Age related resistance to avian leukosis virus. III. Infectious virus, neutralising antibody and tumours in chickens inoculated at various ages

Maas, H. J. L.; Boer, G. F. de; Groenendal, J.E.

doi:10.1080/03079458208436103

Cited by 25 publications

(13 citation statements)

References 17 publications

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“…Susceptibility to ALV lymphomagenesis is developmentally regulated, as birds must be infected before 2 weeks of age in order to develop bursal lymphomas (Maas et al, 1982). This developmental window represents the stage when immature bursal cells are present that can populate the bursa in transplantation experiments (Purchase et al, 1979).…”

Section: Discussionmentioning

confidence: 99%

“…This resistance is encoded by the target bursal cells, as shown by transplantation of bursal progenitors between lymphoma-susceptible and -resistant birds (Purchase et al, 1979). Tumor susceptibility is also developmentally regulated in the lymphoma-susceptible strains, as birds must be infected with ALV before 2 weeks of age to eciently form tumors (Burmester et al, 1960;Maas et al, 1982). It is not known why immature bursal cells are the target for ALV lymphomagenesis.…”

Section: Introductionmentioning

confidence: 99%

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Resistance to avian leukosis virus lymphomagenesis occurs subsequent to proviral c-myc integration

1999

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Most chicken strains are highly susceptible to avian leukosis virus (ALV) induction of bursal lymphoma, involving proviral integration within the c-myc protooncogene, while certain strains are genetically resistant to lymphomagenesis. A nested PCR assay was developed to analyse the appearance of proviral c-myc integrations after ALV infection of lymphoma-susceptible birds, and to determine whether these integrations arise in lymphoma-resistant birds. Proviral c-myc integrations are detected in bursa and other tissues from 6 day-old lymphoma-susceptible birds infected as embryos. The abundance of bursal cells carrying these integrations increases roughly 40-fold by 35 days of age, indicating that these cells hyperproliferate within the bursal environment. Bursal cells with proviral c-myc integrations also arise soon after infection of lymphomaresistant embryos. However, these cells expand much more slowly than cells from lymphoma-susceptible birds. Both strains show the same rate of viral infection, so that resistance to lymphomagenesis occurs at a step subsequent to proviral c-myc integration. Proviral c-erbB gene integrations arise at the same frequency in bursa and other tissues of both strains, and they do not increase in abundance during development. These ®ndings indicate that the mechanism of resistance to lymphomagenesis involves speci®c inhibition of cells with proviral c-myc integrations within the bursa.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Resistance to avian leukosis virus lymphomagenesis occurs subsequent to proviral c-myc integration

1999

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“…RNA was extracted from day 15 embryos, when hematopoietic bursal migrants have colonized the anlage (25), day 16 when most lymphoid cells are in follicles, day 18 with vigorously dividing embryonic follicular populations, and day 21 initiating posthatching physiology, including disappearance of transplantable stem cell and myc-target populations (7,8). Fig.…”

Section: Analysis Of Expression During Normal Bursal Developmentmentioning

confidence: 99%

“…6). In this system, tumor induction by c-myc requires a target cell population present only during embryonic bursal development (7,8) and produces, as its initial histological manifestation, multiple preneoplastic lesions called transformed follicles (TF) (9)(10)(11). The cells comprising TF are a monomorphic population of IgM-positive lymphoblasts that display surface antigens of early bursal cells and that retain stem cell function (8,10).…”

mentioning

confidence: 99%

Analysis of gene expression during myc oncogene-induced lymphomagenesis in the bursa of Fabricius

Neiman

Ruddell

Jasoni

et al. 2001

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

122

101

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The transcriptional effects of deregulated myc gene overexpression are implicated in tumorigenesis in a spectrum of experimental and naturally occurring neoplasms. In follicles of the chicken bursa of Fabricius, myc induction of B-cell neoplasia requires a target cell population present during early bursal development and progresses through preneoplastic transformed follicles to metastatic lymphomas. We developed a chicken immune system cDNA microarray to analyze broad changes in gene expression that occur during normal embryonic B-cell development and during mycinduced neoplastic transformation in the bursa. The number of mRNAs showing at least 3-fold change was greater during mycinduced lymphomagenesis than during normal development, and hierarchical cluster analysis of expression patterns revealed that levels of several hundred mRNAs varied in concert with levels of myc overexpression. A set of 41 mRNAs were most consistently elevated in myc-overexpressing preneoplastic and neoplastic cells, most involved in processes thought to be subject to regulation by Myc. The mRNAs for another cluster of genes were overexpressed in neoplasia independent of myc expression level, including a small subset with the expression signature of embryonic bursal lymphocytes. Overexpression of myc, and some of the genes overexpressed with myc, may be important for generation of preneoplastic transformed follicles. However, expression profiles of late metastatic tumors showed a large variation in concert with myc expression levels, and some showed minimal myc overexpression. Therefore, high-level myc overexpression may be more important in the early induction of these lymphomas than in maintenance of late-stage metastases.

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“…In contrast, LTR-enhanced transcription is stable at all stages of B-cell development in resistant birds, suggesting that the transcription factors mediating LTR-enhanced transcription are differentially regulated during B-cell development in resistant and susceptible birds. The lability of LTR-enhanced transcription in immature bursal lymphocytes correlates with the agedependent susceptibility of birds to ALV-induced lymphomas before 2 weeks of age (Maas et al, 1982). This suggests that stable LTR-enhanced transcription in the immature bursal target cells of resistant birds could produce the observed lower levels of Myc expression, which fail to promote effectively the growth of transformed follicles.…”

Section: Discussionmentioning

confidence: 86%

Reduced Myc overexpression and normal B-cell differentiation mediate resistance to avian leukosis virus lymphomagenesis

et al. 2004

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Age related resistance to avian leukosis virus. III. Infectious virus, neutralising antibody and tumours in chickens inoculated at various ages

Cited by 25 publications

References 17 publications

Resistance to avian leukosis virus lymphomagenesis occurs subsequent to proviral c-myc integration

Resistance to avian leukosis virus lymphomagenesis occurs subsequent to proviral c-myc integration

Analysis of gene expression during myc oncogene-induced lymphomagenesis in the bursa of Fabricius

Reduced Myc overexpression and normal B-cell differentiation mediate resistance to avian leukosis virus lymphomagenesis

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