr-Abl inhibitor nilotinib caused a very similar gene expression signature, validating the identified differentially regulated genes as a read-out of Bcr-Abl activity and implying that Bcr-Abl is the functionally central target of dasatinib in CML cells. Dasatinib 252-261 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 20-27 19383348-2 2008 The highly specific Bcr-Abl inhibitor nilotinib caused a very similar gene expression signature, validating the identified differentially regulated genes as a read-out of Bcr-Abl activity and implying that Bcr-Abl is the functionally central target of dasatinib in CML cells. Dasatinib 252-261 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 171-178 19383348-2 2008 The highly specific Bcr-Abl inhibitor nilotinib caused a very similar gene expression signature, validating the identified differentially regulated genes as a read-out of Bcr-Abl activity and implying that Bcr-Abl is the functionally central target of dasatinib in CML cells. Dasatinib 252-261 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 171-178 19383348-4 2008 Expression of both proteins is upregulated upon Bcr-Abl expression and inhibited by dasatinib and nilotinib. Dasatinib 84-93 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 48-55 18827790-8 2008 Dasatinib and nilotinib are the most extensively studied second-generation BCR-ABL tyrosine kinase inhibitors, and are currently approved for treating patients following imatinib failure. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 75-82 18759691-4 2008 In order to override this resistance, several second generation ATP-competitive Abl TKIs including dasatinib, nilotinib, bosutinib and INNO-406 have been developed. Dasatinib 99-108 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 80-83 18477770-8 2008 In 3 additional patients, isolated CNS relapse occurred during dasatinib therapy; and in 2 of them, it was caused by expansion of a BCR-ABL-mutated dasatinib-resistant clone, implying selection pressure exerted by the compound in the CNS. Dasatinib 148-157 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 132-139 18519516-0 2008 Centrosome aberrations and G1 phase arrest after in vitro and in vivo treatment with the SRC/ABL inhibitor dasatinib. Dasatinib 107-116 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 93-96 18519516-1 2008 BACKGROUND: Dasatinib is a multitargeted inhibitor of ABL, the SRC family, and other tyrosine kinases. Dasatinib 12-21 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 54-57 18326784-0 2008 Dual inhibition of c-abl and PDGF receptor signaling by dasatinib and nilotinib for the treatment of dermal fibrosis. Dasatinib 56-65 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 19-24 18326784-2 2008 The aim of the present study was to evaluate the antifibrotic potential of dasatinib and nilotinib, 2 novel inhibitors of c-abl and PDGF, which are well tolerated and have recently been approved. Dasatinib 75-84 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 122-127 18541900-1 2008 PURPOSE: Dasatinib is a BCR-ABL inhibitor, 325-fold more potent than imatinib against unmutated BCR-ABL in vitro. Dasatinib 9-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 24-31 18541900-1 2008 PURPOSE: Dasatinib is a BCR-ABL inhibitor, 325-fold more potent than imatinib against unmutated BCR-ABL in vitro. Dasatinib 9-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 96-103 18559612-2 2008 The tyrosine kinase (TK) inhibitor dasatinib is 325-fold more potent against Bcr-Abl TK than imatinib in vitro, significantly inhibiting wild-type KIT and platelet-derived growth factor receptor beta TKs, and is active against cells carrying the mutant KIT-D816V gene. Dasatinib 35-44 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 77-84 18366061-3 2008 The treatment of advanced Ph+ leukemia with selective ABL-kinase inhibitors such as Imatinib, Nilotinib and Dasatinib is initially effective but rapidly followed by resistance mainly because of specific mutations in BCR/ABL. Dasatinib 108-117 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 54-57 18366061-3 2008 The treatment of advanced Ph+ leukemia with selective ABL-kinase inhibitors such as Imatinib, Nilotinib and Dasatinib is initially effective but rapidly followed by resistance mainly because of specific mutations in BCR/ABL. Dasatinib 108-117 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 216-223 18395492-0 2008 The Src/ABL kinase inhibitor dasatinib (BMS-354825) inhibits function of normal human T-lymphocytes in vitro. Dasatinib 29-38 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 8-11 18395492-0 2008 The Src/ABL kinase inhibitor dasatinib (BMS-354825) inhibits function of normal human T-lymphocytes in vitro. Dasatinib 40-50 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 8-11 18395492-1 2008 Dasatinib (BMS-354825) is a Src/ABL tyrosine kinase inhibitor currently approved for the treatment of chronic myeloid leukemia. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 32-35 18395492-2 2008 Dasatinib has increased potency against ABL compared to the current therapy imatinib, and is effective in many cases where disease is resistant to imatinib. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 40-43 18491988-3 2008 This discovery prompted the development of new Abl kinase inhibitors, among which nilotinib and dasatinib have gained regulatory approval. Dasatinib 96-105 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 47-50 18491988-4 2008 Despite excellent results in patients with imatinib-resistant or imatinib-intolerant CML treated with nilotinib or dasatinib, early indications suggest that: the cross-resistant Bcr-Abl(T315I) mutant is disproportionately represented among patients who relapse on these therapies; each Abl inhibitor exhibits vulnerabilities to certain kinase domain mutations. Dasatinib 115-124 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 178-185 18491988-4 2008 Despite excellent results in patients with imatinib-resistant or imatinib-intolerant CML treated with nilotinib or dasatinib, early indications suggest that: the cross-resistant Bcr-Abl(T315I) mutant is disproportionately represented among patients who relapse on these therapies; each Abl inhibitor exhibits vulnerabilities to certain kinase domain mutations. Dasatinib 115-124 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 182-185 18191450-2 2008 Dasatinib exhibited the strongest potency against BCR-ABL with little selectivity over SFKs. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 50-57 18191450-5 2008 Both nilotinib and INNO-406 were potent inhibitors of the dasatinib-resistant T315A, F317L and F317V BCR-ABL mutations. Dasatinib 58-67 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 101-108 18401416-1 2008 Dasatinib, a potent inhibitor of BCR-ABL in vitro, is effective for patients with chronic myelogenous leukemia (CML) resistant or intolerant to imatinib. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 33-40 18401417-9 2008 Moreover, dasatinib was active in a NUP214-ABL1-positive leukemia xenograft murine model and in marrow lymphoblasts from a patient with NUP214-ABL1-positive T-ALL. Dasatinib 10-19 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 143-147 18348294-1 2008 The majority of patients with chronic-phase (CP) chronic myeloid leukemia (CML) who are treated with Bcr-Abl tyrosine kinase inhibitors such as imatinib and dasatinib achieve cytogenetic disease remission (ie, Philadelphia chromosome-positive cells undetectable by cytogenetic evaluation). Dasatinib 157-166 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 101-108 18413841-1 2008 PURPOSE: The dual BCR-ABL/SRC kinase inhibitor dasatinib entered the clinic for the treatment of chronic myeloid leukemia and Ph+ acute lymphoblastic leukemia. Dasatinib 47-56 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 18-25 18367669-2 2008 The second-line inhibitors nilotinib and dasatinib are effective in patients with imatinib resistance resulting from Bcr-Abl kinase domain mutations. Dasatinib 41-50 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 117-124 18367669-6 2008 Combining SGX393 with nilotinib or dasatinib preempted emergence of resistant subclones, including Bcr-Abl(T315I). Dasatinib 35-44 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 99-106 17851552-0 2008 A new case with rare e6a2 BCR-ABL fusion transcript developing two new resistance mutations during imatinib mesylate, which were replaced by T315I after subsequent dasatinib treatment. Dasatinib 164-173 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 26-33 18398719-5 2008 This function leads to resistance to ABL kinase small molecular inhibitors (SMIs) imatinib (IM), dasatinib and nilotinib, and contributes to malignant progression of the disease. Dasatinib 97-106 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 37-40 18448557-8 2008 Dasatinib, a dual Bcr-Abl/Src kinase inhibitor, has shown efficacy against all imatinib-resistant Bcr-Abl mutations except for T315I. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 18-25 18448557-8 2008 Dasatinib, a dual Bcr-Abl/Src kinase inhibitor, has shown efficacy against all imatinib-resistant Bcr-Abl mutations except for T315I. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 98-105 19254884-5 2008 Dasatinib is also an oral kinase inhibitor, but it has increased potency for Brc-Abl compared with imatinib. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 81-84 17962511-1 2008 Dasatinib is an oral small molecule inhibitor of Abl and Src family tyrosine kinases (SFK), including p56(Lck) (Lck). Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 49-52 18245668-0 2008 IkappaB kinase beta inhibition induces cell death in Imatinib-resistant and T315I Dasatinib-resistant BCR-ABL+ cells. Dasatinib 82-91 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 102-109 18245668-7 2008 These data indicate that blockage of BCR-ABL-induced NF-kappaB activation via IkappaB kinase beta inhibition represents a potential new approach for treatment of Imatinib- or Dasatinib-resistant forms of chronic myelogenous leukemia. Dasatinib 175-184 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 37-44 18202781-3 2008 Dasatinib, an oral multi-targeted inhibitor of several kinases including BCR-ABL and SRC-family kinases, is also active against c-KIT and PDGFR. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 73-80 18346528-6 2008 Imatinib resistance has, in part, been addressed with the introduction of the new BCR-ABL inhibitors, namely dasatinib and nilotinib. Dasatinib 109-118 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 82-89 18215092-1 2008 Dasatinib is a small-molecule inhibitor of multiple tyrosine kinases, including BCR-ABL, SRC, c-KIT, ephrin A receptor and platelet-derived growth factor-beta receptor kinases, at nanomolar concentrations. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 80-87 18215092-2 2008 In vitro, dasatinib is 325-fold more potent than imatinib against cells expressing wild-type BCR-ABL. Dasatinib 10-19 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 93-100 18673174-8 2008 In order to address the resistance of mutated BCR-ABL to imatinib, 2(nd) generation inhibitors such as dasatinib, and nilotinib were developed. Dasatinib 103-112 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 46-53 18401881-8 2008 Dasatinib, with increased binding potency (325-fold greater potency than imatinib for wild-type BCR-ABL), inhibition of both the active and inactive formation of BCR-ABL, and targeting of SRC family kinases, is the only agent approved for the treatment of patients with imatinib-resistant or -intolerant CML and Ph+ ALL. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 96-103 18401881-8 2008 Dasatinib, with increased binding potency (325-fold greater potency than imatinib for wild-type BCR-ABL), inhibition of both the active and inactive formation of BCR-ABL, and targeting of SRC family kinases, is the only agent approved for the treatment of patients with imatinib-resistant or -intolerant CML and Ph+ ALL. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 162-169 18436994-0 2008 Dasatinib treatment can overcome imatinib and nilotinib resistance in CML patient carrying F359I mutation of BCR-ABL oncogene. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 109-116 18436994-2 2008 In most CML cases with BCR-ABL mutations leading to imatinib resistance the second generation of tyrosine kinase inhibitors (TKI- e.g. nilotinib or dasatinib) may be effective. Dasatinib 148-157 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 23-30 18203007-6 2008 The dual SFK/BCR-ABL inhibitor dasatinib is now clinically available and has markedly greater potency compared with imatinib against native BCR-ABL and the majority of imatinib-resistant BCR-ABL mutants. Dasatinib 31-40 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 13-20 18203007-6 2008 The dual SFK/BCR-ABL inhibitor dasatinib is now clinically available and has markedly greater potency compared with imatinib against native BCR-ABL and the majority of imatinib-resistant BCR-ABL mutants. Dasatinib 31-40 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 140-147 18203007-6 2008 The dual SFK/BCR-ABL inhibitor dasatinib is now clinically available and has markedly greater potency compared with imatinib against native BCR-ABL and the majority of imatinib-resistant BCR-ABL mutants. Dasatinib 31-40 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 140-147 19248584-9 2008 Dasatinib, dual Bcr-Abl/Src kinase inhibitor, is of high activity and induces hematologic and cytogenetic responses in patients with chronic myelogenous leukaemia in blast crisis. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 16-23 18056927-14 2007 Dasatinib is the second BCR-ABL inhibitor to become available. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 24-31 18056927-16 2007 Dasatinib also inhibits SRC kinase, which may play a role in both maintaining BCR-ABL activity and in BCR-ABL independent signaling pathways. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 78-85 18056927-16 2007 Dasatinib also inhibits SRC kinase, which may play a role in both maintaining BCR-ABL activity and in BCR-ABL independent signaling pathways. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 102-109 18056932-16 2007 The second generation BCR-ABL inhibitor, dasatinib, can block the activity of many of these mutations; however, the T315I mutation, at present, is resistant to all available kinase inhibitors. Dasatinib 41-50 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 22-29 17720881-0 2007 Chemical proteomic profiles of the BCR-ABL inhibitors imatinib, nilotinib, and dasatinib reveal novel kinase and nonkinase targets. Dasatinib 79-88 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 35-42 17720881-2 2007 Because many patients develop imatinib resistance, 2 second-generation drugs, nilotinib and dasatinib, displaying increased potency against BCR-ABL were developed. Dasatinib 92-101 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 140-147 17785585-1 2007 Dasatinib and nilotinib are potent tyrosine kinase inhibitors (TKIs) with activity against many imatinib-resistant chronic myeloid leukemia (CML) clones with BCR-ABL kinase domain (KD) mutations, except T315I. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 158-165 18035968-2 2007 In an in vitro study, dasatinib had 325-fold greater potency than imatinib for inhibiting unmutated BCR-ABL. Dasatinib 22-31 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 100-107 18067005-3 2007 The investigation of therapeutic options post-imatinib failure resulted in the development and regulatory approval of dasatinib, a BCR-ABL and SRC-family kinase inhibitor. Dasatinib 118-127 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 131-138 19662183-6 2007 We set out to develop a novel drug whose affinity for Abl is higher than that of imatinib and whose specificity in inhibiting Lyn is higher than that of SFK/Abl inhibitors such as dasatinib (Sprycel) or bosutinib (SKI-606). Dasatinib 180-189 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 157-160 17268817-0 2007 Dasatinib, an orally active small molecule inhibitor of both the src and abl kinases, selectively inhibits growth of basal-type/"triple-negative" breast cancer cell lines growing in vitro. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 73-76 17268817-1 2007 Dasatinib is an orally active small molecule kinase inhibitor of both the src and abl proteins. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 82-85 18158072-9 2007 Dasatinib has shown in vitro and in vivo activity against BCR-ABL, including mutations that are resistant to other available TK inhibitors. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 58-65 18158072-17 2007 CONCLUSIONS: Dasatinib has a wider spectrum of activity against a broader range of BCR-ABL forms than existing TK inhibitors. Dasatinib 13-22 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 83-90 18020922-0 2007 Management of Bcr-Abl-positive leukemias with dasatinib. Dasatinib 46-55 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 14-21 17496200-3 2007 We also provide a perspective on how the second-line Abl inhibitors dasatinib and nilotinib are faring in the treatment of imatinib-resistant CML, especially in relation to specific KD mutations. Dasatinib 68-77 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 53-56 17496201-2 2007 Dasatinib, a novel, oral, multitargeted kinase inhibitor of BCR-ABL and SRC family kinases, has previously induced responses in patients with imatinib-resistant or -intolerant Ph-positive ALL. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 60-67 17964981-4 2007 The emergence of resistance to the Bcr-Abl inhibitor imatinib mesylate in patients with Philadelphia chromosome-positive (Ph+) ALL has prompted the development of second-generation compounds active against mutant forms, including dasatinib and nilotinib. Dasatinib 230-239 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 35-42 17727673-13 2007 For systemic treatment and prophylaxis, BCR/ABL kinase inhibitors crossing the blood-brain barrier such as dasatinib should be considered in patients with CNS relapse. Dasatinib 107-116 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 40-47 17929114-8 2007 Dasatinib (formerly BMS-354825), AP23464, SKI-606, and PD166326 are classified as Src/Abl inhibitors, while nilotinib (AMN107) and INNO-406 (NS-187) belong to the latter subclass of inhibitors. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 86-89 17970610-16 2007 dasatinib is a next-generation kinase inhibitor that binds to both SrC and to multiple conformations of BCR-ABL. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 104-111 17853901-3 2007 The second-generation BCR-ABL inhibitors nilotinib (Tasigna; Novartis) and dasatinib (Sprycel; Bristol-Myers Squibb) have shown significant activity after imatinib failure in clinical trials, but still face similar obstacles to imatinib, including negligible activity against the frequent BCR-ABL T315I mutation and modest effects in advanced phases of CML. Dasatinib 75-84 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 22-29 17853901-3 2007 The second-generation BCR-ABL inhibitors nilotinib (Tasigna; Novartis) and dasatinib (Sprycel; Bristol-Myers Squibb) have shown significant activity after imatinib failure in clinical trials, but still face similar obstacles to imatinib, including negligible activity against the frequent BCR-ABL T315I mutation and modest effects in advanced phases of CML. Dasatinib 75-84 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 289-296 17701954-9 2007 Dasatinib is a multitargeted kinase inhibitor of BCR-ABL, SRC, C-KIT, PDGFRs, and ephrin A receptor kinases. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 49-56 17710227-3 2007 Analysis of BCR-ABL genotypes in CML patients who relapsed after sequential treatment with the ABL inhibitors imatinib and dasatinib revealed evolving resistant BCR-ABL kinase domain mutations in all cases. Dasatinib 123-132 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 12-19 17721511-5 2007 Quantitative profiling of the drugs imatinib (Gleevec), dasatinib (Sprycel) and bosutinib in K562 cells confirms known targets including ABL and SRC family kinases and identifies the receptor tyrosine kinase DDR1 and the oxidoreductase NQO2 as novel targets of imatinib. Dasatinib 56-65 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 137-140 17684099-0 2007 The Btk tyrosine kinase is a major target of the Bcr-Abl inhibitor dasatinib. Dasatinib 67-76 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 49-56 17317857-3 2007 Dasatinib, a significantly more potent inhibitor of BCR-ABL, is safe and effective in this population. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 52-59 17213809-1 2007 Dasatinib is an ATP-competitive, multi-targeted SRC and ABL kinase inhibitor that can bind BCR-ABL in both the active and inactive conformations. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 91-98 17213809-3 2007 The fact because the combination of imatinib and dasatinib shows the additive/synergistic growth inhibition on wild-type p210 BCR-ABL-expressing cells, we reasoned that these ABL kinase inhibitors might induce the different molecular pathways. Dasatinib 49-58 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 126-133 17591830-4 2007 The understanding of mechanisms of imatinib resistance has led to the development of novel BCR-ABL inhibitors; among these, dasatinib emerged as the most promising, being approximately 300-fold more potent than imatinib; it also inhibits SRC family kinases. Dasatinib 124-133 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 91-98 17208297-0 2007 BCR-ABL mutant kinetics in CML patients treated with dasatinib. Dasatinib 53-62 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 0-7 17208297-2 2007 Here, we monitored the mutated BCR-ABL transcripts during the follow-up of 12 CML patients treated with dasatinib. Dasatinib 104-113 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 31-38 17208297-4 2007 Clinical responses were correlated to the in vitro sensitivity of BCR-ABL mutants to dasatinib, however, some discrepancies were observed in a subfraction of CML patients, suggesting subtle differences between in vitro observations and clinical entities and/or the onset of other mechanisms responsible for dasatinib resistance. Dasatinib 85-94 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 66-73 17264298-2 2007 Dasatinib is a novel, potent, oral, multitargeted kinase inhibitor of BCR-ABL and SRC-family kinases that showed marked efficacy in a phase 1 trial of patients with imatinib-resistant CML. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 70-77 17218385-8 2007 Notably, the dasatinib/PD184352 regimen was active against leukemic cells exhibiting various forms of imatinib mesylate resistance, including Bcr/Abl overexpression, Lyn activation, and several Bcr/Abl kinase domain mutations (eg, E255K, M351T), but not T315I. Dasatinib 13-22 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 142-149 17218385-8 2007 Notably, the dasatinib/PD184352 regimen was active against leukemic cells exhibiting various forms of imatinib mesylate resistance, including Bcr/Abl overexpression, Lyn activation, and several Bcr/Abl kinase domain mutations (eg, E255K, M351T), but not T315I. Dasatinib 13-22 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 194-201 17185463-3 2007 Dasatinib is a novel, oral, multitargeted kinase inhibitor of BCR-ABL and SRC family kinases. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 62-69 17431118-1 2007 Dasatinib (BMS-354825) is a novel, oral, potent, multi-targeted kinase inhibitor of Bcr-Abl and Src family kinases (SFK) and is a promising cancer therapeutic agent. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 84-91 17431118-2 2007 Preclinical data indicate that dasatinib is 325-fold more potent than imatinib against cells expressing wild-type Bcr-Abl, and that dasatinib is active against 18 of 19 Bcr-Abl mutations known to cause imatinib resistance. Dasatinib 31-40 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 114-121 17431118-2 2007 Preclinical data indicate that dasatinib is 325-fold more potent than imatinib against cells expressing wild-type Bcr-Abl, and that dasatinib is active against 18 of 19 Bcr-Abl mutations known to cause imatinib resistance. Dasatinib 132-141 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 169-176 17431118-10 2007 Our findings indicate that inhibition of Stat5 signaling downstream of Bcr-Abl/SFKs contributes to the action of dasatinib, and, conversely, that increasing cell density up-regulates Stat5 activation and confers resistance to dasatinib. Dasatinib 113-122 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 71-78 17431118-11 2007 Moreover, the level of phosphorylated Stat5 in CML cells represents a mechanistically relevant biomarker for monitoring inhibition of Bcr-Abl signaling by dasatinib in CML patients using convenient immunocytochemical assays. Dasatinib 155-164 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 134-141 17138817-2 2007 Dasatinib, a novel, highly potent, oral, multitargeted kinase inhibitor of BCR-ABL and SRC family kinases, induced cytogenetic responses in a phase 1 study in imatinib-resistant or -intolerant CML and was well tolerated. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 75-82 17138817-7 2007 Dasatinib also induced molecular responses, reducing BCR-ABL/ABL transcript ratios from 66% at baseline to 2.6% at 9 months. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 53-60 17138817-7 2007 Dasatinib also induced molecular responses, reducing BCR-ABL/ABL transcript ratios from 66% at baseline to 2.6% at 9 months. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 57-60 17167796-4 2007 While Imatinib binding is highly sensitive to the activation state of the enzyme, the computed binding profile of Dasatinib is remarkably tolerant to the conformational state of ABL. Dasatinib 114-123 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 178-181 17382019-1 2007 Imatinib and other Abl tyrosine kinase inhibitors (TKIs), such as dasatinib and nilotinib, have significantly improved the outcome of patients with chronic myeloid leukemia. Dasatinib 66-75 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 19-22 17382023-3 2007 For patients who develop resistance to imatinib, the Bcr-Abl signaling pathway is often re-activated, second generation tyrosine kinase inhibitors, such as dasatinib or nilotinib, might restore the kinase inhibition. Dasatinib 156-165 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 53-60 17355221-5 2007 Initial data on the second-generation BCR-ABL inhibitors, dasatinib and nilotinib, indicate a potentially greater efficacy than imatinib, but the improvement is likely to be modest. Dasatinib 58-67 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 38-45 17339191-1 2007 The emergence of resistance to the Bcr-Abl inhibitor imatinib mesylate in patients with Philadelphia chromosome-positive (Ph+) leukemia has prompted the development of second-generation compounds active against several imatinib-insensitive mutant forms of Bcr-Abl, including dasatinib (BMS-354825; Bristol-Myers Squibb). Dasatinib 275-284 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 35-42 17373201-6 2007 Dasatinib is a multi-targeted tyrosine kinase inhibitor active in vitro against most cell lines containing BCR-ABL mutations that confer resistance to imatinib. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 107-114 17329198-0 2007 Second-line treatment with dasatinib in patients resistant to imatinib can select novel inhibitor-specific BCR-ABL mutants in Ph+ ALL. Dasatinib 27-36 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 107-114 16990603-2 2007 The T315I BCR-ABL mutation mediates resistance to imatinib, nilotinib, and dasatinib. Dasatinib 75-84 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 10-17 17315048-1 2007 Dasatinib is an orally bioavailable potent inhibitor of multiple tyrosine kinases, including ABL and SRC. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 93-96 17315048-2 2007 Preclinical studies have shown dasatinib to be a much more potent inhibitor of BCR-ABL than imatinib is, and to harbor efficacy against nearly all imatinib-resistant BCR-ABL mutants. Dasatinib 31-40 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 79-86 17315048-2 2007 Preclinical studies have shown dasatinib to be a much more potent inhibitor of BCR-ABL than imatinib is, and to harbor efficacy against nearly all imatinib-resistant BCR-ABL mutants. Dasatinib 31-40 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 166-173 17106016-4 2006 Dasatinib is 300 times more potent than imatinib at BCR-ABL inhibition, has few side effects, and inhibits the SRC family kinases. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 52-59 17145844-3 2006 To improve treatment options, dasatinib (BMS-354825) was developed as a novel, oral, multi-targeted kinase inhibitor of BCR-ABL and SRC family kinases. Dasatinib 30-39 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 120-127 17145844-7 2006 RESULTS: Following a single oral administration of dasatinib at a preclinical efficacious dose of 1.25 or 2.5 mg/kg, tumoral phospho-BCR-ABL/phospho-CrkL were maximally inhibited at approximately 3 hours and recovered to basal levels by 24 hours. Dasatinib 51-60 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 133-140 17145844-9 2006 Pharmacokinetic/biomarker modeling predicted that the plasma concentration of dasatinib required to inhibit 90% of phospho-BCR-ABL in vivo was 10.9 ng/mL in mice and 14.6 ng/mL in humans, which is within the range of concentrations achieved in CML patients who responded to dasatinib treatment in the clinic. Dasatinib 78-87 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 123-130 17145844-10 2006 CONCLUSIONS: Phospho-BCR-ABL/phospho-CrkL are likely to be useful clinical biomarkers for the assessment of BCR-ABL kinase inhibition by dasatinib. Dasatinib 137-146 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 21-28 17145844-10 2006 CONCLUSIONS: Phospho-BCR-ABL/phospho-CrkL are likely to be useful clinical biomarkers for the assessment of BCR-ABL kinase inhibition by dasatinib. Dasatinib 137-146 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 108-115 17155893-0 2006 Targeting ABL and SRC kinases in chronic myeloid leukemia: experience with dasatinib. Dasatinib 75-84 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 10-13 17155893-3 2006 One such agent, dasatinib (formerly BMS-354825), is approximately 300-fold more potent against BCR-ABL than imatinib, and is active against all tested ABL mutant isoforms, except for T315I. Dasatinib 16-25 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 95-102 17155893-3 2006 One such agent, dasatinib (formerly BMS-354825), is approximately 300-fold more potent against BCR-ABL than imatinib, and is active against all tested ABL mutant isoforms, except for T315I. Dasatinib 16-25 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 99-102 17155893-5 2006 Studies exploring the efficacy of dasatinib as front-line therapy in patients with BCR-ABL-expressing hematologic malignancies are underway. Dasatinib 34-43 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 83-90 17114651-0 2006 Presence or the emergence of a F317L BCR-ABL mutation may be associated with resistance to dasatinib in Philadelphia chromosome-positive leukemia. Dasatinib 91-100 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 37-44 18221045-4 2006 To override resistance, several second generation ATP competitive Abl kinase inhibitors such as dasatinib, nilotinib and INNO-406 have been developed. Dasatinib 96-105 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 66-69 16772610-1 2006 BMS-354825 (dasatinib) and AMN107 (nilotinib) are potent alternate Abl inhibitors with activity against many imatinib mesylate-resistant BCR-ABL kinase domain (KD) mutants, except T315I. Dasatinib 12-21 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 67-70 16772610-1 2006 BMS-354825 (dasatinib) and AMN107 (nilotinib) are potent alternate Abl inhibitors with activity against many imatinib mesylate-resistant BCR-ABL kinase domain (KD) mutants, except T315I. Dasatinib 12-21 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 141-144 16772610-3 2006 Although ENU is expected to induce mutations in multiple proteins, resistant clones were almost exclusively BCR-ABL KD mutant at relevant concentrations of nilotinib and dasatinib, consistent with a central role of KD mutations for resistance to these drugs. Dasatinib 170-179 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 112-115 17020995-3 2006 RESULTS: Treatment with dasatinib attenuated the levels of autophosphorylated Bcr-Abl, p-CrkL, phospho-signal transducer and activator of transcription 5 (p-STAT5), p-c-Src, and p-Lyn; inhibited the activity of Lyn and c-Src; and induced apoptosis of the cultured CML cells. Dasatinib 24-33 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 82-85 17020995-4 2006 Combined treatment of cultured human CML and BaF3 cells with vorinostat and dasatinib induced more apoptosis than either agent alone, as well as synergistically induced loss of clonogenic survival, which was associated with greater depletion of Bcr-Abl, p-CrkL, and p-STAT5 levels. Dasatinib 76-85 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 249-252 17020995-5 2006 Cotreatment with dasatinib and vorinostat also attenuated the levels of Bcr-AblE255K and Bcr-AblT315I and induced apoptosis of BaF3 cells with ectopic expression of the mutant forms of Bcr-Abl. Dasatinib 17-26 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 76-79 17020995-6 2006 Finally, cotreatment of the primary CML cells with vorinostat and dasatinib induced more loss of cell viability and depleted Bcr-Abl or Bcr-AblT315I, p-STAT5, and p-CrkL levels than either agent alone. Dasatinib 66-75 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 129-132 17076652-6 2006 Dasatinib (formerly BMS-354825), AP23464, SKI-606 and PD166326 are classified as Src/Abl inhibitors while AMN107 and NS-187 (INNO-406) belong to the latter subclass of inhibitors. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 85-88 16434489-3 2006 Dasatinib (BMS-354825) is a novel orally bioavailable SRC/ABL inhibitor that has activity against multiple imatinib-resistant BCR-ABL isoforms in vitro that is presently showing considerable promise in early-phase clinical trials of chronic myeloid leukemia (CML). Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 58-61 16434489-3 2006 Dasatinib (BMS-354825) is a novel orally bioavailable SRC/ABL inhibitor that has activity against multiple imatinib-resistant BCR-ABL isoforms in vitro that is presently showing considerable promise in early-phase clinical trials of chronic myeloid leukemia (CML). Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 126-133 16721371-9 2006 Dasatinib (BMS-354825), which inhibits Abl and Src family kinases, is another promising new clinical candidate for CML that has shown good efficacy in CML patients. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 39-42 16775234-2 2006 We evaluated dasatinib, a BCR-ABL inhibitor that targets most imatinib-resistant BCR-ABL mutations, in patients with chronic myelogenous leukemia (CML) or Ph-positive acute lymphoblastic leukemia (ALL). Dasatinib 13-22 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 26-33 16775234-2 2006 We evaluated dasatinib, a BCR-ABL inhibitor that targets most imatinib-resistant BCR-ABL mutations, in patients with chronic myelogenous leukemia (CML) or Ph-positive acute lymphoblastic leukemia (ALL). Dasatinib 13-22 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 81-88 16469872-1 2006 Dasatinib (BMS-354825), a novel dual SRC/BCR-ABL kinase inhibitor, exhibits greater potency than imatinib mesylate (IM) and inhibits the majority of kinase mutations in IM-resistant chronic myeloid leukemia (CML). Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 41-48 16740718-0 2006 The structure of Dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants. Dasatinib 17-26 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 59-62 16740718-0 2006 The structure of Dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants. Dasatinib 17-26 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 139-142 16740718-4 2006 Dasatinib (BMS-354825) is a multitargeted tyrosine kinase inhibitor that targets oncogenic pathways and is a more potent inhibitor than imatinib against wild-type BCR-ABL. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 163-170 16740718-6 2006 Analysis of the crystal structure of dasatinib-bound ABL kinase suggests that the increased binding affinity of dasatinib over imatinib is at least partially due to its ability to recognize multiple states of BCR-ABL. Dasatinib 37-46 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 53-56 16740718-6 2006 Analysis of the crystal structure of dasatinib-bound ABL kinase suggests that the increased binding affinity of dasatinib over imatinib is at least partially due to its ability to recognize multiple states of BCR-ABL. Dasatinib 37-46 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 209-216 16740718-6 2006 Analysis of the crystal structure of dasatinib-bound ABL kinase suggests that the increased binding affinity of dasatinib over imatinib is at least partially due to its ability to recognize multiple states of BCR-ABL. Dasatinib 112-121 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 53-56 16740718-6 2006 Analysis of the crystal structure of dasatinib-bound ABL kinase suggests that the increased binding affinity of dasatinib over imatinib is at least partially due to its ability to recognize multiple states of BCR-ABL. Dasatinib 112-121 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 209-216 16740718-7 2006 The structure also provides an explanation for the activity of dasatinib against imatinib-resistant BCR-ABL mutants. Dasatinib 63-72 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 100-107 16343892-3 2006 To counteract this problem, two new BCR-ABL kinase inhibitors for imatinib-refractory disease are currently in clinical trials: the imatinib derivative AMN107 and the dual-specificity SRC/ABL inhibitor dasatinib. Dasatinib 202-211 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 36-43 16343892-3 2006 To counteract this problem, two new BCR-ABL kinase inhibitors for imatinib-refractory disease are currently in clinical trials: the imatinib derivative AMN107 and the dual-specificity SRC/ABL inhibitor dasatinib. Dasatinib 202-211 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 40-43 16397263-0 2006 Dasatinib (BMS-354825), a dual SRC/ABL kinase inhibitor, inhibits the kinase activity of wild-type, juxtamembrane, and activation loop mutant KIT isoforms associated with human malignancies. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 35-38 16397263-4 2006 Dasatinib (formerly BMS-354825) is a small-molecule, ATP-competitive inhibitor of SRC and ABL tyrosine kinases with potency in the low nanomolar range. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 90-93 16542059-1 2006 Dasatinib [BMS 354825] is an orally active, small molecule, dual inhibitor of both SRC and ABL kinases that is under development with Bristol-Myers Squibb for the treatment of patients with chronic myelogenous leukaemia (CML) and imatinib-acquired resistance/intolerance. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 91-94 17124064-5 2006 Still newer inhibitors active against T315I mutant BCR-ABL may overcome primary and secondary resistance to dasatinib and nilotinib. Dasatinib 108-117 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 51-58 16230377-2 2005 The novel SFK/Abl inhibitor, dasatinib (BMS-354825), is a promising therapeutic agent with oral bioavailability. Dasatinib 29-38 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 14-17 16230377-3 2005 Dasatinib has been shown to inhibit growth of Bcr-Abl-dependent chronic myeloid leukemia xenografts in nude mice. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 50-53 15858616-0 2005 Abl inhibitor BMS354825 binding mode in Abelson kinase revealed by molecular docking studies. Dasatinib 14-23 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 0-3 16304378-5 2005 These agents, dasatinib (BMS-354825) and AMN107, are more potent inhibitors of BCR-ABL than imatinib, and moreover, harbor activity against nearly all imatinib-resistant BCR-ABL kinase domain mutant forms tested in vitro. Dasatinib 14-23 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 79-86 16304378-5 2005 These agents, dasatinib (BMS-354825) and AMN107, are more potent inhibitors of BCR-ABL than imatinib, and moreover, harbor activity against nearly all imatinib-resistant BCR-ABL kinase domain mutant forms tested in vitro. Dasatinib 14-23 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 170-177 33814500-0 2021 BCR/ABL1-positive B-lymphoblastic Lymphoma Successfully Treated with Dasatinib-combined Chemotherapy. Dasatinib 69-78 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 4-8 33814500-6 2021 She was diagnosed with BCR-ABL1-positive B-LBL and administered dasatinib and prednisolone. Dasatinib 64-73 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 27-31 33772839-2 2021 A simple analytical method using high-performance liquid chromatography/electrospray ionization tandem mass spectrometry has been developed and validated for simultaneous quantification of BCR-ABL and Bruton"s tyrosine kinase inhibitors (TKIs) used for chronic leukemia (imatinib, dasatinib, bosutinib, nilotinib, and ibrutinib) in human plasma. Dasatinib 281-290 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 189-196 17317816-6 2007 The IC(50) values of nilotinib and dasatinib are at least 10- to 100-fold lower for BCR-ABL compared with imatinib. Dasatinib 35-44 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 84-91 34830455-6 2021 In this study, we used specific gene knockdown to clearly demonstrate that the deficiency of p38alpha greatly enhanced the therapeutic efficacy in growth suppression and cytotoxicity of TKIs, first-generation imatinib, and second generation dasatinib by approximately 2.5-3.0-fold in BCR-ABL-positive CML-derived leukemia K562 and KMB5 cells. Dasatinib 241-250 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 284-291 34599372-0 2021 Investigation on the interaction behavior of afatinib, dasatinib, and imatinib docked to the BCR-ABL protein. Dasatinib 55-64 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 93-100 34433624-9 2021 Dasatinib also enhanced NK cell cytotoxicity against K562 bearing the BCR-ABL1 T315I TKI resistance-conferring mutation, depending on KIR3DL1/HLA-Bw4 allotypes. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 74-78 34195988-1 2021 Dasatinib is a second-generation BCR-ABL1 tyrosine kinase inhibitor approved for patients with chronic myeloid leukaemia (CML). Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 37-41 34276365-7 2021 Moreover, employing immortalized cell lines and primary CD34-positive progenitors, we demonstrate that these modifications lead to reduced BCR-ABL1 sensitivity to imatinib, dasatinib and ponatinib but not nilotinib. Dasatinib 173-182 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 143-147 35550008-7 2022 Downregulation of cAbl by RNA-interference in Control-ECs or its inhibition with dasatinib resulted in genomic instability and the failure to form tubes, whereas upregulation of cAbl with DPH reduced DNA damage and apoptosis in PAH-ECs. Dasatinib 81-90 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 18-22 35551463-2 2022 The approval of BCR::ABL1 tyrosine kinase inhibitors (TKI) such as imatinib, dasatinib, nilotinib and ponatinib marked a milestone in targeted therapy only for a subset of patients carrying the translocation t(9;22)(q34;q11). Dasatinib 77-86 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 21-25 35256549-0 2022 Dasatinib-induced reversible pulmonary arterial hypertension in a pediatric patient with BCR/ABL1+ lymphoblastic lymphoma from chronic myeloid leukemia. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 93-97 35402127-1 2022 The BCR-ABL1 tyrosine kinase inhibitor dasatinib is effective in chronic myeloid leukemia (CML) treatment. Dasatinib 39-48 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 8-12 35092492-2 2022 For this purpose, dasatinib is the second-generation tyrosine kinase inhibitor that is used for inhibition of BCR-ABL. Dasatinib 18-27 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 110-117 35164068-6 2022 Our results showed that 2-hydroxyestradiol (2HE2), a metabolite of estradiol, and dasatinib, an Abl/Src kinase inhibitor, were significantly effective in overcoming MSC-mediated platinum drug resistance. Dasatinib 82-91 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 96-99 33976882-1 2021 Dasatinib is a potent and effective second-generation oral tyrosine kinase inhibitor that is clinically indicated for the treatment of imatinib-resistant or imatinib-intolerant breakpoint cluster region-Abelson (BCR-ABL)-positive chronic myeloid leukaemia (CML) or for Philadelphia chromosome-positive acute lymphocytic leukaemia. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 212-219 33390067-3 2021 The patient-derived Ph-like ALL RANBP2-ABL1 fusion gene was transduced into Ba/F3 cells and allowed to become resistant to the tyrosine kinase inhibitors (TKIs) imatinib or dasatinib, followed by secondary resistance to ponatinib. Dasatinib 173-182 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 39-43 34054462-10 2021 Patients with JAK2-positive BCR-ABL-positive CML had a good hematological and cytogenetic response to dasatinib. Dasatinib 102-111 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 28-35 34054462-11 2021 In such rare coexistence of JAK and BCR-ABL, dasatinib is a good option due to multi-kinase activity. Dasatinib 45-54 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 36-43 33748144-3 2021 Although the use of the BCR-ABL tyrosine kinase inhibitors (TKIs), such as imatinib, nilotinib, dasatinib, bosutinib, and ponatinib have increased the overall survival of CML patients, their use is limited by drug resistance and severe adverse effects. Dasatinib 96-105 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 24-31 33407162-2 2021 The drug has been shown to act as a potent multikinase inhibitor by blocking not only the BCR-ABL1 gene sequence but also the SRC kinase family, though unexpected adverse events such as pleural effusion have recently been reported in patients undergoing treatment with dasatinib. Dasatinib 269-278 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 94-98 33376671-2 2021 We reported a case of AML with BCR-ABL1 patient who was successfully treated with dasatinib alone; additionally, we previously reported another case of long-term remission maintained with imatinib monotherapy. Dasatinib 82-91 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 35-39 33291786-1 2020 Dasatinib is a multi-target kinase inhibitor, whose targets include BCR-ABL, SRC family kinases, and various cancer kinases. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 68-75 33074527-5 2020 Patients with Philadelphia chromosome (Ph)-positive or Ph-like ALL with ABL-class fusion should be treated with dasatinib. Dasatinib 112-121 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 72-75 33155931-2 2021 The therapeutic targets for CML patients which are mediated with BCR/ABL1 oncogenic are tyrosine kinase inhibitors such as imatinib, dasatinib, and nilotinib. Dasatinib 133-142 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 69-73 32248338-1 2020 Dasatinib is a tyrosine kinase inhibitor for the treatment of BCR-ABL-positive chronic myeloid leukaemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukaemia (ALL). Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 62-69 31688632-1 2020 Dasatinib is a second-generation potent and efficacious oral tyrosine kinase inhibitor frequently used for imatinib-resistant or intolerant BCR-ABL-positive chronic myeloid leukemia and for Philadelphia chromosome-positive acute lymphocytic leukemia. Dasatinib 0-9 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 140-147 32536651-1 2020 We report the case of a 56-year-old man with chronic myeloid leukemia (CML) who developed dasatinib-induced interstitial lung disease (ILD) 7 years after starting dasatinib, a BCR-ABL1 inhibitor. Dasatinib 90-99 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 180-184 32536651-7 2020 The present case and relevant literature suggest that dasatinib-induced ILD can present as NSIP after an extended period, responds to corticosteroids, and is amenable to re-challenge at a lower-dose or with alternative BCR-ABL1 inhibitors. Dasatinib 54-63 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 223-227 32879093-0 2020 Combination of axitinib with dasatinib improves the outcome of a chronic myeloid leukemia patient with BCR-ABL1 T315I mutation. Dasatinib 29-38 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 107-111 32879093-5 2020 A 38-year-old male CML patient developed a BCR-ABL1 gene mutation of T315I after 2.5 years of TKI treatment, including imatinib and dasatinib. Dasatinib 132-141 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 47-51 32568522-5 2020 We demonstrate that a PROTAC linking nimbolide to the kinase and BCR-ABL fusion oncogene inhibitor dasatinib, BT1, selectively degrades BCR-ABL over c-ABL in leukemia cancer cells, compared to previously reported cereblon or VHL-recruiting BCR-ABL degraders that show opposite selectivity or in some cases inactivity. Dasatinib 99-108 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 65-72 32568522-5 2020 We demonstrate that a PROTAC linking nimbolide to the kinase and BCR-ABL fusion oncogene inhibitor dasatinib, BT1, selectively degrades BCR-ABL over c-ABL in leukemia cancer cells, compared to previously reported cereblon or VHL-recruiting BCR-ABL degraders that show opposite selectivity or in some cases inactivity. Dasatinib 99-108 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 136-143 32568522-5 2020 We demonstrate that a PROTAC linking nimbolide to the kinase and BCR-ABL fusion oncogene inhibitor dasatinib, BT1, selectively degrades BCR-ABL over c-ABL in leukemia cancer cells, compared to previously reported cereblon or VHL-recruiting BCR-ABL degraders that show opposite selectivity or in some cases inactivity. Dasatinib 99-108 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 149-154 32568522-5 2020 We demonstrate that a PROTAC linking nimbolide to the kinase and BCR-ABL fusion oncogene inhibitor dasatinib, BT1, selectively degrades BCR-ABL over c-ABL in leukemia cancer cells, compared to previously reported cereblon or VHL-recruiting BCR-ABL degraders that show opposite selectivity or in some cases inactivity. Dasatinib 99-108 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 136-143 32667912-6 2020 ABL1 tyrosine kinase inhibitors (TKIs), including imatinib, nilotinib, and dasatinib, are used clinically for treating CML. Dasatinib 75-84 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 0-4 32279331-5 2020 In ETV6-ABL1 positive patients, a durable CHR was achieved by 4/9 patients (imatinib 1/5, nilotinib 2/3, dasatinib 1/1). Dasatinib 105-114 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 8-12 32424388-3 2020 As an example, the crystal structure of the kinase inhibitor dasatinib bound to the Abl1 kinase shows a hydrogen bond between the drug and residue Thr315 and very few contacts between the drug and residues Val299 and Phe317, yet mutations in those residues lead to drug resistance. Dasatinib 61-70 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 84-88 32654459-2 2020 Methods: Imatinib-, nilotinib-, and/or dasatinib-resistant patients with CML who screened BCR-ABL mutation (s) in Peking University People"s Hospital between June 2001 and September 2019 were retrospectively reviewed. Dasatinib 39-48 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 94-97 32654459-6 2020 In total, 291 (50.5%) imatinib-, 152 (63.9%) nilotinib-, and 160 (57.3%) dasatinib-resistant cases developed BCR-ABL mutation (s) . Dasatinib 73-82 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 113-116 32654459-10 2020 Other variables associated with developing BCR-ABL mutation (s) in imatinib-, nilotinib-, or dasatinib-resistant cases included male gender, younger age, no comorbidity, advanced phase before starting current TKI therapy, longer interval from diagnosis to starting current TKI therapy, acquired resistance, and TKI resistance due to progression to advanced phase or hematologic failure. Dasatinib 93-102 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 47-50