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A cellular oncogene (c-Ki- ras ) is amplified, overexpressed, and located within karyotypic abnormalities in mouse adrenocortical tumour cells

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TLDR
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

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Amplification of N-myc in untreated human neuroblastomas correlates with advanced disease stage

TL;DR: N-myc amplification is highly correlated with advanced stages of disease (P less than 0.001) and with the ability to grow in vitro as an established cell line, both of which are associated with a poor prognosis.
Journal ArticleDOI

A new variant of glycoprotein cd44 confers metastatic potential to rat carcinoma cells

TL;DR: Using a monoclonal antibody raised against a surface glycoprotein of the metastasizing rat pancreatic carcinoma cell line BSp73ASML, cDNA clones have been isolated that encode glycoproteins with partial homology to CD44, a presumed adhesion molecule.
Journal ArticleDOI

Amplified DNA with limited homology to myc cellular oncogene is shared by human neuroblastoma cell lines and a neuroblastoma tumour.

TL;DR: It is shown here that a DNA domain detectable by partial homology to the myc oncogene is amplified up to 140-fold in cell lines derived from different human neuroblastomas and in a neuroblastoma tumour, but not in other tumour cells showing cytological evidence for gene amplification.
Journal ArticleDOI

Cellular Oncogenes and Multistep Carcinogenesis

TL;DR: Two dozen cellular proto-oncogenes have been discovered to date through the study of retroviruses and the use of gene transfer, and recent work provides experimental strategies by which many of them, as well as oncogene of DNA tumor viruses, may be placed into functional categories.
Journal ArticleDOI

The Molecular Genetics of Cellular Oncogenes

TL;DR: Structural and Functional Properties of Translocation Breakpoints near Cellular Oncogenes and the Functional Significance of Diff erences Between c-onc' s and v-onC' s are studied.
References
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Journal ArticleDOI

Many tumors induced by the mouse mammary tumor virus contain a provirus integrated in the same region of the host genome.

TL;DR: It is proposed that tumorigenesis by MMTV is strongly favored by proviral insertion within the int1 locus, perhaps as a consequence of enhanced expression of a novel cellular oncogene.
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Human c-myc onc gene is located on the region of chromosome 8 that is translocated in Burkitt lymphoma cells

TL;DR: Using a DNA probe that is specific for the complete gene (c-myc), different somatic cell hybrids possessing varying numbers of human chromosomes were analyzed by the Southern blotting technique and results indicate that the human c- myc gene is located on chromosome 8.
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Activation of a cellular onc gene by promoter insertion in ALV-induced lymphoid leukosis

TL;DR: The data indicate that, as a rare event, the ALV provirus integrates adjacent to the c-myc gene and that transcription, initiating from a viral promoter, causes enhanced expression of c- myc, leading to neoplastic transformation.
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A cellular oncogene is translocated to the Philadelphia chromosome in chronic myelocytic leukaemia

TL;DR: Positive hybridization is found when the 22q−(the Philadelphia chromosome), and not the 9q+ derivative of the translocation, is present in the cell hybrids, and this finding is a direct demonstration of a reciprocal exchange between the two chromosomes and suggests a role for the c-abl gene in the generation of CML.
Journal ArticleDOI

Translocation of the c-myc gene into the immunoglobulin heavy chain locus in human Burkitt lymphoma and murine plasmacytoma cells

TL;DR: It is shown that transformation of human Burkitt lymphomas and murine plasmacytomas is frequently accompanied by the somatic rearrangement of a cellular analogue of an avian retrovirus transforming gene, c-myc, which provides a molecular basis for considering the role that specific translocations might play in malignant transformation.
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