Management of Antiangiogenic Therapy-Induced Hypertension

Jesus-Gonzalez, Nilka de; Robinson, Emily S.; Moslehi, Javid; Humphreys, Benjamin D.

doi:10.1161/hypertensionaha.112.196774

Cited by 97 publications

(69 citation statements)

References 66 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…[50][51][52] The impact of the different categories of antihypertensive drugs on the cancer evolution and prognosis has not been investigated. 53 The antihypertensive drugs are numerous and there are not enough data available in the different combinations of cancer, cancer evolution, cancer treatment and antihypertensive drug class to enable the publication of guidelines. For long, antihypertensive drugs have been considered to be a carcinogen, but there is not enough evidence in the literature to obtain a coherent view or consensus and there are some data to indicate that antihypertensive drugs could even be beneficial.…”

Section: Discussionmentioning

confidence: 99%

Chronic arterial hypertension impedes glioma growth: a multiparametric MRI study in the rat

et al. 2015

View full text Add to dashboard Cite

Glioblastoma is the most aggressive brain tumor and is almost always fatal. These tumors are highly vascularized and angiogenesis is one of the pre-eminent mechanisms underlying their growth. Chronic arterial hypertension (CAH) is a common and worldwide pathology that markedlly alters the structure and function of the vasculature. Yet, essential hypertension is associated in the brain with potential locally impaired vasoreactivity, disturbed perfusion supply and hypoxia phenomena. Even though CAH is a global burden and has an important impact on brain function, nothing is known about the way this frequent pathology would interact with the evolution of glioma. We sought to determine if arterial hypertension influences gliobastoma growth. In the present study, rat glioma C6 tumor cells were implanted in the caudate-putamen of spontaneously hypertensive rats (SHR) or their normotensive controls, the Wistar-Kyoto (WKY) rats. The evolution of the tumor was sequentially analyzed by multiparametric magnetic resonance imaging and the inflammatory response was examined by histochemistry. We found that CAH significantly attenuates the growth of the tumor as, at 21 days, the volume of the tumor was 85.4±34.7 and 126.1±28.8 mm(3), respectively, in hypertensive and normotensive rats (P<0.02). Moreover, cerebral blood volume and cerebral blood flow were greater in the tumors of hypertensive rats (P<0.05). The lesser growth of the tumor observed in normotensive animals was not due to an enhanced rejection of the tumor cells in WKY rats, the inflammatory response being similar in both groups. For the first time, these results show that CAH impedes the growth of glioblastoma and illustrate the need to further study the impact of hypertension on the evolution of brain tumors.

show abstract

Section: Discussionmentioning

confidence: 99%

Chronic arterial hypertension impedes glioma growth: a multiparametric MRI study in the rat

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Hypertension is a frequent side effect of anti-VEGF therapy (38). However, the impact of baseline hypertension on the development of high-grade hypertension during bevacizumab therapy is less well documented.…”

Section: Discussionmentioning

confidence: 99%

Safety of bevacizumab in clinical practice for recurrent ovarian cancer: A retrospective cohort study

Selle¹,

Emile²,

Pautier³

et al. 2016

Oncology Letters

View full text Add to dashboard Cite

Abstract. The poor outcome of patients with recurrent ovarian cancer constitutes a continuous challenge for decision-making in clinical practice. In this setting, molecular targets have recently been identified, and novel compounds are now available. Bevacizumab has been introduced for the treatment of patients with ovarian cancer and is, to date, the most extensively investigated targeted therapy in this setting. However, potential toxicities are associated with the use of this monoclonal antibody. These toxicities have been reported in clinical trials, and can also be observed outside of trials. As limited data is currently available regarding the safety of bevacizumab treatment in daily clinical practice, the current retrospective study was designed to evaluate this. Data from 156 patients with recurrent ovarian cancer who had

show abstract

“…OS-RC-2 human RCC cells (2x10 5 per p-96 plate) were transfected with various vectors. Transfection was performed on cells in plates at 60% confluence using 9 µl Lipofectamine 2000™ (Applied Biosystems, Life Technologies, Foster City, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

“…Although there are numerous methods of detecting localized RCC, in the majority of cases the disease is difficult to diagnose (3). Furthermore, it is still controversial whether immunotherapy and antiangiogenic therapy are effective treatments for RCC (4,5). Hence, it is necessary to find novel biomarkers for the diagnosis and treatment of this disease.…”

Section: Introductionmentioning

confidence: 99%

Smad4 suppresses the progression of renal cell carcinoma via the activation of forkhead box protein H1

Liu

et al. 2014

Molecular Medicine Reports

View full text Add to dashboard Cite

Abstract. Smad4 has recently been identified as a tumor suppressor gene in a variety of cancers, yet the role of Smad4 in renal cell carcinoma (RCC) remained to be elusive. Therefore, the aim of the present study was to explore the function of Smad4 in RCC. The expression of Smad4 reduced the growth rate of RCC. The levels of Smad4 and forkhead box protein H1 (FOXH1) mRNA were reduced, while the levels of estrogen receptor were increased in RCC cells compared with those in human renal epithelial cells (P<0.01). Western blot analysis showed an identical trend among the three molecules. Glutathione S-transferase pull-down and immunoprecipitation assays proved the interaction between Smad4 and FOXH1. An immunofluorescence assay revealed that Smad4 and FOXH1 were colocalized in the nuclei of RCC cells. Smad4 interacts with Smad2 and migrates into the nucleus, where it interacts with FOXH1 to repress the protein expression of estrogen receptor. These results indicate that Smad4 acts as a tumor suppressor by activating FOXH1, and then suppressing the expression of estrogen receptor, in addition to tumor migration and invasion. Hence, Smad4 should be investigated as a potential target for the treatment for RCC.

show abstract

Management of Antiangiogenic Therapy-Induced Hypertension

Cited by 97 publications

References 66 publications

Chronic arterial hypertension impedes glioma growth: a multiparametric MRI study in the rat

Chronic arterial hypertension impedes glioma growth: a multiparametric MRI study in the rat

Safety of bevacizumab in clinical practice for recurrent ovarian cancer: A retrospective cohort study

Smad4 suppresses the progression of renal cell carcinoma via the activation of forkhead box protein H1

Contact Info

Product

Resources

About