Chromosomal aberrations in human neuroblastomas

Gm, Brodeur; Sekhon, Gurbax S.; Goldstein, Milton N.

doi:10.1002/1097-0142(197711)40:5<2256::aid-cncr2820400536>3.0.co;2-1

Cited by 294 publications

(135 citation statements)

References 18 publications

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“…For instance, several regions of chromosome 1p, including 1p36 and 1p22, have been implicated in the tumorigenesis of a wide range of malignancies. [37][38][39][40][41][42][43][44][45][46][47][48][49] Prior LOH studies in NB have used a variety of techniques and most have focused on 1p36. The incidence of 1p36 LOH in the literature ranges from 19 to 36%.…”

Section: Discussionmentioning

confidence: 99%

Clinical Categories of Neuroblastoma Are Associated with Different Patterns of Loss of Heterozygosity on Chromosome Arm 1p

Mora

Cheung

Kushner

et al. 2000

The Journal of Molecular Diagnostics

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Section: Discussionmentioning

confidence: 99%

Clinical Categories of Neuroblastoma Are Associated with Different Patterns of Loss of Heterozygosity on Chromosome Arm 1p

Mora

Cheung

Kushner

et al. 2000

The Journal of Molecular Diagnostics

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“…A panel of 12 neuroblastoma cell lines established from patients at different stages of treatment was used in this study: a matched pair derived from the same patient at diagnosis (BE(1)N) and relapse (BE(2)N); 14 a pair (SHSY5Y and SHEP1) derived from the same parental line SKNSH at relapse; 15 one at diagnosis, IMR-32; 16 and the rest at relapse, LAN1, 17 SKNAS, 18 SKNJC2, NB1691, 19 LS, 20 NGP, 21 and LAN6. 22 The p53/ MDM2/p14 ARF genomic status of most cell lines has been described previously, 7,18,23 except for one line established at Memorial Sloan-Kettering Cancer Center (MSKCC): SKNJC2 has a p53 nonsense mutation at codon 204.…”

Section: Cell Lines and Human Tissuesmentioning

confidence: 99%

Checkpoint kinase inhibitor synergizes with DNA‐damaging agents in G₁ checkpoint‐defective neuroblastoma

Xu¹,

Cheung²,

Wei³

et al. 2011

Intl Journal of Cancer

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Checkpoint kinase inhibitors can enhance the cancer killing action of DNA-damaging chemotherapeutic agents by disrupting the S/G 2 cell cycle checkpoints. The in vitro and in vivo effects of the Chk1/2 inhibitor AZD7762 when combined with these agents were examined using neuroblastoma cell lines with known p53/MDM2/p14 ARF genomic status. Four of four p53 mutant lines and three of five MDM2/p14 ARF abnormal lines were defective in G 1 checkpoint, correlating with failure to induce endogenous p21 after treatment with DNA-damaging agents. In cytotoxicity assays, these G 1 checkpoint-defective lines were more resistant to DNA-damaging agents when compared to G 1 checkpoint intact lines, yet becoming more sensitive when AZD7762 was added. Moreover, AZD7762 abrogated DNA damage-induced S/G 2 checkpoint arrest both in vitro and in vivo. In xenograft models, a significant delay in tumor growth accompanied by histological evidence of increased apoptosis was observed, when AZD7762 was added to the DNA-damaging drug gemcitabine. These results suggest a therapeutic potential of combination therapy using checkpoint kinase inhibitor and chemotherapy to reverse or prevent drug resistance in treating neuroblastomas with defective G 1 checkpoints.

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“…The neuroblastoma cell lines SHSY5Y (Ciccarone et al, 1989) and NGP (Brodeur et al, 1977) were kindly provided by Drs P Lovat and D Tweddle (University of Newcastle upon Tyne). Cells were grown in RPMI 1640 (Dutch modification, supplemented with 10% v/v foetal bovine serum, and antibiotics (Gibco BRL)) at 378C/5% CO 2 .…”

Section: Cell Culture and Drug Solutionsmentioning

confidence: 99%

Schedule-dependent response of neuroblastoma cell lines to combinations of etoposide and cisplatin

et al. 2002

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The growth inhibitory effects of cisplatin and etoposide on neuroblastoma cell lines were investigated in several scheduled combinations. Results were analyzed using median effect and combination index analyses. In all schedules in which cisplatin was administered prior to etoposide a synergistic effect was observed. Conversely, an antagonistic effect was seen in all schedules where etoposide was administered before cisplatin. The design of the widely used OPEC protocol (oncovins, platinum agents, epipodophyllotoxins and cyclophosphamide) for management of the paediatric solid tumour neuroblastoma was based on clinical and in vitro evaluations of sequentially scheduled cisplatin and the epipodophyllotoxin, teniposide. These studies indicated that, for optimal anti-tumour effect, cisplatin should be administered prior to the epipodophyllotoxin (Hayes et al, 1981;Shafford et al, 1984;Pritchard et al, 1985).In several more recent clinical protocols for neuroblastoma, this apparently optimal order of drug administration has not been retained. The order of administration has been reversed in some regimens (Gordon et al, 1992;Tweddle et al, 2001) or the drugs are administered concurrently (reviewed in Pinkerton et al, 2000). If the OPEC rationale was correct, this altered scheduling pattern could result in sub-optimal response. Furthermore, in many of these schedules, cisplatin has been replaced by carboplatin. This will accentuate the change in order of administration because, despite the fact that carboplatin forms essentially the same final DNA adducts as cisplatin, the cytotoxic cross-linked structures develop more slowly than with cisplatin (Knox et al, 1986).The present study was aimed at determining, using contemporary methods of analysis, whether the currently used epipodophyllotoxin, etoposide, in combination with cisplatin, caused effects on neuroblastoma cell lines that were dependent upon the relative timings of the drug exposures. MATERIALS AND METHODS Cell culture and drug solutionsThe neuroblastoma cell lines SHSY5Y (Ciccarone et al, 1989) and NGP (Brodeur et al, 1977) were kindly provided by Drs P Lovat and D Tweddle (University of Newcastle upon Tyne). Cells were grown in RPMI 1640 (Dutch modification, supplemented with 10% v/v foetal bovine serum, and antibiotics (Gibco BRL)) at 378C/5% CO 2 . Frequent tests for mycoplasma infection were always negative. Etoposide was dissolved in methanol and stored at 7208C. Cisplatin was freshly dissolved in DMSO just prior to each experiment and immediately diluted into medium. During drug exposures, the concentrations of methanol and DMSO were kept below 1% and 0.001% respectively in treated and control wells. Sulphorhodamine B (SRB) assayFor each experiment, cells were inoculated into three 96-well tissue culture plates and incubated for 24 h prior to starting drug exposures (time zero). Plates were exposed to graded concentrations of either: the first drug in the schedule only followed by the diluent for the second drug; the diluent for the first drug in the s...

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Chromosomal aberrations in human neuroblastomas

Cited by 294 publications

References 18 publications

Clinical Categories of Neuroblastoma Are Associated with Different Patterns of Loss of Heterozygosity on Chromosome Arm 1p

Clinical Categories of Neuroblastoma Are Associated with Different Patterns of Loss of Heterozygosity on Chromosome Arm 1p

Checkpoint kinase inhibitor synergizes with DNA‐damaging agents in G₁ checkpoint‐defective neuroblastoma

Schedule-dependent response of neuroblastoma cell lines to combinations of etoposide and cisplatin

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Chromosomal aberrations in human neuroblastomas

Cited by 294 publications

References 18 publications

Clinical Categories of Neuroblastoma Are Associated with Different Patterns of Loss of Heterozygosity on Chromosome Arm 1p

Clinical Categories of Neuroblastoma Are Associated with Different Patterns of Loss of Heterozygosity on Chromosome Arm 1p

Checkpoint kinase inhibitor synergizes with DNA‐damaging agents in G1 checkpoint‐defective neuroblastoma

Schedule-dependent response of neuroblastoma cell lines to combinations of etoposide and cisplatin

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Checkpoint kinase inhibitor synergizes with DNA‐damaging agents in G₁ checkpoint‐defective neuroblastoma