Carotid and brachiocephalic arteries stenosis with long term use of sorafenib

Maraiki, Fatma; Aljubran, Ali

doi:10.1016/j.hemonc.2013.06.005

Cited by 5 publications

(2 citation statements)

References 3 publications

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“…25 In view of sorafenib therapy associating with myocardial ischemia, 26,27 and some case reports revealing that long-term sorafenib application causes coronary stenosis and atherosclerosis in carotid artery, inhibiting the VEGF/VEGFR pathway by sorafenib may contribute to such adverse effects. 28 Moreover, sorafenib-induced inhibition of PDGFR and FGFR1 can affect VSMCs, contributing to vascular remodeling and neointimal hyperplasia. 9 Additionally, a new study also suggests that sorafenib can affect cardiac metabolism, suggesting that sorafenib cardiotoxicity is related to its deleterious effects on specific cardiac metabolic pathways.…”

Section: Dovepressmentioning

confidence: 99%

Understanding Sorafenib-Induced Cardiovascular Toxicity: Mechanisms and Treatment Implications

Li,

Zhang,

et al. 2024

DDDT

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Tyrosine kinase inhibitors (TKIs) have been recognized as crucial agents for treating various tumors, and one of their key targets is the intracellular site of the vascular endothelial growth factor receptor (VEGFR). While TKIs have demonstrated their effectiveness in solid tumor patients and increased life expectancy, they can also lead to adverse cardiovascular effects including hypertension, thromboembolism, cardiac ischemia, and left ventricular dysfunction. Among the TKIs, sorafenib was the first approved agent and it exerts anti-tumor effects on hepatocellular carcinoma (HCC) and renal cell carcinoma (RCC) by inhibiting angiogenesis and tumor cell proliferation through targeting VEGFR and RAF. Unfortunately, the adverse cardiovascular effects caused by sorafenib not only affect solid tumor patients but also limit its application in curing other diseases. This review explores the mechanisms underlying sorafenib-induced cardiovascular adverse effects, including endothelial dysfunction, mitochondrial dysfunction, endoplasmic reticulum stress, dysregulated autophagy, and ferroptosis. It also discusses potential treatment strategies, such as antioxidants and renin-angiotensin system inhibitors, and highlights the association between sorafenib-induced hypertension and treatment efficacy in cancer patients. Furthermore, emerging research suggests a link between sorafenibinduced glycolysis, drug resistance, and cardiovascular toxicity, necessitating further investigation. Overall, understanding these mechanisms is crucial for optimizing sorafenib therapy and minimizing cardiovascular risks in cancer patients.

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Section: Dovepressmentioning

confidence: 99%

Understanding Sorafenib-Induced Cardiovascular Toxicity: Mechanisms and Treatment Implications

Li,

Zhang,

et al. 2024

DDDT

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“…152 Similarly, while significant carotid artery disease can be noted with sorafenib, this seems to be the exception rather than the rule in patients presenting with stroke while undergoing therapy VEGF signaling pathway TKIs. 153-156 …”

Section: Cerebrovascular Eventsmentioning

confidence: 99%

Vascular Toxicities of Cancer Therapies

et al. 2016

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Since the late 1990s, there has been a steady decline in cancer-related mortality, in part related to the introduction of so-called “targeted therapies”. Intended to interfere with a specific molecular pathway, these therapies have, paradoxically, led to a number of “off-target” effects. The latest examples are tyrosine kinase inhibitors targeting the Philadelphia Chromosome mutation product, which have been associated with progressive atherosclerosis and acute vascular events. Additionally, agents designed to interfere with the vascular growth factor signaling pathway have vascular side effects ranging from hypertension to arterial events and cardiomyocyte toxicity. Interestingly, the risk of cardiotoxicity with drugs such as trastuzumab is predicted by preexisting cardiovascular risk factors and disease, posing the question of a vascular component to the pathophysiology. The effect on the coronary circulation has been the leading explanation for cardiotoxicity of 5-Fluorouracil and may be the underlying the mechanism of presentation of apical ballooning syndrome with various chemotherapeutics. Classical chemotherapeutics such as cisplatin, often used in combination with bleomycin and vinca alkaloids, can lead to vascular events including acute coronary thrombosis, may be associated with an increased long-term cardiovascular risk. This review is intended to provide an update on the evolving spectrum of vascular toxicities with cancer therapeutics, particularly as it pertains to clinical practice as well as the conceptualization of cardiovascular diseases. Vascular toxicity with cancer therapy: the old and the new, an evolving avenue.

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