Activation of a cellular onc gene by promoter insertion in ALV-induced lymphoid leukosis

Hayward, William S.; Neel, Benjamin G.; Astrin, Susan M.

doi:10.1038/290475a0

Cited by 1,540 publications

(758 citation statements)

References 54 publications

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“…c-myc, present at 8q, was one of the first cellular oncogene cloned (25,26). However, much has been recently learned about the biology of the gene itself (27).…”

Section: Figurementioning

confidence: 99%

Loss of p53 and c-myc Overrepresentation in Stage T2-3N1-3M0 Prostate Cancer are Potential Markers for Cancer Progression

et al. 2002

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To determine whether genetic changes are markers of cancer progression and patient survival in Stage T 2-3 N 1-3 M 0 prostatic carcinoma, we compared 26 patients who died of tumor relapse after prostatectomy and lymphadenectomy (case group) with 26 matched patients who were alive at the time of the matched case's death (control group). Nine unmatched cases were also included in this study. In 37 cases, paired primary tumors (119 foci) and lymph node metastases (114 foci) were available for study. Fluorescence in situ hybridization (FISH) with centromere-specific probes for chromosomes 7, 8, and 17 and region-specific probes for D7S486 (7q31), c-myc (8q24), LPL (8p22), and p53 (17p13) was performed on available primary carcinomas and lymph node metastases. In primary tumor foci, ؉7q31, ؊8p22, ؉c-myc, substantial additional increases of myc (AI-c-myc), and ؊p53 were observed in 65%, 74%, 43%, 29%, and 31% of foci, respectively. AI-c-myc was strongly associated with higher cancer Gleason score (P ‫؍‬ .003). Heterogeneity of genetic changes was frequently observed among multiple cancer foci. Lymph node metastases of prostate cancer usually shared genetic changes with paired primary tumors. In addition, the genetic change pattern with ؊8p, ؉c-myc or AI-c-myc, ؉7q, and ؉p53 was slightly higher in lymph node metastases (22%) than in primary tumors (6%) (P ‫؍‬ .08). In matched case and control patients, simultaneous gain of 7q31 (؉7q31) and CEP7 (؉CEP7) was identified in 59% and 68% of specimens for case and control groups, respectively (P ‫؍‬ .48). Loss of 8p22 (؊8p22) was identified in 77% and 69% of specimens for case and control groups, respectively (P ‫؍‬ 1.0). Simultaneous gain of c-myc (؉c-myc) and CEP8 (؉CEP8) without overt additional increase of c-myc copy number relative to CEP8 copy number, was identified in 38% and 54% of specimens for case and control groups, respectively (P ‫؍‬ .27). AI-c-myc was identified in 54% and 23% of specimens for case and control groups, respectively (odds ratio ‫؍‬ 3.0, P ‫؍‬ .06). Loss of p53 (؊p53) was identified in 46% and 15% of specimens for case and control groups, respectively (odds ratio Prostate cancer is the most common malignancy and the second leading cause of cancer death in men in the United States (1). Patients with pelvic lymph node metastases of prostatic carcinoma, but no evidence of systemic progression are commonly classified as having Stage T 2-3 N 1-3 M 0 prostate cancer (2). These cancers have an indeterminate natural history (3). Choosing different types of therapy (radiation, surgery, or hormonal therapy) for these

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“…c-myc, present at 8q, was one of the first cellular oncogene cloned (25,26). However, much has been recently learned about the biology of the gene itself (27).…”

Section: Figurementioning

confidence: 99%

Loss of p53 and c-myc Overrepresentation in Stage T2-3N1-3M0 Prostate Cancer are Potential Markers for Cancer Progression

et al. 2002

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“…A model supporting this notion comes from the studies on the chicken leukaemogenesis induced by the non-acute avian leukosis virus (ALV). By integrating close to the cellular oncogene, c-myc, the ALV provirus via its transcriptional promoter or enhancer element can lead to increased levels of c-myc transcription 5,6 23,24 . using the probes shown at the bottom of Figure 2.…”

Section: C-myc Translocation In Manca Cellsmentioning

confidence: 99%

Activation of a translocated human c-myc gene by an enhancer in the immunoglobulin heavy-chain locus

Hayday

Gillies

Saito

et al. 1984

Nature

Self Cite

257

112

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“…This collapse of host regulatory function for the oncogene might involve actual demethylation of the host sequence incorporated into the virion (Breznik & Cogen, 1982) or physical separation of the oncogene from the methylated host DNA sequence responsible for its repression. Integration of the avian leukosis viral genome next to a specific cellular oncogene has been shown to occur, and to transcriptionally activate the gene (Hayward et al, 1981).…”

Section: -Mc Depletion During Tumour Developmentmentioning

confidence: 99%

5-Methylcytosine depletion during tumour development: An extension of the miscoding concept

Nyce¹,

Weinhouse²,

Magee³

1983

Br J Cancer

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Perhaps the most ubiquitous aspect of tumours and the neoplastic cells of which they are composed is their loss of the ability to control cellular functions in a normal way. During the development of the malignant state, the neoplastic cell becomes increasingly refractory to both the internal and external stimulae which integrate its normal counterparts into functional tissues and organ systems. This lack of integration is associated with alterations in the expression of a host of gene products, including, for example, the ectopic biosynthesis of hormones (

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Activation of a cellular onc gene by promoter insertion in ALV-induced lymphoid leukosis

Cited by 1,540 publications

References 54 publications

Loss of p53 and c-myc Overrepresentation in Stage T2-3N1-3M0 Prostate Cancer are Potential Markers for Cancer Progression

Loss of p53 and c-myc Overrepresentation in Stage T2-3N1-3M0 Prostate Cancer are Potential Markers for Cancer Progression

Activation of a translocated human c-myc gene by an enhancer in the immunoglobulin heavy-chain locus

5-Methylcytosine depletion during tumour development: An extension of the miscoding concept

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