c-erbB activation in avian leukosis virus-induced erythroblastosis: Clustered integration sites and the arrangement of provirus in the c-erbB alleles

M. A. Raines, W. G. Lewis, L. B. Crittenden, Hsing-Jien Kung

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Abstract

There is considerable evidence that links the activation of cellular genes to oncogenesis. We previously reported that structural rearrangements in the cellular oncogene c-erbB correlate with the development of erythroblastosis induced by avian leukosis virus (ALV). c-erbB recently has been shown to be related to the gene encoding growth factor receptor. We now have characterized the detailed mechanisms of c-erbB activation by ALV proviruses. We report here that the ALV proviral integration sites are clustered 5' to the region where homology to v-erbB starts, suggesting that interruption in this region of c-erbB is important for its activation. The proviruses are oriented in the same transcriptional direction as c-erbB and usually are full-size. The latter finding is in contrast to the frequent deletions observed within the c-myc-linked proviruses in B-cell lymphomas. We have also identified a second c-erbB allele, which differs from the previously known allele primarily by a deletion in an intron region. This allele is also oncogenic upon mutation by an ALV provirus.

Original languageEnglish (US)
Pages (from-to)2287-2291
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume82
Issue number8
StatePublished - 1985
Externally publishedYes

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Avian Leukosis Virus
Proviruses
Alleles
Virus Integration
Growth Factor Receptors
B-Cell Lymphoma
Oncogenes
Introns
Transcriptional Activation
Carcinogenesis
Mutation
Genes

ASJC Scopus subject areas

  • General
  • Genetics

Cite this

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title = "c-erbB activation in avian leukosis virus-induced erythroblastosis: Clustered integration sites and the arrangement of provirus in the c-erbB alleles",
abstract = "There is considerable evidence that links the activation of cellular genes to oncogenesis. We previously reported that structural rearrangements in the cellular oncogene c-erbB correlate with the development of erythroblastosis induced by avian leukosis virus (ALV). c-erbB recently has been shown to be related to the gene encoding growth factor receptor. We now have characterized the detailed mechanisms of c-erbB activation by ALV proviruses. We report here that the ALV proviral integration sites are clustered 5' to the region where homology to v-erbB starts, suggesting that interruption in this region of c-erbB is important for its activation. The proviruses are oriented in the same transcriptional direction as c-erbB and usually are full-size. The latter finding is in contrast to the frequent deletions observed within the c-myc-linked proviruses in B-cell lymphomas. We have also identified a second c-erbB allele, which differs from the previously known allele primarily by a deletion in an intron region. This allele is also oncogenic upon mutation by an ALV provirus.",
author = "Raines, {M. A.} and Lewis, {W. G.} and Crittenden, {L. B.} and Hsing-Jien Kung",
year = "1985",
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journal = "Proceedings of the National Academy of Sciences of the United States of America",
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T1 - c-erbB activation in avian leukosis virus-induced erythroblastosis

T2 - Clustered integration sites and the arrangement of provirus in the c-erbB alleles

AU - Raines, M. A.

AU - Lewis, W. G.

AU - Crittenden, L. B.

AU - Kung, Hsing-Jien

PY - 1985

Y1 - 1985

N2 - There is considerable evidence that links the activation of cellular genes to oncogenesis. We previously reported that structural rearrangements in the cellular oncogene c-erbB correlate with the development of erythroblastosis induced by avian leukosis virus (ALV). c-erbB recently has been shown to be related to the gene encoding growth factor receptor. We now have characterized the detailed mechanisms of c-erbB activation by ALV proviruses. We report here that the ALV proviral integration sites are clustered 5' to the region where homology to v-erbB starts, suggesting that interruption in this region of c-erbB is important for its activation. The proviruses are oriented in the same transcriptional direction as c-erbB and usually are full-size. The latter finding is in contrast to the frequent deletions observed within the c-myc-linked proviruses in B-cell lymphomas. We have also identified a second c-erbB allele, which differs from the previously known allele primarily by a deletion in an intron region. This allele is also oncogenic upon mutation by an ALV provirus.

AB - There is considerable evidence that links the activation of cellular genes to oncogenesis. We previously reported that structural rearrangements in the cellular oncogene c-erbB correlate with the development of erythroblastosis induced by avian leukosis virus (ALV). c-erbB recently has been shown to be related to the gene encoding growth factor receptor. We now have characterized the detailed mechanisms of c-erbB activation by ALV proviruses. We report here that the ALV proviral integration sites are clustered 5' to the region where homology to v-erbB starts, suggesting that interruption in this region of c-erbB is important for its activation. The proviruses are oriented in the same transcriptional direction as c-erbB and usually are full-size. The latter finding is in contrast to the frequent deletions observed within the c-myc-linked proviruses in B-cell lymphomas. We have also identified a second c-erbB allele, which differs from the previously known allele primarily by a deletion in an intron region. This allele is also oncogenic upon mutation by an ALV provirus.

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