Homogeneously staining regions on marker chromosomes in malignancy

Kovács, G.

doi:10.1002/ijc.2910230304

Cited by 45 publications

(23 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A similar finding has been re ported for HSRs in a number of human tumors (Biedler and Spengler, 1976;B ai .aban-Mai.enbaum and G ilbert, 1977;K ovacs, 1979). Other HSRs, however, exhibit intermediate staining (Kovacs, 1979;M iller et al, 1979) or are intensely stained (B iedler and Spengler, 1976;B ostock et al, 1979) after C-banding. The reason for these differences should become clearer as more is learned about the DNA composition of the HSRs.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Homogeneously staining chromosome regions and double minutes in a mouse adrenocortical tumor cell line

George

Francke

1980

Cytogenet Genome Res

View full text Add to dashboard Cite

We have used a number of banding techniques to analyze the chromosomal content of two sublines of the steroid-secreting mouse adrenocortical tumor cell line Y1. One of the sublines contains marker chromosomes with large “homogeneously staining regions” (HSRs). The other subline contains numerous double minutes, but no HSR. The presence of marker chromosomes shared by both sublines indicates their derivation from a common precursor. Both sublines are karyotypically stable, have similar growth rates, and exhibit positive staining for Δ⁵,3β-Hydroxysteroid dehydrogenase.

show abstract

Section: Discussionmentioning

confidence: 99%

“…The Johns Hopkins Medical School, 720 Rutland Avenue, Baltimore, MD 21205 (USA). and HSRs have been described in tumors of a number of species in a variety of cell types (for references, see L evan et al, 1977;Bar ker and Hsu, 1979; Kovacs, 1979), but they are rarely found together in the same cell.…”

mentioning

confidence: 99%

Homogeneously staining chromosome regions and double minutes in a mouse adrenocortical tumor cell line

George

Francke

1980

Cytogenet Genome Res

View full text Add to dashboard Cite

show abstract

“…At the time of the DNA isolations, the mean (± SD) number ofdm per cell for the cell lines Y1-DM, Cl.2a, and Cl.3b was 69 + 57 (6-220), 32 ± 19 , and 27 ± 24 , respectively (range in parentheses). Therefore, despite the differences in the relative abundance ofpYdl-DISCUSSION HSRs and dm have been described in various tumor cell types of human and animal origin (19)(20)(21)(22). Evidence has been presented that these chromosomal anomalies result from a process of gene amplification (1,(3)(4)(5)22).…”

Section: Specific Association Of Amplified Sequences With Y1 Dmmentioning

confidence: 99%

Amplified DNA sequences in Y1 mouse adrenal tumor cells: association with double minutes and localization to a homogeneously staining chromosomal region.

George¹,

Powers²

1982

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…Tumorigenesis is accompanied by a variety of molecular processes including DNA rearrangements (18, 21), oncogene activation (2) and amplification (5,24,25), and the appearance of double-minute chromosomes and homogeneously staining regions containing amplified DNA sequences (7,10,16).…”

mentioning

confidence: 99%

Carcinogen-mediated methotrexate resistance and dihydrofolate reductase amplification in Chinese hamster cells.

Kleinberger¹,

Etkin²,

Lavi³

1986

Mol. Cell. Biol.

View full text Add to dashboard Cite

We have investigated different parameters characterizing carcinogen-mediated enhancement of methotrexate resistance in Chinese hamster ovary (CHO) cells and in simian virus 40-transformed Chinese hamster embryo (C060) cells. We show that this enhancement reflects dihydrofolate reductase (dhfr) gene amplification. The carcinogens used in this work are alkylating agents and UV irradiation. Both types of carcinogens induce a transient enhancement of methotrexate resistance which increases gradually from the time of treatment to 72 to 96 h later and decreases thereafter. Increasing doses of carcinogens decrease cell survival and increase the enhancement of methotrexate resistance. Enhancement was observed when cells were treated at different stages in the cell cycle, and it was maximal when cells were treated during the early S phase. These studies of carcinogen-mediated dhfr gene amplification coupled with our earlier studies on viral DNA amplification in simian virus 40-transformed cells demonstrate that the same parameters characterize the amplification of both genes. Possible cellular mechanisms responsible for the carcinogen-mediated gene amplification phenomenon are discussed.Although environmental agents have been shown to play an important role in the initiation of most human cancers, little is known about the molecular mechanisms underlying their action. Tumorigenesis is accompanied by a variety of molecular processes including DNA rearrangements (18, 21), oncogene activation (2) and amplification (5,24,25), and the appearance of double-minute chromosomes and homogeneously staining regions containing amplified DNA sequences (7,10,16).In recent years we studied the effect of chemical and physical carcinogens on one of these cancer-related phenomena, namely, gene amplification, in an attempt to establish its possible role in the initiation events of carcinogenesis. To study gene amplification immediately after exposure to the carcinogens rather than after the long process of establishing cell lines containing amplified genes, we have constructed an experimental model system consisting of simian virus 40 (SV40)-transformed Chinese hamster cells (C060) (12). In this system SV40 amplification can be monitored by molecular hybridization. Exposure of these cells to a variety of chemical and physical carcinogens has been shown to result in the amplification of SV40 DNA sequences. This amplification requires an active origin of replication and a functional T antigen. The amplification phenomenon is transient, reaching a maximal level on the third and fourth day after treatment with carcinogen, and disappears within a few more days (12,14,15). Exposure to carcinogens is followed by a prolonged S phase. Treatment of a synchronized population of cells obtained by isoleucine starvation results in increased SV40 amplification (Y. Berko and S. Lavi, manuscript in preparation).Further studies in our laboratory revealed transient amplification of additional DNA sequences including the dhfr and rasH genes in response to carc...

show abstract

Homogeneously staining regions on marker chromosomes in malignancy

Cited by 45 publications

References 15 publications

Homogeneously staining chromosome regions and double minutes in a mouse adrenocortical tumor cell line

Homogeneously staining chromosome regions and double minutes in a mouse adrenocortical tumor cell line

Amplified DNA sequences in Y1 mouse adrenal tumor cells: association with double minutes and localization to a homogeneously staining chromosomal region.

Carcinogen-mediated methotrexate resistance and dihydrofolate reductase amplification in Chinese hamster cells.

Contact Info

Product

Resources

About