Abnormalities of chromosome 1p in human neuroblastoma tumors and cell lines

Gilbert, Fiona J.; Balaban, Gloria; Moorhead, Paul S.; Bianchi, Diana W.; Schlesinger, Harvey

doi:10.1016/0165-4608(82)90105-4

Cited by 164 publications

(69 citation statements)

References 12 publications

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“…The same author and his associates in 1981 reported structural abnormalities of lp-in 7/10 cases they investigated. However the partial lp monosomy was confirmed by Haag et al (1981), Gilbert et al (1982 and Trent (1983). Other workers used conventional staining without the benefit of the banding techniques.…”

Section: Discussionsupporting

confidence: 61%

“…The presence of the marker chromosomes in a fairly reasonable proportion would support the theory of the clonal derivation of this tumour. However 80% of the published karyotypes had modes that are in the peridiploid range (Brewster & Garrett, 1965;Wakonig-Vaartaja et al, 1971;Brodeur et al, 1977Brodeur et al, , 1981Haag et al, 1981;Gilbert et al, 1982). Double minutes were found in 1% of the metaphases of our neuroblastomas.…”

Section: Discussionmentioning

confidence: 92%

“…However, these were also found frequently in glial as well as other neurogenic tumours. Some workers reported deletion of the short arm of chromosome number 1 in some of their neuroblastomas (Brodeur et al, 1977(Brodeur et al, , 1981Haag et al, 1981;Gilbert et al, 1982 andTrent, 1983).…”

mentioning

confidence: 99%

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Chromosomal analysis of neuroblastoma

Hafez¹,

el-Meadday²,

Sheir³

et al. 1985

Br J Cancer

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Summary Ten children with abdominal neuroblastoma were included in the study. Biopsies from the neuroblastomas were taken during surgical operations, nine from the primary tumours and one from a metastasis. Histopathology was done for diagnosis. Chromosomal cultures of neuroblastoma cells and peripheral blood lymphocytes were performed.The peripheral blood lymphocytes revealed normal chromosomal complements. The 10 tumours were in the peridiploid range with random gains or losses of chromosomes. Deletion of the short arm of chromosome number 1 distal to band p31 occurred in 6 tumours. Other structural changes and giant markers were found. It was concluded that a regulatory gene controlling the transformation gene of neuroblastoma, is present at or distal to lp31.

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Section: Discussionsupporting

confidence: 61%

Section: Discussionmentioning

confidence: 92%

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Chromosomal analysis of neuroblastoma

Hafez¹,

el-Meadday²,

Sheir³

et al. 1985

Br J Cancer

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“…UET-13 cells were cultured in Dulbecco's modified Eagle's medium (DMEM) with 10% Tet system approved fetal bovine serum (T-FBS) (Takara) at 37°C under a humidified 5% CO 2 atmosphere. EFT cell lines (EES-1 [20], SCCH196 [21], RD-ES and SK-ES1 [5], NCR-EW2 and NCR-EW3 [19], and W-ES [13]) and neuroblastoma (NB) cell lines (NB69 and NB9 [15] and GOTO [47]) were cultured in RPMI 1640 with 10% FBS. A rhabdomyosarcoma cell line, NRS-1 (40), was cultured in Eagle's minimal essential medium with 10% FBS.…”

Section: Methodsmentioning

confidence: 99%

Inducible Expression of Chimeric EWS/ETS Proteins Confers Ewing's Family Tumor-Like Phenotypes to Human Mesenchymal Progenitor Cells

Miyagawa

Okita

Nakaijima

et al. 2008

Molecular and Cellular Biology

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Ewing's family tumor (EFT) is a rare pediatric tumor of unclear origin that occurs in bone and soft tissue. Specific chromosomal translocations found in EFT cause EWS to fuse to a subset of ets transcription factor genes (ETS), generating chimeric EWS/ETS proteins. These proteins are believed to play a crucial role in the onset and progression of EFT. However, the mechanisms responsible for the EWS/ETS-mediated onset remain unclear. Here we report the establishment of a tetracycline-controlled EWS/ETS-inducible system in human bone marrow-derived mesenchymal progenitor cells (MPCs). Ectopic expression of both EWS/FLI1 and EWS/ERG proteins resulted in a dramatic change of morphology, i.e., from a mesenchymal spindle shape to a small round-to-polygonal cell, one of the characteristics of EFT. EWS/ETS also induced immunophenotypic changes in MPCs, including the disappearance of the mesenchyme-positive markers CD10 and CD13 and the up-regulation of the EFT-positive markers CD54, CD99, CD117, and CD271. Furthermore, a prominent shift from the gene expression profile of MPCs to that of EFT was observed in the presence of EWS/ETS. Together with the observation that EWS/ETS enhances the ability of cells to invade Matrigel, these results suggest that EWS/ETS proteins contribute to alterations of cellular features and confer an EFT-like phenotype to human MPCs.Ewing's family tumor (EFT) is a rare childhood cancer arising mainly in bone and soft tissue. Since EFT has a poor prognosis, it is important to elucidate the underlying pathogenic mechanisms for establishing a more effective therapeutic strategy. EFT is characterized by the presence of chimeric genes composed of EWS and ets transcription factor genes (ETS) formed by specific chromosomal translocations, i.e., EWS/FLI1, t(11;22)(q24;q12); EWS/ERG, t(21;22)(q12;q12); EWS/ETV1, t(7;22)(p22;q12); EWS/E1AF, t(17;22)(q12;q12); and EWS/FEV, t(2;22)(q33;q12) (26). The products of these chimeric genes behave as aberrant transcriptional regulators and are believed to play a crucial role in the onset and progression of EFT (3,36). Indeed, recent studies have revealed that the induction of EWS/FLI1 proteins can trigger transformation in certain cell types, including NIH 3T3 cells (36), C2C12 myoblasts (12), and murine primary bone marrow-derived mesenchymal progenitor cells (MPCs) (6, 45, 52). However, studies have also indicated that overexpression of EWS/ FLI1 provokes apoptosis and growth arrest in mouse normal embryonic fibroblasts and primary human fibroblasts (10, 31), hence hampering understanding of the precise role of EWS/ ETS proteins in the development of EFT. The function of EWS/ETS proteins would be greatly influenced by cell type, and thus the cells that can originate EFTs might be more susceptible to the tumorigenic effects of EWS/ETS.Although the cell origin of EFT is still unknown, the expression of neuronal markers in spite of the occurrence in bone and soft tissues has kept open the debate as to a potential mesenchymal or neuroectodermal origin. As described ...

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“…Gilbert and et al (1982) reported that the high frequency of deletions and other rearrangements of 1p were held to be the most common genetic aberration of NB tumour cells. 11 aberrations of CAs (particularly deletions) at band p32, q21 and q32 on chromosome 1 were detected in our patients (Table 1).…”

Section: Discussionmentioning

confidence: 99%

Chromosome Imbalances and Alterations of AURKA and MYCN Genes in Children with Neuroblastoma

Yılmaz¹,

Demırhan²,

Erdoğan³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Background: Neuroblastoma (NB), like most human cancers, is characterized by genomic instability, manifested at the chromosomal level as allelic gain, loss or rearrangement. Genetics methods, as well as conventional and molecular cytogenetics may provide valuable clues for the identification of target loci and successful search for major genes in neuroblastoma. We aimed to investigate AURKA and MYCN gene rearrangements and the chromosomal aberrations (CAs) to determine the prognosis of neuroblastoma. Methods: We performed cytogenetic analysis by G-banding in 25 cases [11 girls (44%) and 14 boys (66%)] and in 25 controls. Fluorescence in situ hybridization (FISH) with AURKA and MYCN gene probes was also used on interphase nuclei to screen for alterations. Results: Some 18.4% of patient cells exhibited CAs., with a significant difference between patient and control groups in the frequencies (P<0.0001). Some 72% of the cells had structural aberrations, and only 28% had numerical chnages in patients. Structural aberrations consisted of deletions, translocations, breaks and fragility in various chromosomes, 84% and 52% of the patients having deletions and translocations, respectively. Among these expressed CAs, there was a higher frequency at 1q21, 1q32, 2q21, 2q31, 2p24, 4q31, 9q11, 9q22, 13q14, 14q11.2, 14q24, and

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Abnormalities of chromosome 1p in human neuroblastoma tumors and cell lines

Cited by 164 publications

References 12 publications

Chromosomal analysis of neuroblastoma

Chromosomal analysis of neuroblastoma

Inducible Expression of Chimeric EWS/ETS Proteins Confers Ewing's Family Tumor-Like Phenotypes to Human Mesenchymal Progenitor Cells

Chromosome Imbalances and Alterations of AURKA and MYCN Genes in Children with Neuroblastoma

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