Rapid cloning of multiple amplified nucleotide sequences from human neuroblastoma cell lines by phenol emulsion competitive DNA reassociation

Shiloh, Yosef; Rose, Elise; Colletti-Feener, Chris; Korf, Bruce R.; Kunkel, Louis M.; Latt, Samuel A.

doi:10.1016/0378-1119(87)90473-2

Cited by 19 publications

(13 citation statements)

References 31 publications

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“…Competitive DNA reassociation techniques were used to select for amplified MboI fragments (24) in breast tumor DNA obtained from a patient with advanced disease. A plasmid library was created using the multifunctional pSPORTl vector (Life Technologies, Gaithersburg, MD) and DNA enriched for amplified sequences.…”

Section: Isolation Of the Amplified Jc-a Fragmentmentioning

confidence: 99%

Assessing sequential oncogene amplification in human breast cancer

et al. 1995

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Studies of amplification and/or overexpression of c-myc, HER-2/neu, and H-ras in breast cancer have shown that each is associated with a poor prognosis. The purpose of this study was to explore the possibility that there is a preferred sequence of amplification of these oncogenes in breast cancer. The frequencies of amplification and patterns of co-amplification of c-myc, HER-Yneu, and H-ras were studied in a group of 84 breast cancers. The data suggested a preferred sequence of amplification that consisted of c-myc amplification-HER-2heu amplification-H-ras amplification. This model was supported by loglinear analysis. In addition, the levels of amplification of JC-A, a DNA fragment newly isolated from a patient with advanced breast cancer, were studied in 61 of these cases. The data suggested that JC-A amplification occurred early. Loglinear analysis supported a model in which JC-A amplification occurred either before or after c-myc amplification but was unrelated to Her-2heu or ras amplification. 0 1995 Wiley-Liss, Inc.

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Section: Isolation Of the Amplified Jc-a Fragmentmentioning

confidence: 99%

Assessing sequential oncogene amplification in human breast cancer

et al. 1995

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“…Circular DNAs harboring MYC were also present (Von Hoff et al, 1988). Other studies have shown that the size and sequence of amplified regions differ between the neuroblastoma tumors and cell lines (Montgomery et al, 1983;Shiloh et al, 1985Shiloh et al, , 1986Shiloh et al, , 1987Amler and Schwab, 1989;Kato et al, 1989). These results led us to consider MYCN amplification in two different contexts: one is rearrangement in the initial stage of amplification, and the other is rearrangement during subsequent stages.…”

Section: Discussionmentioning

confidence: 94%

“…These results led us to consider MYCN amplification in two different contexts: one is rearrangement in the initial stage of amplification, and the other is rearrangement during subsequent stages. This consideration leads to the episomeformation-plus-segregation model (Stark et al, 1989), with an initial recombination during the subsequent intermediate states and further rearrangements during the formation of MYCN amplicons. Regardless of whether or not this model fits MYCN amplification in human neuroblastomas from a cloning bias, but rather due to the smallness of the core of the amplicons retained in this cell line.…”

Section: Discussionmentioning

confidence: 99%

“…Gene amplification in mammalian cells is found most commonly in drug-resistance genes (Schimke, 1984;Stark et al, 1989) and cellular proto-oncogenes (Alitalo and Schwab, 1986;Schwab, 1986; Schwab and Amler, 1990). Understanding the molecular mechanism by which the MYCN locus is amplified is of great value in elucidating the correlation between this phenomenon and the poor prognosis for human neuroblastomas (Brodeur et al, 1984;Schwab et al, 1984).…”

Section: Introductionmentioning

confidence: 99%

“…There have been several studies aimed at understanding the structural organization of amplified regions Montgomery et al, 1983;Shiloh et al, 1985Shiloh et al, , 1986Shiloh et al, , 1987Kinder et al, 1986;Zehnbauer et al, 1988;Amler and Schwab, 1989;Kato et al, 1989; Akiyama and Nishi, 1991;Nishi et al, 1992), whereas others have tried to discover the mechanism operative during the early events of amplification (Von Hoff et al, 1988;IIunt et al, 1900).…”

Section: Introductionmentioning

confidence: 99%

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Structural organization of MYCN amplicons of neuroblastoma tumors, xenografts, and cell lines characterized by the sequences encompassing the MYCN amplicons in a human neuroblastoma cell line

Akiyama

Kanda

Yamada

et al. 1993

Genes Chromosomes & Cancer

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We characterized differences in the structural organization of the MYCN amplicons of a number of neuroblastomas by analyzing 8 contigs spanning 330 kb cloned from the MYCN amplicon of a neuroblastoma cell line. Some regions were amplified in almost all specimens, the conserved regions (CRs), and others were differentially amplified in some subsets, the non-conserved regions (NCRs). CRs constituted only 20% of the 330 kb region, with the remainder being NCRs. The regions that inevitably co-segregate with the MYCN gene make up the core, whereas flanking regions are retained at random. If a histogram of the frequency with which the amplified NCR sequences from one specimen match those of the cell line MC-NB-I shows a random distribution, the NCRs would co-segregate with MYCN as a result of random events. However, both the tumors and cell lines/xenografts showed a distribution with two distinct peaks; one from a group containing a small number of sequences with a fairly high degree of homology to the NCRs of MC-NB-I, and the other from a group containing a large number of sequences with little homology. These results indicate that the flanking segments are preferentially co-segregated with MYCN by a non-random mechanism.

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Isolation of Genomic Fragments from Polymorphic Regions by Representational Difference Analysis

Baldocchi

Flaherty

1997

Methods

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Rapid cloning of multiple amplified nucleotide sequences from human neuroblastoma cell lines by phenol emulsion competitive DNA reassociation

Cited by 19 publications

References 31 publications

Assessing sequential oncogene amplification in human breast cancer

Assessing sequential oncogene amplification in human breast cancer

Structural organization of MYCN amplicons of neuroblastoma tumors, xenografts, and cell lines characterized by the sequences encompassing the MYCN amplicons in a human neuroblastoma cell line

Isolation of Genomic Fragments from Polymorphic Regions by Representational Difference Analysis

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