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Cardiotoxicity of the cancer therapeutic agent imatinib mesylate
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What this work says
Outgoing claims: the papers this work cites, builds on, or argues with.
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The Mitochondrial Biogenesis Regulatory Program in Cardiac Adaptation to Ischemia—A Putative Target for Therapeutic Intervention
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STRESS signaling pathways that modulate cardiac myocyte apoptosis
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Interpretation of echocardiographic measurements: A call for standardization
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XBP1 mRNA Is Induced by ATF6 and Spliced by IRE1 in Response to ER Stress to Produce a Highly Active Transcription Factor
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Endoplasmic reticulum stress initiates apoptotic death induced by STI571 inhibition of p210 bcr–abl tyrosine kinase
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Recommendations for Quantitation of the Left Ventricle by Two-Dimensional Echocardiography
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Diversity in the Mechanisms of Neuronal Cell Death
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Cycling, stressed-out and nervous: cellular functions of c-Abl
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Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death
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JNK phosphorylation of 14-3-3 proteins regulates nuclear targeting of c-Abl in the apoptotic response to DNA damage
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Requirement of Src kinases Lyn, Hck and Fgr for BCR-ABL1-induced B-lymphoblastic leukemia but not chronic myeloid leukemia
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Caenorhabditis elegans ABL-1 antagonizes p53-mediated germline apoptosis after ionizing irradiation
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Translational control in stress and apoptosis
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JNK promotes Bax translocation to mitochondria through phosphorylation of 14‐3‐3 proteins
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Trastuzumab plus Adjuvant Chemotherapy for Operable HER2-Positive Breast Cancer
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Activation of the Cytoplasmic c-Abl Tyrosine Kinase by Reactive Oxygen Species
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Direct Activation of Mitochondrial Apoptosis Machinery by c-Jun N-terminal Kinase in Adult Cardiac Myocytes
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Catalase Activity Is Regulated by c-Abl and Arg in the Oxidative Stress Response
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Glutathione Peroxidase 1 Is Regulated by the c-Abl and Arg Tyrosine Kinases
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Protein Kinase Cδ Activation Induces Apoptosis in Response to Cardiac Ischemia and Reperfusion Damage
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Signaling the Unfolded Protein Response from the Endoplasmic Reticulum
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In Vivo Eradication of Human BCR/ABL-Positive Leukemia Cells With an ABL Kinase Inhibitor
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Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C δ
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ASK1 is essential for endoplasmic reticulum stress-induced neuronal cell death triggered by expanded polyglutamine repeats
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Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification
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A Selective Inhibitor of eIF2α Dephosphorylation Protects Cells from ER Stress
inferredcites →https://doi.org/10.1126/science.287.5453.664openalex-snapshot
Coupling of Stress in the ER to Activation of JNK Protein Kinases by Transmembrane Protein Kinase IRE1
inferredcites →https://doi.org/10.1126/science.288.5467.870openalex-snapshot
Requirement of JNK for Stress- Induced Activation of the Cytochrome c-Mediated Death Pathway
inferredcites →https://doi.org/10.1128/mcb.21.18.6233-6242.2001openalex-snapshot
Targeting of the c-Abl Tyrosine Kinase to Mitochondria in Endoplasmic Reticulum Stress-Induced Apoptosis
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XBP-1 Regulates a Subset of Endoplasmic Reticulum Resident Chaperone Genes in the Unfolded Protein Response
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Modulation of Anthracycline-Induced Myofibrillar Disarray in Rat Ventricular Myocytes by Neuregulin-1β and Anti-erbB2
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Translational control in the endoplasmic reticulum stress response
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Translational control in the endoplasmic reticulum stress response
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Imatinib mesylate inhibits the profibrogenic activity of TGF-β and prevents bleomycin-mediated lung fibrosis
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Reversal of experimental pulmonary hypertension by PDGF inhibition
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A novel mechanism for imatinib mesylate–induced cell death of BCR-ABL–positive human leukemic cells: caspase-independent, necrosis-like programmed cell death mediated by serine protease activity
inferredcites →https://doi.org/10.1182/blood-2004-08-3097openalex-snapshot
The development of imatinib as a therapeutic agent for chronic myeloid leukemia
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Establishment of a murine model for therapy-treated chronic myelogenous leukemia using the tyrosine kinase inhibitor STI571
What points at this work
Incoming claims: where this work appears in other papers’ reference lists and arguments.
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Chronic Myelogenous Leukemia
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Investigative Approaches to Drug Therapy
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Tyrosine Kinase Inhibitors
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Toward Personalized Therapy for Cancer
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Targeted Therapy in Chronic Myeloid Leukemia
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PDGF Receptor and its Antagonists: Role in Treatment of PAH
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Leucémie myéloïde chronique
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Side Effects and Sequelae of Treatment for Chronic Myeloid Leukemia in Childhood and Adolescence
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Adverse Events Associated with ATP-Competitive BCR-ABL1 Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia
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Pathophysiology of Cardiac Toxicity
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Intracellular Cardiac Signaling Pathways Altered by Cancer Therapies
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Epistructural Re-engineering of Imatinib to Eliminate Adverse Side Effects
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The Pharmacologist’s Point of View: Mechanisms of Cardiotoxicity
inferred← citeshttps://doi.org/10.1007/978-3-319-43096-6_2openalex-snapshot
Cardiotoxicity of Anticancer Therapies
inferred← citeshttps://doi.org/10.1007/978-3-319-93402-0_6openalex-snapshot
Cardiovascular Damage Induced by Anti-BCR-ABL TKIs
inferred← citeshttps://doi.org/10.1007/978-3-319-93402-0_7openalex-snapshot
Heart Failure and Left Ventricular Dysfunction
inferred← citeshttps://doi.org/10.1007/978-3-540-75863-1_12openalex-snapshot
Heart, Coronary Arteries, Aorta and Great Vessels, Arteries and Veins, Microcirculation
inferred← citeshttps://doi.org/10.1007/978-3-642-11792-3_10openalex-snapshot
Fulfilling a Therapeutic Imperative in Cancer Treatment: Control of Multi-target Drug Impact
inferred← citeshttps://doi.org/10.1007/978-3-642-11792-3_11openalex-snapshot
Inducing Folding By Crating the Target
inferred← citeshttps://doi.org/10.1007/978-3-642-11792-3_12openalex-snapshot
Wrapper Drugs as Therapeutic Editors of Side Effects
inferred← citeshttps://doi.org/10.1007/978-3-642-11792-3_8openalex-snapshot
Re-engineering an Anticancer Drug to Make It Safer: Modifying Imatinib to Curb Its Side Effects
inferred← citeshttps://doi.org/10.1007/978-3-642-15742-4_63openalex-snapshot
Pulmonary Toxicity of Imatinib and Other BCR-ABL Tyrosine Kinase Inhibitors
inferred← citeshttps://doi.org/10.1007/978-3-642-15742-4_65openalex-snapshot
Cardiogenic Causes of Respiratory Failure in Patients with Hematological Malignancies
inferred← citeshttps://doi.org/10.1007/978-3-642-15742-4_9openalex-snapshot
Cardiovascular Complications of Cancer Therapeutics
inferred← citeshttps://doi.org/10.1007/978-3-642-38664-0_16openalex-snapshot
Targeting of Platelet-Derived Growth Factor Signaling in Pulmonary Arterial Hypertension
inferred← citeshttps://doi.org/10.1007/978-3-662-46943-9_16openalex-snapshot
Safety Pharmacology of Anticancer Agents
inferred← citeshttps://doi.org/10.1007/s00108-011-2895-3openalex-snapshot
Neue Tyrosinkinase- und EGFR-Inhibitoren in der Tumortherapie
inferred← citeshttps://doi.org/10.1007/s00112-006-1454-9openalex-snapshot
Neue Therapieansätze in der pädiatrischen Onkologie
inferred← citeshttps://doi.org/10.1007/s00204-011-0729-7openalex-snapshot
The safety profile of imatinib in CML and GIST: long-term considerations
inferred← citeshttps://doi.org/10.1007/s00204-012-0813-7openalex-snapshot
Imatinib: the controversial discussion on cardiotoxicity induced by endoplasmic reticulum (ER) stress
inferred← citeshttps://doi.org/10.1007/s00204-019-02448-zopenalex-snapshot
Upregulation of phosphoinositide 3-kinase prevents sunitinib-induced cardiotoxicity in vitro and in vivo
inferred← citeshttps://doi.org/10.1007/s00204-025-04159-0openalex-snapshot
Evaluating the use of rodents as in vitro, in vivo and ex vivo experimental models for the assessment of tyrosine kinase inhibitor-induced cardiotoxicity: a systematic review
inferred← citeshttps://doi.org/10.1007/s00210-025-03946-xopenalex-snapshot
Cilostazol alleviates imatinib-induced myocardial injury in rats by modulating the TGF-β1/MAPK, SHC/Grb2/SOS signaling pathways and upregulating miRNA-195-5P
inferred← citeshttps://doi.org/10.1007/s00223-010-9429-1openalex-snapshot
Imatinib Mesylate Does Not Increase Bone Volume In Vivo
inferred← citeshttps://doi.org/10.1007/s00228-024-03675-9openalex-snapshot
Imatinib pharmacokinetics and creatine kinase levels in chronic myeloid leukemia patients: implications for therapeutic response and monitoring
inferred← citeshttps://doi.org/10.1007/s00246-010-9880-9openalex-snapshot
The Mitochondrial Permeability Transition Pore and the Cardiac Necrotic Program
inferred← citeshttps://doi.org/10.1007/s00277-009-0866-8openalex-snapshot
Imatinib and cardiac failure in idiopathic hypereosinophilic syndrome
inferred← citeshttps://doi.org/10.1007/s00277-015-2318-yopenalex-snapshot
Management of adverse events associated with tyrosine kinase inhibitors in chronic myeloid leukemia
inferred← citeshttps://doi.org/10.1007/s00280-010-1372-3openalex-snapshot
A phase I open-label study evaluating the cardiovascular safety of sorafenib in patients with advanced cancer
inferred← citeshttps://doi.org/10.1007/s00280-013-2160-7openalex-snapshot
Analysis of the potential effect of ponatinib on the QTc interval in patients with refractory hematological malignancies
inferred← citeshttps://doi.org/10.1007/s00281-013-0371-yopenalex-snapshot
The unfolded protein response triggered by environmental factors
inferred← citeshttps://doi.org/10.1007/s00345-010-0558-yopenalex-snapshot
Treatment with tyrosine kinase inhibitors in patients with metastatic renal cell carcinoma is associated with drug-induced hyperparathyroidism: a single center experience in 59 patients
inferred← citeshttps://doi.org/10.1007/s00392-007-0567-zopenalex-snapshot
Severe cardiomyopathy in a patient with renal cell carcinoma after treatment with the novel tyrosine kinase inhibitor sunitinib
inferred← citeshttps://doi.org/10.1007/s00392-009-0752-3openalex-snapshot
Significant improvement of right ventricular function by imatinib mesylate in scleroderma-associated pulmonary arterial hypertension
inferred← citeshttps://doi.org/10.1007/s00394-017-1482-3openalex-snapshot
Chronic treatment with prebiotics, probiotics and synbiotics attenuated cardiac dysfunction by improving cardiac mitochondrial dysfunction in male obese insulin-resistant rats
inferred← citeshttps://doi.org/10.1007/s00395-009-0004-8openalex-snapshot
The mitochondrial permeability transition pore and ischemia-reperfusion injury
inferred← citeshttps://doi.org/10.1007/s00395-022-00974-zopenalex-snapshot
Imatinib attenuates reperfusion injury in a rat model of acute myocardial infarction
inferred← citeshttps://doi.org/10.1007/s00403-014-1532-0openalex-snapshot
Attenuation of fibrosis with selective inhibition of c-Abl by siRNA in systemic sclerosis dermal fibroblasts
inferred← citeshttps://doi.org/10.1007/s00467-011-1892-zopenalex-snapshot
The PDGF family in renal fibrosis
inferred← citeshttps://doi.org/10.1007/s00761-013-2500-6openalex-snapshot
Risiko und Management von Nebenwirkungen zielgerichteter Therapien
inferred← citeshttps://doi.org/10.1007/s10528-022-10282-9openalex-snapshot
Using In Silico Bioinformatics Algorithms for the Accurate Prediction of the Impact of Spike Protein Mutations on the Pathogenicity, Stability, and Functionality of the SARS-CoV-2 Virus and Analysis of Potential Therapeutic Targets
inferred← citeshttps://doi.org/10.1007/s10529-014-1453-1openalex-snapshot
An optical multi-sensing system for detection of cardiovascular toxicity
inferred← citeshttps://doi.org/10.1007/s10549-008-0032-3openalex-snapshot
Treatment of metastatic breast cancer: looking towards the future
inferred← citeshttps://doi.org/10.1007/s10555-010-9206-7openalex-snapshot
Targeted therapy for gastrointestinal stromal tumors: current status and future perspectives
inferred← citeshttps://doi.org/10.1007/s10557-016-6709-7openalex-snapshot
Protein Quality Control Dysfunction in Cardiovascular Complications Induced by Anti-Cancer Drugs
inferred← citeshttps://doi.org/10.1007/s10637-009-9252-6openalex-snapshot
Acute left ventricular dysfunction induced by a panHER and VEGFR tyrosine kinase inhibitor in a phase I trial
inferred← citeshttps://doi.org/10.1007/s10637-010-9546-8openalex-snapshot
Frequency and management of troponin I elevation in patients treated with molecular targeted therapies in phase I trials
inferred← citeshttps://doi.org/10.1007/s10741-015-9502-yopenalex-snapshot
Chemotherapy-induced cardiomyopathy
inferred← citeshttps://doi.org/10.1007/s10741-020-09926-yopenalex-snapshot
Early diagnosis, clinical management, and follow-up of cardiovascular events with ponatinib
inferred← citeshttps://doi.org/10.1007/s10863-007-9070-5openalex-snapshot
The cancer cell’s “power plants” as promising therapeutic targets: An overview
inferred← citeshttps://doi.org/10.1007/s11010-012-1252-8openalex-snapshot
BGP-15, a PARP-inhibitor, prevents imatinib-induced cardiotoxicity by activating Akt and suppressing JNK and p38 MAP kinases
inferred← citeshttps://doi.org/10.1007/s11010-024-05014-zopenalex-snapshot
The role of the ER stress sensor IRE1 in cardiovascular diseases
inferred← citeshttps://doi.org/10.1007/s11060-006-9302-2openalex-snapshot
Phase II study of imatinib mesylate and hydroxyurea for recurrent grade III malignant gliomas
inferred← citeshttps://doi.org/10.1007/s11239-020-02263-9openalex-snapshot
Emerging cancer therapies and cardiovascular risk
inferred← citeshttps://doi.org/10.1007/s11481-013-9484-2openalex-snapshot
Targeting the PDGF Signaling Pathway in the Treatment of Non-Malignant Diseases
inferred← citeshttps://doi.org/10.1007/s11523-009-0106-0openalex-snapshot
Cardiovascular toxicities: clues to optimal administration of vascular endothelial growth factor signaling pathway inhibitors
inferred← citeshttps://doi.org/10.1007/s11739-011-0744-yopenalex-snapshot
Cardiovascular toxicity of anticancer-targeted therapy: emerging issues in the era of cardio-oncology
inferred← citeshttps://doi.org/10.1007/s11805-008-0290-1openalex-snapshot
Analysis of cardiotoxicity from rh-endostatin therapy combined with chemotherapy
inferred← citeshttps://doi.org/10.1007/s11864-023-01088-xopenalex-snapshot
Which Second-Line Tyrosine Kinase Inhibitor(s) for Chronic Myeloid Leukemia?
inferred← citeshttps://doi.org/10.1007/s11864-023-01149-1openalex-snapshot
Cardiovascular Adverse Events of Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia: Clinical Relevance, Impact on Outcome, Preventive Measures and Treatment Strategies
inferred← citeshttps://doi.org/10.1007/s11864-023-01175-zopenalex-snapshot
A Comprehensive Review of Cancer Drug–Induced Cardiotoxicity in Blood Cancer Patients: Current Perspectives and Therapeutic Strategies
inferred← citeshttps://doi.org/10.1007/s11886-009-0025-9openalex-snapshot
Cardiac dysfunction induced by novel targeted anticancer therapy: An emerging issue
inferred← citeshttps://doi.org/10.1007/s11886-015-0603-yopenalex-snapshot
Cardiotoxicity due to Chemotherapy: the Role of Biomarkers
inferred← citeshttps://doi.org/10.1007/s11897-010-0031-7openalex-snapshot
Right Ventricular Failure: A Novel Era of Targeted Therapy
inferred← citeshttps://doi.org/10.1007/s11897-024-00658-wopenalex-snapshot
Is There a Mitochondrial Protection via Remote Ischemic Conditioning in Settings of Anticancer Therapy Cardiotoxicity?
inferred← citeshttps://doi.org/10.1007/s11899-007-0012-4openalex-snapshot
Second-generation tyrosine kinase inhibitors as therapy for chronic myeloid leukemia
inferred← citeshttps://doi.org/10.1007/s11899-016-0309-2openalex-snapshot
Long-Term Side Effects of Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia
inferred← citeshttps://doi.org/10.1007/s11899-017-0369-yopenalex-snapshot
Beyond Anthracyclines: Preemptive Management of Cardiovascular Toxicity in the Era of Targeted Agents for Hematologic Malignancies
inferred← citeshttps://doi.org/10.1007/s11899-020-00560-xopenalex-snapshot
Mechanisms of Cardiovascular Toxicity of BCR-ABL1 Tyrosine Kinase Inhibitors in Chronic Myelogenous Leukemia
inferred← citeshttps://doi.org/10.1007/s11912-018-0696-8openalex-snapshot
Pharmacogenetics of Chemotherapy-Induced Cardiotoxicity
inferred← citeshttps://doi.org/10.1007/s11926-009-0032-2openalex-snapshot
Tyrosine kinase inhibitors in systemic sclerosis: The case for imatinib
inferred← citeshttps://doi.org/10.1007/s11926-010-0146-6openalex-snapshot
Imatinib and the Treatment of Fibrosis: Recent Trials and Tribulations
inferred← citeshttps://doi.org/10.1007/s11936-017-0524-8openalex-snapshot
Cardiovascular Complications of Targeted Therapies for Chronic Myeloid Leukemia
inferred← citeshttps://doi.org/10.1007/s11936-018-0649-4openalex-snapshot
Cardiotoxicity of Novel Targeted Chemotherapeutic Agents
inferred← citeshttps://doi.org/10.1007/s11936-024-01067-xopenalex-snapshot
Clinical Relevance and Mechanistic Underpinnings of Tyrosine Kinase Inhibitor Associated Cardiotoxicities
inferred← citeshttps://doi.org/10.1007/s12012-007-0016-2openalex-snapshot
Pathophysiology and diagnosis of cancer drug induced cardiomyopathy
inferred← citeshttps://doi.org/10.1007/s12012-011-9141-zopenalex-snapshot
Timely Recognition of Cardiovascular Toxicity by Anticancer Agents: A Common Objective of the Pharmacologist, Oncologist and Cardiologist
inferred← citeshttps://doi.org/10.1007/s12012-012-9164-0openalex-snapshot
Cardiac Toxicity of Targeted Therapies Used in the Treatment for Solid Tumours: A Review
inferred← citeshttps://doi.org/10.1007/s12012-012-9173-zopenalex-snapshot
Biological Drugs: Classic Adverse Effects and New Clinical Evidences
inferred← citeshttps://doi.org/10.1007/s12012-016-9386-7openalex-snapshot
The Myocyte-Damaging Effects of the BCR-ABL1-Targeted Tyrosine Kinase Inhibitors Increase with Potency and Decrease with Specificity
inferred← citeshttps://doi.org/10.1007/s12012-017-9429-8openalex-snapshot
Unanticipated Cardiotoxicity Associated with Targeted Anticancer Therapy in Patients with Hematologic Malignancies Patients: Natural History and Risk Factors
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