The p73 gene is less involved in the development but involved in the progression of neuroblastoma.

Yang, Hong-Wei; Piao, Hui Ying; Chen, Y Z; Takita, Junko; Kobayashi, M; Taniwaki, Masanori; Hashizume, Kohei; Hanada, Ryoji; Yamamoto, Keisuke; Taki, Tomohiko; Bessho, Fumio; Yanagisawa, Masami; Hayashi, Yasuhide

doi:10.3892/ijmm.5.4.379

Cited by 12 publications

(22 citation statements)

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“…KIF1B-b expression in the seven cell lines is signi®cantly higher than that of favorable and unfavorable NBs 16, NB-19, NB-69, GOTO, SK-N-SH, CHP-134, LAN-1, LAN-2, and SJNB-1*SJNB-5, SJNB-7, and SJNB-8. SCMC-N2*SCMC-N5 were established by us (Komuro et al, 1993;Kong et al, 1997;Yang et al, 2000), while SJNB-1 * SJNB-5, SJNB-7, and SJNB-8 were a generous gift from Dr AT Look. The other cell lines including NB-1 (Imashuku et al, 1973) were obtained from the Japanese Cancer Research Resources Bank (http://cellbank.nihs.go.jp).…”

Section: Cell Lines and Primary Tumorsmentioning

confidence: 99%

“…The gel was dried and exposed to X-ray ®lm. After an abnormal band was identi®ed, then direct sequencing was carried out on the PCR product of the band (Kong et al, 1997;Yang et al, 2000).…”

Section: Pcr ± Sscp and Direct Sequencingmentioning

confidence: 99%

“…High molecular weight DNA was extracted from 24 cell lines by proteinase K digestion and phenol/ chloroform extraction (Kong et al, 1997;Yang et al, 2000).…”

Section: Cell Lines and Primary Tumorsmentioning

confidence: 99%

“…The primers from introns used for this study are shown in Table 2. PCR ampli®cation was performed with a GeneAmp PCR system-9700 (Perkin Elmer, Norwalk, CT, USA) as follows (Kong et al, 1997;Yang et al, 2000): denaturing at 948C followed by a 35 cycle ampli®cation (948C for 30 s, appropriate annealing temperature for 30 s, 728C for 30 s) and 7 min extention at 728C. The reaction mixture contained 50 ng of genomic DNA or 1 ml cDNA, 0.8 mM of each primer, 100 mM of each dNTP, 16PCR bu er, and 0.25 units of Taq polymerase in a ®nal volume of 5 ml.…”

Section: Pcr ± Sscp and Direct Sequencingmentioning

confidence: 99%

“…Several genes on distal 1p have been suggested as potential candidate tumor suppressor genes for NB. These include the cyclin dependent kinase (CDK) homologue CDC2L1 (Lahti et al, 1994); the zinc ®nger-containing transcription factors PAX7 (Shapiro et al, 1993), ID3 (Deed et al, 1994) and E2F2 (Saito et al, 1995); the tumor necrosis factor receptor 2 (TNFR2) (Beltinger et al, 1996); p73 gene (Kaghad et al, 1997;Yang et al, 2000) and DNA fragmentation factor 45 (DFF45) (Leek et al, 1997;Yang et al, 2001). None of them have shown any evidence as being a tumor suppressor gene for NB.…”

Section: Introductionmentioning

confidence: 99%

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Genomic structure and mutational analysis of the human KIF1B gene which is homozygously deleted in neuroblastoma at chromosome 1p36.2

et al. 2001

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In order to clone candidate tumor suppressor genes whose loss contributes to the pathogenesis of neuroblastoma (NB), we performed polymerase chain reaction (PCR) screening using a high-density sequence tagged site-content map within a commonly deleted region (chromosome band 1p36) in 24 NB cell lines. We found a *480 kb homozygously deleted region at chromosome band 1p36.2 in one of the 24 NB cell lines, NB-1, and cloned the human homologue (KIF1B-b) of the mouseKif1B-b gene in this region. The KIF1B-b gene had at least 47 exons, all of which had a classic exon ± intron boundary structure. Mouse Kif1B is a microtubule-based putative anterograde motor protein for the transport of mitochondria in neural cells. We performed mutational analysis of the KIF1B-b gene in 23 cell lines using 46 sets of primers and also an allelic imbalance (AI) analysis of KIF1B-b in 50 fresh NB samples. A missense mutation at codon 1554, GTG (Gly) to ATG (Met), silent mutations at codon 409 (ACG to ACA) and codon 1721 (ACC to ACT), and polymorphisms at codon 170, GAT (Asp) to GAA (Glu), and at codon 1087, TAT (Tyr), to TGT (Cys), were all identi®ed, although their functional signi®cances remain to be determined. The AI for KIF1B-b was slightly higher (38%) than those for the other two markers (D1S244, D1S1350) (35 and 32%) within the commonly deleted region (1p36). Reverse transcriptase-PCR analysis of the KIF1B-b gene revealed obvious expression in all NB cell lines except NB-1, although decreased expression of the KIF1B-b gene was found in a subset of early-and advanced-stage NBs. These results suggest that the KIF1B-b gene may not be a candidate for tumor suppressor gene of NB. Oncogene (2001) 20, 5075 ± 5083.

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Section: Cell Lines and Primary Tumorsmentioning

confidence: 99%

Section: Pcr ± Sscp and Direct Sequencingmentioning

confidence: 99%

“…High molecular weight DNA was extracted from 24 cell lines by proteinase K digestion and phenol/ chloroform extraction (Kong et al, 1997;Yang et al, 2000).…”

Section: Cell Lines and Primary Tumorsmentioning

confidence: 99%

Section: Pcr ± Sscp and Direct Sequencingmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Genomic structure and mutational analysis of the human KIF1B gene which is homozygously deleted in neuroblastoma at chromosome 1p36.2

et al. 2001

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Aberrations of the hSNF5/INI1 gene are restricted to malignant rhabdoid tumors or atypical teratoid/rhabdoid tumors in pediatric solid tumors

Uno

Takita

Yokomori

et al. 2002

Genes Chromosomes & Cancer

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The hSNF5/INI1 gene, which encodes a subunit of the SWI/SNF family of chromatin-remodeling complexes and is located at 22q11.2, has been reported as a tumor suppressor gene inactivated in malignant rhabdoid tumors (MRTs). We analyzed this gene in varieties of pediatric solid tumors including MRTs, using the reverse transcription-polymerase chain reaction (PCR) and PCR-single strand conformation polymorphism method. We found 5 homozygous deletions, 2 truncated mutations, one missense mutation, and one silent mutation of the hSNF5/INI1 gene in 7 MRT cell lines, and one homozygous deletion, one microdeletion, one splicing acceptor site mutation, and one absence of expression in 7 fresh tumor tissues of MRT and atypical teratoid (AT)/rhabdoid tumors (RTs). Homozygous deletions were also found in one (KYM-1) of 8 rhabdomyosarcoma (RMS) cell lines. To investigate characteristics of the KYM-1 cell line, we have established KYM-1 tumors in nude mice into which KYM-1 cells were transplanted. Notably, we found that MyoD1, known as a marker for RMS, was not expressed in the KYM-1 cell line as well as MRT cell lines and fresh tumors. Histopathologic, cytogenetic, and molecular studies of the KYM-1 cell line and KYM-1 tumors in nude mice have revealed that this RMS cell line should be MRT rather than RMS. RMS-carrying aberrations of the hSNF5/INI1 gene should be reevaluated. No aberrations of this gene were found in the other 34 cell lines or 80 fresh tumor specimens except the single nucleotide polymorphisms in the 3' noncoding region. These results suggest that alterations of the hSNF5/INI1 gene were restricted to MRTs or AT/RTs in pediatric solid tumors.

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Homozygous deletion in a neuroblastoma cell line defined by a high‐density STS map spanning human chromosome band 1p36

Chen

Soeda²,

Yang

et al. 2001

Genes Chromosomes & Cancer

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Recent molecular studies have shown a relatively high rate of loss of heterozygosity (LOH) in neuroblastoma (NB) as well as other types of tumors in human chromosome band 1p36. To identify candidate tumor suppressor genes in NB, we searched for homozygous deletions in NB cell lines with PCR according to a high-density sequence tagged site (STS)-content map spanning 1p35-36. Among 25 NB cell lines examined, only one cell line, NB-1, showed no signal with 27 STSs in a 480 kb region in 1p36.2. The sequence analysis has revealed that the defective region included seven known genes (E4, KIF1B, SCYA5, PGD, Cortistatin, DFF45, and PEX14), nine expressed sequence tags (ESTs), and two microsatellite markers. These genes are related to apoptosis, an ubiquitin-proteasome pathway, a neuronal microtubule-associated motor molecule, and components of a common translocation machinery. The region between the DFF45 and KIF1B genes was defined as homozygous deletion by Southern blotting. The search in LOH regions with high-density STSs may be useful for the isolation and identification of tumor suppressor genes in other tumors as well as NBs.

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The p73 gene is less involved in the development but involved in the progression of neuroblastoma.

Cited by 12 publications

References 0 publications

Genomic structure and mutational analysis of the human KIF1B gene which is homozygously deleted in neuroblastoma at chromosome 1p36.2

Genomic structure and mutational analysis of the human KIF1B gene which is homozygously deleted in neuroblastoma at chromosome 1p36.2

Aberrations of the hSNF5/INI1 gene are restricted to malignant rhabdoid tumors or atypical teratoid/rhabdoid tumors in pediatric solid tumors

Homozygous deletion in a neuroblastoma cell line defined by a high‐density STS map spanning human chromosome band 1p36

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