Vascular Endothelial Growth Factor A c.*237C&gt;T polymorphism is associated with bevacizumab efficacy and related hypertension in metastatic colorectal cancer

Sibertin-Blanc, Camille; Mancini, Julien; Fabre, Aurélie; Lagarde, Arnaud; Grande, Jean Del; Levy, Nicolas; Seitz, Jean‐François; Olschwang, Sylviane; Dahan, Laétitia

doi:10.1016/j.dld.2014.12.013

Cited by 27 publications

(19 citation statements)

References 40 publications

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“…Jain et al performed a meta-analysis of bevacizumab treated patients across six different trials and identified carriers of rs1870377 as having greater risk of developing grade 2+ HTN (Jain et al, 2010). Etienne-Grimaldi et al genotyped women with locally recurrent or metastatic breast cancer receiving bevacizumab-containing therapy and found a significant association between rs2010963 and all-grade HTN (Etienne-Grimaldi et al, 2011), though with the opposite direction of effect as reported by Schneider et al In bevacizumab-treated patients with metastatic colorectal cancer, Morita et al identified rs699947 and rs833061 to be associated with early grade 2+ HTN (during the first two months of treatment) and rs699947and rs3025039 to be associated with grade 2+ HTN during the entire treatment period (Morita et al, 2013); the direction of effect for rs833061 agreed with that of Schneider et al Sibertin-Blanc et al identified an association of rs3025039 with incidence of all-grade HTN in metastatic colorectal cancer patients (Sibertin-Blanc et al, 2015), with a direction of effect that contradicts that in the Morita et al study. Finally, Gampenrieder et al found an association between rs2010963 and the incidence of bevacizumab-induced HTN in metastatic breast cancer patients (Gampenrieder et al, 2016), with a direction of effect that agrees with Schneider et al but not Etienne-Grimaldi et al…”

Section: Pharmacogeneticsmentioning

confidence: 71%

Bevacizumab-induced hypertension: Clinical presentation and molecular understanding

Kroetz

2018

Pharmacology & Therapeutics

111

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Bevacizumab is a vascular endothelial growth factor-A-specific angiogenesis inhibitor indicated as an adjunct to chemotherapy for the treatment of several types of cancer. Hypertension is commonly observed during bevacizumab treatment, and high-grade toxicity can limit therapy and lead to other cardiovascular complications. The factors that contribute to interindividual variability in blood pressure response to bevacizumab treatment are not well understood. In this review, we outline research efforts to understand the mechanisms and pathophysiology of hypertension resulting from bevacizumab treatment. Moreover, we highlight current knowledge of the pharmacogenetics of bevacizumab-induced hypertension, which may be used to develop strategies to prevent or minimize this toxicity.

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Section: Pharmacogeneticsmentioning

confidence: 71%

Bevacizumab-induced hypertension: Clinical presentation and molecular understanding

Kroetz

2018

Pharmacology & Therapeutics

111

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“…It has been reported that hypertension development was linked with better antitumor efficacy in subjects treated with bevacizumab and the antiangiogenic TKIs [ 58 , 104 , 106 – 112 ] however, it was not a consistent finding in some studies [ 113 – 115 ]. In 4 prospective studies in patients with advanced RCC treated with sunitinib, rise in blood pressure over 140 mm Hg was associated with better antitumor efficacy (median OS, median PFS, and objective response rates were 30.9 versus 7.2 months, 12.5 versus 2.5 months, and 55 versus 9 percent, respectively) [ 111 ].…”

Section: Vegfr and Hypertensionmentioning

confidence: 97%

“…The significant rise in blood pressure were observed as early as in the first week of treatment [ 101 , 102 ]. There are several reports that the are some SNPs that are linked with a higher risk for hypertension development during TKI therapy [ 103 , 104 ]. However, no factors are yet known to predict the magnitude of blood pressure rise [ 105 ].…”

Section: Vegfr and Hypertensionmentioning

confidence: 99%

Hypertension in malignancy-an underappreciated problem

Małyszko

Kozłowski³

et al. 2018

Oncotarget

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Hypertension is one of the most common comorbidities in cancer patients with malignancy, in particular, in the elderly. On the other hand, hypertension is a long-term consequence of antineoplastic treatment, including both chemotherapy and targeted agents. Several chemotherapeutics and targeted drugs may be responsible for development or worsening of the hypertension. The most common side effect of anti-VEGF (vascular endothelial growth factor) treatment is hypertension. However, pathogenesis of hypertension in patients receiving this therapy appears to be associated with multiple pathways and is not yet fully understood. Development of hypertension was associated with improved antitumor efficacy in patients treated with anti-antiangiogenic drugs in some but not in all studies. Drugs used commonly as adjuvants such as steroids, erythropoietin stimulating agents etc, may also cause rise in blood pressure or exacerbate preexisiting hypertension. Hypotensive therapy is crucial to manage hypertension during certain antineoplastic treatment. The choice and dose of antihypertensive drugs depend upon the presence of organ dysfunction, comorbidities, and/or adverse effects. In addition, severity of the hypertension and the urgency of blood pressure control should also be taken into consideration. As there are no specific guidelines on the hypertension treatment in cancer patients we should follow the available guidelines to obtain the best possible outcomes and pay the attention to the individualization of the therapy according to the actual situation.

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“…It has been reported that single-nucleotide polymorphisms in VEGF, VEGFR2, ABCB1 (ATP-binding cassette sub-family B member 1), and eNOS genes predict the rise in blood pressure and/or hypertension in TKI-treated patients [136][137][138]. Other genetic variants have been associated with bevacizumab-induced hypertension [139][140][141]. All these changes at the cellular level contribute to the increase in vascular tone and vascular remodeling during anti-VEGF treatment.…”

Section: Hypertensionmentioning

confidence: 99%

Nephrotoxicity of Anti-Angiogenic Therapies

et al. 2021

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The use of inhibitors of vascular endothelial growth factor (VEGF)/vascular endothelial growth factor receptor 2 (VEGFR2) signaling for the treatment of cancer has increased over the last decade. This signaling pathway plays a fundamental role in angiogenesis and also in kidney physiology. The emergence of anti-angiogenic therapies has led to adverse nephrotoxic effects, despite improving the outcomes of patients. In this review, we will present the different anti-angiogenic therapies targeting the VEGFR pathway in association with the incidence of renal manifestations during their use. In addition, we will discuss, in detail, the pathophysiological mechanisms of frequent renal diseases such as hypertension, proteinuria, renal dysfunction, and electrolyte disorders. Finally, we will outline the cellular damage described following these therapies.

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Vascular Endothelial Growth Factor A c.*237C>T polymorphism is associated with bevacizumab efficacy and related hypertension in metastatic colorectal cancer

Cited by 27 publications

References 40 publications

Bevacizumab-induced hypertension: Clinical presentation and molecular understanding

Bevacizumab-induced hypertension: Clinical presentation and molecular understanding

Hypertension in malignancy-an underappreciated problem

Nephrotoxicity of Anti-Angiogenic Therapies

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