Results 21 to 30 of about 106,545 (283)

Exploiting mitochondrial dysfunction for effective elimination of imatinib-resistant leukemic cells.

open access: yesPLoS ONE, 2011
Challenges today concern chronic myeloid leukemia (CML) patients resistant to imatinib. There is growing evidence that imatinib-resistant leukemic cells present abnormal glucose metabolism but the impact on mitochondria has been neglected. Our work aimed
Jérome Kluza   +14 more
doaj   +1 more source

Delivery as nanoparticles reduces imatinib mesylate-induced cardiotoxicity and improves anticancer activity [PDF]

open access: yes, 2015
Clinical effectiveness of imatinib mesylate in cancer treatment is compromised by its off-target cardiotoxicity. In the present study, we have developed physically stable imatinib mesylate-loaded poly(lactide-co-glycolide) nanoparticles (INPs) that could
Balakumar, Krishnamoorthy   +6 more
core   +2 more sources

Heterogeneity of Metabolic Vulnerability in Imatinib-Resistant Gastrointestinal Stromal Tumor

open access: yesCells, 2020
Metabolic reprogramming is a hallmark of cancer cells in response to targeted therapy. Decreased glycolytic activity with enhanced mitochondrial respiration secondary to imatinib has been shown in imatinib-sensitive gastrointestional stromal tumors (GIST)
Wen-Kuan Huang   +10 more
doaj   +1 more source

Management of imatinib-resistant CML patients [PDF]

open access: yes, 2007
Imatinib has had marked impact on outcomes in chronic myelogenous leukemia (CML) patients for all stages of the disease and is endorsed by international treatment guidelines as the first line option.
Branford S   +21 more
core   +1 more source

Induction of autophagy has protective roles in imatinib-induced cardiotoxicity

open access: yesToxicology Reports, 2021
Cardiotoxicity is one of the severe adverse effects of chemotherapeutic agents. Imatinib was previously reported to induce cardiotoxicity. Autophagy is an intracellular bulk protein and organelle degradation process, but its roles in cardiac diseases are
Miyuki Kobara   +3 more
doaj  

Imatinib Mesylate Reduces Neurotrophic Factors and pERK and pAKT Expression in Urinary Bladder of Female Mice With Cyclophosphamide-Induced Cystitis

open access: yesFrontiers in Systems Neuroscience, 2022
Imatinib mesylate is a tyrosine kinase inhibitor that inhibits platelet-derived growth factor receptor (PDGFR)-α, -β, stem cell factor receptor (c-KIT), and BCR-ABL.
Megan Perkins   +4 more
doaj   +1 more source

Integrating microfluidics and biosensing on a single flexible acoustic device using hybrid modes [PDF]

open access: yes, 2020
Integration of microfluidics and biosensing functionalities on a single device holds promise in continuous health monitoring and disease diagnosis for point-of-care applications.
Dodd, Linzi   +10 more
core   +5 more sources

Imatinib withdrawal syndrome and longer duration of imatinib have a close association with a lower molecular relapse after treatment discontinuation: the KID study

open access: yesHaematologica, 2016
The aim of the Korean Imatinib Discontinuation Study was to identify predictors for safe and successful imatinib discontinuation. A total of 90 patients with a follow-up of ≥12 months were analyzed.
Sung-Eun Lee   +20 more
doaj   +1 more source

Role for targeted resection in the multidisciplinary treatment of metastatic gastrointestinal stromal tumor [PDF]

open access: yes, 2019
The management of advanced gastrointestinal stromal tumors (GISTs) has evolved in the modern era due to the discovery of c-kit mutations and the development of tyrosine kinase inhibitors (TKIs).
Feizpour, Cyrus   +4 more
core   +1 more source

Imatinib Use in Pregnancy

open access: yesTurkish Journal of Hematology, 2012
The outcome in patients with chronic myeloid leukemia (CML) has dramatically improved over the last decade due to the widespread use of novel tyrosine kinase inhibitors such as imatinib. As overall survival has improved, the number of women with CML that wish to become pregnant has increased.
Debbie Jafta, Michael J Webb
openaire   +4 more sources

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