scholarly journals Proof-of-concept single-arm trial of bevacizumab therapy for brain arteriovenous malformation

2021 ◽  
Vol 3 (1) ◽  
pp. e000114
Author(s):  
Rachel Muster ◽  
Nerissa Ko ◽  
Wade Smith ◽  
Hua Su ◽  
Melissa A Dickey ◽  
...  
Keyword(s):  
Pilot Study ◽  
Primary Outcome ◽  
Drug Effects ◽  
Primary Outcome Measure ◽  
Vascular Endothelial ◽  
Bevacizumab Treatment ◽  
Registration Number ◽  
Endothelial Growth Factor ◽  
Dose Dependent ◽  
Radiographic Changes

Brain arteriovenous malformations (bAVMs) are relatively rare, although their potential for secondary intracranial haemorrhage (ICH) makes their diagnosis and management essential to the community. Currently, invasive therapies (surgical resection, stereotactic radiosurgery and endovascular embolisation) are the only interventions that offer a reduction in ICH risk. There is no designated medical therapy for bAVM, although there is growing animal and human evidence supporting a role for bevacizumab to reduce the size of AVMs. In this single-arm pilot study, two patients with large bAVMs (deemed unresectable by an interdisciplinary team) received bevacizumab 5 mg/kg every 2 weeks for 12 weeks. Due to limitations of external funding, the intended sample size of 10 participants was not reached. Primary outcome measure was change in bAVM volume from baseline at 26 and 52 weeks. No change in bAVM volume was observed 26 or 52 weeks after bevacizumab treatment. No clinically important adverse events were observed during the 52-week study period. There were no observed instances of ICH. Sera vascular endothelial growth factor levels were reduced at 26 weeks and returned to baseline at 52 weeks. This pilot study is the first to test bevacizumab for patients with bAVMs. Bevacizumab therapy was well tolerated in both subjects. No radiographic changes were observed over the 52-week study period. Subsequent larger clinical trials are in order to assess for dose-dependent efficacy and rarer adverse drug effects.Trial registration number: NCT02314377.

scholarly journals Evaluation of the Response to Ranibizumab Therapy following Bevacizumab Treatment Failure in Eyes with Diabetic Macular Edema

2015 ◽  
Vol 6 (1) ◽  
pp. 44-50 ◽  
Author(s):  
Joel Hanhart ◽  
Itay Chowers
Keyword(s):  
Treatment Failure ◽  
Macular Edema ◽  
Diabetic Macular Edema ◽  
Median Number ◽  
Vascular Endothelial ◽  
Spectral Domain Oct ◽  
Bevacizumab Treatment ◽  
Central Subfield Thickness ◽  
The Mean ◽  
Endothelial Growth Factor

Background/Aims: Bevacizumab and ranibizumab are routinely used to treat diabetic macular edema (DME). We aim to evaluate the usefulness of switching to ranibizumab therapy following bevacizumab treatment failure in eyes with DME. Methods: We performed a retrospective analysis of a consecutive group of patients with DME who received ranibizumab injections following the failure of bevacizumab injections. The injections were delivered following a pro re nata protocol every 4-6 weeks. The data collected included demographics, systemic and ophthalmic findings, as well as the central subfield thickness according to spectral-domain OCT. Results: Eight eyes (5 patients) were included in the study. The median number of bevacizumab injections prior to the switch to ranibizumab was 4, and the median number of ranibizumab injections during the study was 2. The mean follow-up period was 541 ± 258 days. The mean central retinal thickness (CRT) (±SEM) was 539 ± 75 μm before the initiation of bevacizumab treatment, and 524 ± 43 μm after the last bevacizumab injection (p = 0.7). It reduced to 325 ± 26 μm following the ranibizumab injections (p = 0.0063). The best-corrected visual acuity (BCVA) improved in 4 eyes and remained stable in 4 eyes following the ranibizumab injections. Conclusion: A ranibizumab therapy was effective in reducing the CRT in eyes that failed bevacizumab therapy. A BCVA improvement can also occur in these eyes. Switching between anti-vascular endothelial growth factor compounds may be beneficial in eyes with DME.

scholarly journals Bevacizumab Treatment and Treatment Regimes in Branch Retinal Vein Occlusion and Macular Edema

2019 ◽  
pp. 99-103
Keyword(s):  
Macular Edema ◽  
Retinal Vein Occlusion ◽  
Branch Retinal Vein Occlusion ◽  
Vascular Endothelial ◽  
Steroid Injections ◽  
Treatment Regimes ◽  
Vein Occlusion ◽  
Bevacizumab Treatment ◽  
Endothelial Growth Factor ◽  
Retinal Vein Occlusions

Macular edema secondary to retinal vein occlusions is a significant complication affecting the vision. Medical treatment of retinal vein occlusions first started with intraocular steroid injections and then enriched with intraocular Anti-VEGF (Vascular Endothelial Growth Factor) injections. But till now the length and frequency of therapy have not been defined clearly. In this review, the use of bevacizumab in the treatment of branch retinal vein occlusion and macular edema will be summarized in light of the current literature.

scholarly journals P14.08 Bevacizumab treatment for the lesion emerging after the radiotherapy for malignant glioma

2019 ◽  
Vol 21 (Supplement_3) ◽  
pp. iii68-iii68
Author(s):  
K Miwa ◽  
T Ito ◽  
K Yokoyama ◽  
J Shinoda
Keyword(s):  
Malignant Glioma ◽  
Tumor Recurrence ◽  
Clinical Course ◽  
Radiation Necrosis ◽  
Neurological Dysfunction ◽  
Vascular Endothelial ◽  
Recurrent Malignant Glioma ◽  
Positron Emission ◽  
Bevacizumab Treatment ◽  
Endothelial Growth Factor

Abstract BACKGROUND Because blocking vascular endothelial growth factor from reaching leaky capillaries is a logical strategy for the treatment, we reasoned that bevacizumab might be an effective treatment on recurrent malignant glioma and radiation necrosis (RN). In this study, the authors examined to differentiate RN from recurrent malignant glioma, and evaluated the results of bevacizumab treatment in each diagnosis. MATERIAL AND METHODS Four patients of malignant glioma (2 glioblastomas and 2 anaplastic astrocytomas), which demonstrated symptomatic lesion after radiotherapy, were involved in this study. All four patients were treated with bevacizumab on a 10 mg/kg biweekly (one cycle), for a total dose of 30 mg/kg (3 cycles) or furthermore. RN was differentiated from local recurrence in all four patients on the basis of 11C-methionine positron emission tomography and/or clinical course. Clinical evaluation and MRI studies were obtained after bevacizumab treatment in all cases repeatedly as possible. RESULTS Two patients were diagnosed as RN, and another two patients as tumor recurrence. Of the two patients with RN, neurological dysfunction was distinctly alleviated after bevacizumab treatment. Other two patients with tumor recurrence demonstrated no remarkable improvement in neurological dysfunction after bevacizumab treatment. Of all the two patients with RN, post-treatment MRI performed after the bevacizumab therapy showed a significant reduction of the massive lesion. CONCLUSION We concluded that bevacizumab could control the symptomatic massive lesion occurring after radiotherapy, and it might be more effective with the patients of RN, than with those of recurrent tumor.

Vascular Endothelial Growth Factor (VEGF) in Ankylosing Spondylitis - a Pilot Study

2002 ◽  
Vol 152 (9-10) ◽  
pp. 223-225 ◽  
Author(s):  
C. Goldberger ◽  
J. Dulak ◽  
C. Duftner ◽  
F. Weidinger ◽  
A. Falkenbach ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Ankylosing Spondylitis ◽  
Pilot Study ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Bevacizumab treatment for vestibular schwannomas in neurofibromatosis type two: report of two cases, including responses after prior gamma knife and vascular endothelial growth factor inhibition therapy

2011 ◽  
Vol 126 (1) ◽  
pp. 79-82 ◽  
Author(s):  
G K Eminowicz ◽  
R Raman ◽  
J Conibear ◽  
P N Plowman
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Gamma Knife ◽  
Previous History ◽  
Gamma Knife Radiosurgery ◽  
Neurofibromatosis Type ◽  
Vestibular Schwannomas ◽  
Vascular Endothelial ◽  
Bevacizumab Treatment ◽  
Endothelial Growth Factor

AbstractObjectives:Vestibular schwannomas are the hallmark of neurofibromatosis type two. They are difficult to treat, due to their bilateral presentation and the quest for hearing preservation. Our report describes a new treatment approach in this clinical scenario.Case report:We report two cases which confirm that bevacizumab, a monoclonal antibody targeting vascular endothelial growth factor, causes regression of vestibular schwannomas in patients with a previous history of gamma knife radiosurgery or failed treatment with another form of vascular endothelial growth factor targeted therapy.Conclusion:In 2009, Plotkin et al. reported the volumetric response of vestibular schwannomas to bevacizumab treatment, both in untreated patients and in patients previously treated with erlotinib, an epidermal growth factor receptor inhibitor. The presented cases support the use of bevacizumab to treat vestibular schwannomas. Given the extremely slow growth of these tumours, we note the rapidity of volume reduction following bevacizumab therapy.

scholarly journals VEGF Promotes Proliferation of Human Glioblastoma Multiforme Stem-Like Cells through VEGF Receptor 2

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Chengshi Xu ◽  
Xing Wu ◽  
Jianhong Zhu
Keyword(s):  
Glioblastoma Multiforme ◽  
Vegf Receptor ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Tumor Initiating Cells ◽  
Atp Assay ◽  
Human Glioblastoma Multiforme ◽  
Human Gbm ◽  
Endothelial Growth Factor ◽  
Dose Dependent

Cancer stem-like cells, which have been described as tumor-initiating cells or tumor-propagating cells, play a crucial role in our fundamental understanding of glioblastoma multiforme (GBM) and its recurrence. GBM is a lethal cancer, characterized by florid vascularization and aberrantly elevated vascular endothelial growth factor (VEGF). VEGF promotes tumorigenesis and angiogenesis of human GBM stem-like cells (GBSCs). However, whether and how VEGF contributes to GBSCs proliferation remain largely uncertain. In this study, human GBSCs were isolated from surgical specimens of glioblastoma and cultured in medium favored for stem cell growth. Neural Colony-Forming Cell Assay and ATP assay were performed to measure GBSC proliferation under normoxia (20% O2) and hypoxia (1% O2). Our observations demonstrate that exogenous VEGF stimulates GBSC proliferation in a dose-dependent manner via VEGF Receptor 2 (VEGFR2); while VEGF Receptor 1 (VEGFR1) has a negative feedback effect on VEGFR2 when cells were exposed to higher concentration of VEGF. These results suggest that suppressing VEGFR2-dependent GBSC proliferation is a potentially therapeutic strategy in GBM.

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