Treatment of High-Risk Neuroblastoma with Intensive Chemotherapy, Radiotherapy, Autologous Bone Marrow Transplantation, and 13-<i>cis</i>-Retinoic Acid

Matthay, Katherine K.; Villablanca, Judith G.; Seeger, Robert C.; Stram, Daniel O.; Harris, Richard E.; Ramsay, Norma K.C.; Swift, Patrick S.; Shimada, Hiro; Black, C.; Gm, Brodeur; Gerbing, Robert B.; Reynolds, C. Patrick

doi:10.1056/nejm199910143411601

Cited by 1,722 publications

(1,468 citation statements)

References 29 publications

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“…Although several cytogenetic aberrations linked to poor neuroblastoma prognosis have been identified, at the gene level amplification of MYCN is the only aberration that strongly associates with advanced disease, which in turn associates with activated MYC signaling and an immature phenotype . The fully disseminated disease, Stage 4, is highly aggressive and the overall survival of children with this disease stage is less than 40% (Matthay et al 1999). …”

Section: Differential Tumor Hif Expression In Relation To Patient Outmentioning

confidence: 99%

The HIF-2α-Driven Pseudo-Hypoxic Phenotype in Tumor Aggressiveness, Differentiation, and Vascularization

Pietras

Johnsson

Påhlman

2010

Current Topics in Microbiology and Immunology

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Section: Differential Tumor Hif Expression In Relation To Patient Outmentioning

confidence: 99%

The HIF-2α-Driven Pseudo-Hypoxic Phenotype in Tumor Aggressiveness, Differentiation, and Vascularization

Pietras

Johnsson

Påhlman

2010

Current Topics in Microbiology and Immunology

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“…Cytotoxic therapies (doxorubicin, cyclophosphamide, etoposide, irinotecan and cisplatin) still play a major role in neuroblastoma treatment (Furman et al, 1999;Thompson et al, 1999Thompson et al, , 2001Houghton and Santana, 2002;Castel and Canete, 2004;Donfrancesco et al, 2004). Bone marrow or peripheral blood stem cell transplants appear to have some value increasing relapse-free survival, at least in some studies (Matthay et al, 1999;Valteau-Couanet et al, 2000;Imaizumi et al, 2001;Goldsby and Matthay, 2004). Differentiation agents and immunotherapies have also been seen to increase survival in patients having a complete or good partial response during induction therapy.…”

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confidence: 99%

Proapoptotic compound ARC targets Akt and N-myc in neuroblastoma cells

et al. 2007

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We have previously described the identification of a nucleoside analog transcriptional inhibitor ARC (4-amino-6-hydrazino-7-b-D-ribofuranosyl-7H-pyrrolo[2,3-d]-pyrimidine-5-carboxamide) that was able to induce apoptosis in cancer cell lines of different origin. Here, we report the characterization of ARC on a panel of neuroblastoma cell lines. We found that these cell lines were more than 10-fold sensitive to ARC than to the well-known nucleoside analog DRB (5,6-dichloro-1-b-Dribofuranosylbenzimidazole), and that ARC-induced apoptosis proceeds through mitochondrial injury. Also, we observed that ARC-mediated cell death was accompanied by caspase-3 cleavage and repression of antiapoptotic proteins such as Mcl-1 and survivin. Conversely, we found that overexpression of Mcl-1-protected neuroblastoma cell line NB-1691 from ARC-induced apoptosis. Furthermore, we found that while ARC inhibited the phosphorylation of Akt Ser-473 in multiple cancer cell lines, forced expression of myristoylated Akt promoted resistance to ARC-induced apoptosis in neuroblastoma cells. In addition, we observed that ARC was able to downregulate the protein levels of N-myc, a commonly amplified oncogene in neuroblastomas, and Akt protected N-myc from ARCinduced downregulation. These data suggest that ARC may antagonize different antiapoptotic pathways and induce apoptosis in neuroblastoma cells via multiple mechanisms. Overall, ARC could represent an attractive candidate for anticancer drug development against neuroblastomas.

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“…MYCN amplification, 1p deletion, 17q gain) (Seeger et al, 1985;Caron et al, 1996;Bown et al, 1999) in the tumour cells are major adverse prognostic factors. For these patients long-term survival is seldom achieved despite intensive multimodal treatment (Matthay et al, 1999). The availability of repeated noninvasive assessment of treatment response could contribute to improved outcome for children with high-risk neuroblastoma by early evaluation of novel therapy and application of individualised treatment.…”

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confidence: 99%

Noninvasive estimation of tumour viability in a xenograft model of human neuroblastoma with proton magnetic resonance spectroscopy (1H MRS)

et al. 2003

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The aim of the study was to evaluate proton magnetic resonance spectroscopy ( 1 H MRS) for noninvasive biological characterisation of neuroblastoma xenografts in vivo. For designing the experiments, human neuroblastoma xenografts growing subcutaneously in nude rats were analysed in vivo with 1 H MRS and magnetic resonance imaging at 4.7 T. The effects of spontaneous tumour growth and antiangiogenesis treatment, respectively, on spectral characteristics were evaluated. The spectroscopic findings were compared to tumour morphology, proliferation and viable tumour tissue fraction. The results showed that signals from choline (Cho)-containing compounds and mobile lipids (MLs) dominated the spectra. The individual ML/Cho ratios for both treated and untreated tumours were positively correlated with tumour volume (Po0.05). There was an inverse correlation between the ML/Cho ratio and the viable tumour fraction (r ¼ À0.86, Po0.001). Higher ML/Cho ratios concomitant with pronounced histological changes were seen in spectra from tumours treated with the antiangiogenic drug TNP-470, compared to untreated control tumours (Po0.05). In conclusion, the ML/Cho ratio obtained in vivo by 1 H MRS enabled accurate assessment of the viable tumour fraction in a human neuroblastoma xenograft model. 1 H MRS also revealed early metabolic effects of antiangiogenesis treatment. 1 H MRS could prove useful as a tool to monitor experimental therapy in preclinical models of neuroblastoma, and possibly also in children.

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Treatment of High-Risk Neuroblastoma with Intensive Chemotherapy, Radiotherapy, Autologous Bone Marrow Transplantation, and 13-cis-Retinoic Acid

Cited by 1,722 publications

References 29 publications

The HIF-2α-Driven Pseudo-Hypoxic Phenotype in Tumor Aggressiveness, Differentiation, and Vascularization

The HIF-2α-Driven Pseudo-Hypoxic Phenotype in Tumor Aggressiveness, Differentiation, and Vascularization

Proapoptotic compound ARC targets Akt and N-myc in neuroblastoma cells

Noninvasive estimation of tumour viability in a xenograft model of human neuroblastoma with proton magnetic resonance spectroscopy (1H MRS)

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