High Response Rate to Cisplatin/Etoposide Regimen in Childhood Low-Grade Glioma

Massimino, Maura; Spreafico, Filippo; Cefalo, Graziella; Riccardi, Riccardo; Tesoro-Tess, J. D.; Gandola, Lorenza; Riva, Daria; Ruggiero, Antonio; Valentini, Laura; Mazza, Elena; Genitori, Lorenzo; Rocco, Concezio Di; Navarria, Pierina; Casanova, Michela; Ferrari, Andrea; Luksch, Roberto; Terenziani, Monica; Balestrini, M. R.; Colosimo, Cesare; Fossati-Bellani, Franca

doi:10.1200/jco.2002.08.087

Cited by 166 publications

(93 citation statements)

References 43 publications

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“…Children 5 years of age or younger had a notably more favorable rate of response. More recently, Massimino et al 52 reported a 78% PFS over 3 years with cisplatin and etoposide, with improved visual acuity in most patients and acceptable toxicity profiles. Temozolomide has also been shown to be useful in stabilizing disease in more than 50% of patients without significant toxicity 26 and is considered an option in patients with progressive OPG in whom first-line therapy has failed.…”

Section: Chemotherapy For Opgsmentioning

confidence: 99%

Optic pathway gliomas: a review

Binning

Liu

Kestle

et al. 2007

FOC

174

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✓Optic pathway gliomas represent approximately 3–5% of childhood intracranial tumors. They usually occur in children during the first decade of life and are seen in 11–30% of patients with neurofibromatosis Type 1 (NF1). Although these tumors are typically low-grade gliomas, the clinical course and natural history are highly variable, making treatment paradigms difficult. Overall, however, they are often indolent tumors that can be observed over time for progression without initial treatment, especially in patients with NF1. Chemotherapy is the first-line treatment for progressive tumors, and radiation therapy is reserved for patients with progressive disease who are older than 5–7 years. Surgery is reserved for large tumors causing mass effect or hydrocephalus and tumors confined to the orbit or unilateral optic nerve.

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Section: Chemotherapy For Opgsmentioning

confidence: 99%

Optic pathway gliomas: a review

Binning

Liu

Kestle

et al. 2007

FOC

174

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“…There is clear evidence both in vivo and in vitro of strong synergism between carboplatin and etoposide (Stein et al, 1999). A recent study showed the activity of a CBCDA (carboplatin) -VP-16 (etoposide)-based therapy in the treatment of low-grade gliomas in children (Massimino et al, 2002). The efficacy of CBCDA or cisplatin (CDDP) in combination with etoposide has been evaluated in various schedules in other trials in high-grade gliomas with various results (Buckner et al, 1990;Boiardi et al, 1991;Jeremic et al, 1992).…”

mentioning

confidence: 99%

Phase II trial of carboplatin and etoposide for patients with recurrent high-grade glioma

et al. 2004

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We present the results of a phase II trial of carboplatin and etoposide (CE) combination as first-line chemotherapy in patients with recurrent glioblastoma multiforme (GBM) and anaplastic astrocytoma (AA) after surgery and radiotherapy. We assess the activity and the tolerability of this combination. 30 patients with GBM (25) and AA (5) were treated with VP-16 (etoposide) 120 mg m À2 and CBCDA (carboplatin) 100 mg m À2 for 3 days every 4 weeks. Moreover, we performed a retrospective analysis of topoisomerase IIa gene status using chromogenic in situ hybridisation. The median age was 54 years (21 -73 years); Eastern Cooperative Oncology Group performance score was 0-1 in 25 patients and 2 in five patients. All patients had been previously treated with surgical resection (21 radical resections) followed by radiation therapy (40 -60 Gy). We observed six (20%) complete responses, three (10%) partial responses and 12 (40%) stable diseases, with a response rate of 30%. The median time to progression was 4 months, while progression-free survival at 6 months was 33.3%. The median survival time was 10 months. Neutropenia occurred in 9 patients: four patients had grade 4, two patients grade 3 and three patients grade 2. In the conclusion of this clinical trial, the CE combination has shown activity in recurrent GBM and AA, with a good toxicity profile. Alterations in the copy number of topoisomerase IIa gene seem to be a rare event and in our series do not influence response to the CE combination.

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“…Other traditional chemotherapy agents such as CDDP were somehow restricted by their limited ability to across the blood-brain barrier and could not reach the effective concentration in the tumor sites. CDDP alone or combined with other chemotherapy agents has been used to treat the lowgrade, newly diagnosed, or recurrent glioblastoma (45)(46)(47). The obstacle of CDDP being the first-line drug for glioma chemotherapy may only be hindered by its ability to reach the effective concentration at tumor site, because local chemotherapy of glioblastoma multiforme with CDDP followed by irradiation is proven to be well tolerated and effective (48).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of the met receptor tyrosine kinase signaling enhances the chemosensitivity of glioma cell lines to CDDP through activation of p38 MAPK pathway

Lou

Zhou

Yin

et al. 2009

Molecular Cancer Therapeutics

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The Met receptor tyrosine kinase is known to be overexpressed in many solid tumors and plays a crucial role in tumor invasive growth and metastasis. In this study, we showed that hepatocyte growth factor-induced Met activation as well as Met-dependent downstream signaling of AKT and p44/42 mitogen-activated protein kinase (MAPK) could be efficiently blocked by TAT-coupled carboxyl-terminal tail peptide of Met receptor (TCTP), and inactivation of Met signaling significantly enhanced the sensitivity of T98G and U251 glioma cells to cisdiaminedichloroplatinum (CDDP, cisplatin). However, neither phosphoinositide 3-kinase/AKT inhibitor LY294002 nor p44/42 MAPK inhibitor PD98059 alone or combined could imitate the effect of TCTP on chemosensitivity enhancement of T98G cells to CDDP, indicating that Met-dependent inactivation of AKT and p44/42 MAPK signaling was not the main cause for the increased chemosensitivity to CDDP. Further studies revealed that TCTP significantly activated p38 MAPK in T98G and U251 cell lines. Activation of p38 MAPK by sorbitol pretreatment resembled the sensitization effects, whereas inhibition of p38 MAPK activation by its inhibitor SB202190 counteracted the sensitization effects induced by TCTP. Therefore, p38 MAPK activation was one of the major causes for the increased chemosensitivity to CDDP induced by Met inactivation. Taken together, the study indicated that Met receptor played an important role in regulating cell response to chemotherapy and suggested that inhibition of Met signaling could be used in combination with other chemotherapeutic regimens in treatment of tumor patients.

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High Response Rate to Cisplatin/Etoposide Regimen in Childhood Low-Grade Glioma

Abstract: Cisplatin and etoposide combined treatment is one of the most active regimens for LGG in children and allows avoidance of radiotherapy in the vast majority of patients.

Cited by 166 publications

References 43 publications

Optic pathway gliomas: a review

Optic pathway gliomas: a review

Phase II trial of carboplatin and etoposide for patients with recurrent high-grade glioma

Inhibition of the met receptor tyrosine kinase signaling enhances the chemosensitivity of glioma cell lines to CDDP through activation of p38 MAPK pathway

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