Regression of a meningioma during paclitaxel and bevacizumab therapy for breast cancer

Wilson, Thomas J.; Heth, Jason

doi:10.1016/j.jocn.2011.07.024

Cited by 19 publications

(10 citation statements)

References 9 publications

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“…Wilson and Heth reported regression of a partially resected Grade I meningioma after paclitaxel and bevacizumab was used to treat breast cancer for 6 months and 1 year, respectively. 95 Regression of the meningioma was maintained on follow-up MRI 1 year later. Goutagny and colleagues administered bevacizumab at a dose of 5 mg/kg body weight every 2 weeks for 15 months with the primary goal of treating a vestibular schwannoma in a patient with neurofibromatosis Type 2.…”

Section: Clinical Studies Of Vegf Therapymentioning

confidence: 93%

Peritumoral brain edema in intracranial meningiomas: the emergence of vascular endothelial growth factor–directed therapy

Hou

Kshettry

Selman

et al. 2013

FOC

115

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Meningioma is the second most common type of adult intracranial neoplasm. A substantial subset of patients present with peritumoral brain edema (PTBE), which can cause significant morbidity via mass effect, complicate surgical management, and impact the safety of stereotactic radiosurgery. Recent studies suggest a close relationship between vascular endothelial growth factor-A (VEGF-A) expression and PTBE development in meningiomas. The authors performed a systematic review of the literature on the pathogenesis of PTBE in meningiomas, the effectiveness of steroid therapy, the role played by VEGF-A, and the current clinical evidence for antiangiogenic therapy to treat peritumoral brain edema. Mounting evidence suggests VEGF-A is secreted directly by meningioma cells to induce angiogenesis and edemagenesis of tumoral as well as peritumoral brain tissue. The VEGF-A cascade results in recruitment of cerebral-pial vessels and disruption of the tumor-brain barrier, which appear to be requisite for VEGF-A to have an edemagenic effect. Results of preliminary clinical studies suggest VEGF-directed therapy has modest activity against recurrent and progressive meningioma growth but can alleviate PTBE in some patients. A comprehensive understanding of the VEGF-A pathway and its modulators may hold the key to an effective therapeutic approach to treating PTBE associated with meningiomas. Further clinical trials with larger patient cohorts and longer follow-up periods are warranted to confirm the efficacy of VEGF-directed therapy.

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Section: Clinical Studies Of Vegf Therapymentioning

confidence: 93%

Peritumoral brain edema in intracranial meningiomas: the emergence of vascular endothelial growth factor–directed therapy

Hou

Kshettry

Selman

et al. 2013

FOC

115

View full text Add to dashboard Cite

show abstract

“…It has been shown to be efficacious against benign meningioma in vitro and in vivo [85][86][87][88] Some in vitro work has shown that VEGF, as well as two receptors of VEGF, are expressed in AM [89]. A few reports have shown variable degrees of bevacizumab efficacy in treatment of both Grade II and Grade III meningiomas [90][91][92].…”

Section: Bevacizumab (Avastin)mentioning

confidence: 99%

Review of controversies in management of non-benign meningioma

Paldor

Awad

Sufaro

et al. 2016

Journal of Clinical Neuroscience

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“…While several studies indicate that the EGFR/HER2 and downstream AKT/PI3K and ERK/MAPK signalling pathways often remain inhibited by RTK inhibitors in resistant cells, alternative redundant signalling routes are instead engaged and converge on re-activation of common downstream effectors 5 6 7 . Proposed bypassing routes include the activation of kinases downstream of β1 integrin 8 9 , stimulation of the mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) 10 11 12 13 and enhanced autocrine mitogenic signalling 14 15 16 17 18 . While these observations suggest that reactivation of RTK or of alternative signalling routes may restore the proliferative potential of lapatinib-treated breast cancer cells, the downstream effects responsible for conferring resistance to lapatinib remain unknown.…”

mentioning

confidence: 99%

ERRα mediates metabolic adaptations driving lapatinib resistance in breast cancer

et al. 2016

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Despite the initial benefits of treating HER2-amplified breast cancer patients with the tyrosine kinase inhibitor lapatinib, resistance inevitably develops. Here we report that lapatinib induces the degradation of the nuclear receptor ERRα, a master regulator of cellular metabolism, and that the expression of ERRα is restored in lapatinib-resistant breast cancer cells through reactivation of mTOR signalling. Re-expression of ERRα in resistant cells triggers metabolic adaptations favouring mitochondrial energy metabolism through increased glutamine metabolism, as well as ROS detoxification required for cell survival under therapeutic stress conditions. An ERRα inverse agonist counteracts these metabolic adaptations and overcomes lapatinib resistance in a HER2-induced mammary tumour mouse model. This work reveals a molecular mechanism by which ERRα-induced metabolic reprogramming promotes survival of lapatinib-resistant cancer cells and demonstrates the potential of ERRα inhibition as an effective adjuvant therapy in poor outcome HER2-positive breast cancer.

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Regression of a meningioma during paclitaxel and bevacizumab therapy for breast cancer

Cited by 19 publications

References 9 publications

Peritumoral brain edema in intracranial meningiomas: the emergence of vascular endothelial growth factor–directed therapy

Peritumoral brain edema in intracranial meningiomas: the emergence of vascular endothelial growth factor–directed therapy

Review of controversies in management of non-benign meningioma

ERRα mediates metabolic adaptations driving lapatinib resistance in breast cancer

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