Glioblastoma survival in the United States improved after Food and Drug Administration approval of bevacizumab: A population‐based analysis

Johnson, Derek R.; Leeper, Heather; Uhm, Joon H.

doi:10.1002/cncr.28259

Cited by 99 publications

(78 citation statements)

References 23 publications

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“…However, median patient survival does not exceed 15 months after diagnosis, due to recurrence and lack of treatments [3]. Recently, the US Food and Drug Administration (FDA) approved bevacizumab as a new drug for the treatment of glioblastoma, but whether the drug really improves patient survival remains to be determined [4]. A major problem in the treatment of GBM is the high resistance of these tumor cells to chemotherapy and irradiation and, therefore, novel treatment options must be developed.…”

Section: Introductionmentioning

confidence: 99%

Targeting the Potassium Channel Kv1.3 Kills Glioblastoma Cells

et al. 2017

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Background/Aims: Glioblastoma (GBM) is one of the most aggressive cancers, counting for a high number of the newly diagnosed patients with central nervous system (CNS) cancers in the United States and Europe. Major features of GBM include aggressive and invasive growth as well as a high resistance to treatment. Kv1.3, a potassium channel of the shaker family, is expressed in the inner mitochondrial membrane of many cancer cells. Inhibition of mitochondrial Kv1.3 was shown to induce apoptosis in several tumor cells at doses that were not lethal for normal cells. Methods: We investigated the expression of Kv1.3 in different glioma cell lines by immunocytochemistry, western blotting and electron microscopy and analyzed the effect of newly synthesized, mitochondria-targeted, Kv1.3 inhibitors on the induction of cell death in these cells. Finally, we performed in vivo studies on glioma bearing mice. Results: Here, we report that Kv1.3 is expressed in mitochondria of human and murine GL261, A172 and LN308 glioma cells. Treatment with the novel Kv1.3 inhibitors PAPTP or PCARBTP as well as with clofazimine induced massive cell death in glioma cells, while Psora-4 and PAP-1 were almost without effect. However, in vivo experiments revealed that the drugs had no effect on orthotopic brain tumors in vivo. Conclusion: These data serve as proof of principle that Kv1.3 inhibitors kills GBM cells, but drugs that act in vivo against glioblastoma must be developed to translate these findings in vivo.

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Section: Introductionmentioning

confidence: 99%

Targeting the Potassium Channel Kv1.3 Kills Glioblastoma Cells

et al. 2017

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“…21 In May 2009, the U.S. Food and Drug Administration approved bevacizumab (BEV), an anti-angiogenic agent, to treat patients with the recurrent glioblastoma based on radiographic response. [22][23][24] However, a previous study did not show a significant benefit of treatment with BEV alone compared with combined BEV and irinotecan (topoisomerase I inhibitor) in recurrent glioblastoma patients. 24 Whereas, a phase II study demonstrated that a regimen of combined daily TMZ and biweekly BEV had little adverse effects, 25 the median survival duration of glioblastoma patients treated with either TMZ or BEV alone or combined TMZ and BEV was approximately 9 months.…”

Section: Radiotherapy For Glioblastomamentioning

confidence: 94%

Current evidence of temozolomide and bevacizumab in treatment of gliomas

Nanegrungsunk

Onchan

Chattipakorn

2014

Neurological Research

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“…Similarly, a more recent population-based study analysis conducted on progressive GBM showed that Bevacizumab (Avastin) increased the median survival by 1 month with respect to other treatments administered [41].…”

Section: Discussionmentioning

confidence: 99%

Analysis of chemo-predictive assay for targeting cancer stem cells in 41 glioblastoma patients.

Howard

Alberico

Valluri

et al. 2017

JCO

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Introduction: The prognosis of glioblastoma (GBM) treated with standard-of-care maximal surgical resection and concurrent adjuvant temozolomide (TMZ)/radiotherapy remains very poor (less than 15 months). GBMs have been found to contain a small population of cancer stem cells (CSCs) that contribute to tumor propagation, maintenance, and treatment resistance. The highly invasive nature of high-grade gliomas and their inherent resistance to therapy lead to very high rates of recurrence. For these reasons, not all patients with similar diagnoses respond to the same chemotherapy, schedule, or dose. Administration of ineffective anticancer therapy is not only costly but more importantly burdens the patient with unnecessary toxicity and selects for the development of resistant cancer cell clones. We have developed a drug response assay (ChemoID) that identifies the most effective chemotherapy against CSCs and bulk of tumor cells from of a panel of potential treatments, offering great promise for individualized cancer management. Providing the treating physician with drug response information on a panel of approved drugs will aid in personalized therapy selections of the most effective chemotherapy for individual patients, thereby improving outcomes. A prospective study was conducted evaluating the use of the ChemoID drug response assay in GBM patients treated with standard of care. Methods: Forty-one GBM patients (mean age 54 years, 59% male), all eligible for a surgical biopsy, were enrolled in an Institutional Review Board-approved protocol, and fresh tissue samples were collected for drug sensitivity testing. Patients were all treated with standard-of-care TMZ plus radiation with or without maximal surgery, depending on the status of the disease. Patients were prospectively monitored for tumor response, time to recurrence, progression-free survival (PFS), and overall survival (OS). Odds ratio (OR) associations of 12-month recurrence, PFS, and OS outcomes were estimated for CSC, bulk tumor, and combined assay responses for the standard-of-care TMZ treatment; sensitivities/specificities, areas under the curve (AUCs), and risk reclassification www.transonc.com Tr a n s l a t i o n a l O n c o l o g y Volume 10 Number 2 April 2017 pp. 241-254

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Glioblastoma survival in the United States improved after Food and Drug Administration approval of bevacizumab: A population‐based analysis

Cited by 99 publications

References 23 publications

Targeting the Potassium Channel Kv1.3 Kills Glioblastoma Cells

Targeting the Potassium Channel Kv1.3 Kills Glioblastoma Cells

Current evidence of temozolomide and bevacizumab in treatment of gliomas

Analysis of chemo-predictive assay for targeting cancer stem cells in 41 glioblastoma patients.

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