Topic
Double minute
About: Double minute is a research topic. Over the lifetime, 408 publications have been published within this topic receiving 20367 citations.
Papers published on a yearly basis
Papers
TL;DR: In this article, the amplification and expression of the c-myc oncogene in a system other than B-cell lymphomas, namely human lung cancer, was reported.
Abstract: Genetic changes involving the c-myc oncogene have been observed in human tumours. In particular, the c-myc gene is translocated in Burkitt's lymphoma and is amplified in the human promyelocytic leukaemia cell line, HL-60, which contains double minute chromosomes (DMs). More recently, an amplified c-myc gene has been positioned on a chromosomal homogeneous staining region (HSR) in a human colon cancer cell line, COLO 320, with neuroendocrine properties. Furthermore, c-myc is expressed in increased amounts in some human tumour lines, and in some cases, human small cell lung cancers (SCLC) contain DMs and HSRs. These findings prompted us to study the c-myc gene and its RNA expression in a series of human lung cancer cell lines. We now report amplification and expression of the c-myc oncogene in a system other than B-cell lymphomas, namely human lung cancer. Of 18 human lung cancer cell lines tested, 8 showed an amplified 12.5-kilobase (kb) EcoRI c-myc DNA band. Of particular interest are five SCLC lines with a high degree of c-myc DNA amplification (20-76-fold) and greatly increased levels of c-myc RNA. All five lines reside in the variant class of SCLC (SCLC-V) characterized by altered morphology, lack of expression of some SCLC-differentiated functions and more malignant behaviour than pure SCLC. Three of the five lines which have been karyotyped also contain DMs or HSRs. The finding of a greatly amplified c-myc gene in all cell lines of the SCLC-V class examined strongly suggests a role for the c-myc gene in the phenotypic conversion and malignant behaviour of human lung cancer.
968 citations
TL;DR: It is shown that the homogeneously staining regions of the COLO 320 HSR marker chromosome contain amplified c- myc, and it seems reasonable to suspect that amplification of c-myc may have contributed to tumorigenesis.
Abstract: Two human neuroendocrine tumor cell lines derived from a colon carcinoma contain either numerous double minute chromosomes (COLO 320 DM) or a homogeneously staining marker chromosome (COLO 320 HSR). We found amplification and enhanced expression of the cellular oncogene c-myc in both COLO 320 DM and HSR cells, and we were able to show that the homogeneously staining regions of the COLO 320 HSR marker chromosome contain amplified c-myc. From previous and present karyotypes, it appears that the homogeneously staining regions reside on a distorted X chromosome. Therefore, amplification of c-myc has been accompanied by translocation of the gene from its normal position on chromosome 8 (8q24). Because double minute chromosomes were features of primary cultures from the original tumor, it seems reasonable to suspect that amplification of c-myc may have contributed to tumorigenesis.
769 citations
TL;DR: The cellular oncogene c-Ki-ras is amplified 30- to 60-fold in cells of the mouse adrenocortical tumour Y1, contributing to the genesis and/or maintenance of at least some naturally occurring tumours.
Abstract: The cellular oncogene c-Ki-ras is amplified 30- to 60-fold in cells of the mouse adrenocortical tumour Y1 The amplified oncogene is located in double minute chromosomes and in a homogeneously staining chromosomal region, common karyotypical anomalies of tumour cells The amounts of c-Ki-ras specific mRNA and of the protein (p21) encoded by the amplified gene are correspondingly elevated Amplification and enhanced expression of cellular oncogenes may contribute to the genesis and/or maintenance of at least some naturally occurring tumours
464 citations
TL;DR: Large, homogeneously staining chromosome regions which lack the longitudinal differentiation ordinarily revealed by cytogenetic "banding" methods have been found in antifolate-resistant Chinese hamster cells and also in human neuroblastoma cells established in vitro.
Abstract: Large, homogeneously staining chromosome regions which lack the longitudinal differentiation ordinarily revealed by cytogenetic "banding" methods have been found in antifolate-resistant Chinese hamster cells and also in human neuroblastoma cells established in vitro. The drug-resistant cells are characterized by excessive production of the target enzyme, dihydrofolate reducatase, while the human neuroblastoma cells have phenotypes of normal neuronal cells. The homogeneously staining region appears to represent a novel metaphase chromosome anaomaly which may have functional significance in cells with specialized properties.
411 citations
TL;DR: Using DNAs from a panel of Chinese hamster-mouse somatic cell hybrids together with in situ hybridization protocols for gene mapping studies, it is found that these DM-associated, amplified DNA sequences originate from mouse chromosome 10, region C1–C3.
Abstract: We are exploring the origin and function of amplified DNA sequences associated with double minutes (DMs) in a spontaneously transformed derivative of mouse 3T3 cells. Toward that goal, we have constructed a cDNA library using RNA from these cells and have isolated cDNA clones representing sequences that are amplified and overexpressed in these 3T3-DM cells. From results of Northern- and Southern-blot analyses, we conclude that these cDNAs represent two distinct genes, which we have designated mdm-1and mdm-2.Using DNAs from a panel of Chinese hamster-mouse somatic cell hybrids together with in situ hybridization protocols for gene mapping studies, we have found that these DM-associated, amplified DNA sequences originate from mouse chromosome 10, region C1–C3. Sequences homologous to mdm-1and mdm-2are present in the genomes of several species examined, including that of man.
396 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2021 | 4 |
| 2020 | 3 |
| 2019 | 2 |
| 2018 | 4 |
| 2017 | 3 |
| 2016 | 3 |