Deletion variants within the NF-kappa B activation domain of the LMP1 oncogene prevail in acquired immunodeficiency syndrome-related large cell lymphomas and human immunodeficiency virus-negative atypical lymphoproliferations.

@article{Knecht1996DeletionVW,
  title={Deletion variants within the NF-kappa B activation domain of the LMP1 oncogene prevail in acquired immunodeficiency syndrome-related large cell lymphomas and human immunodeficiency virus-negative atypical lymphoproliferations.},
  author={Hans Knecht and Martine Rapha{\"e}l and Cathy McQuain and Sylvia Rothenberger and German Albert Pihan and Sophie Camilleri‐Br{\"o}et and Edith Bachmann and G. R. Kershaw and Saleh Ryan and Ellen L. W. Kittler and Peter J. Quesenberry and Daniel Schlaifer and Bruce A. Woda and Pierre Brousset},
  journal={Blood},
  year={1996},
  volume={87 3},
  pages={
          876-81
        }
}
This sequencing study of 17 acquired immunodeficiency syndrome-related lymphomas (9 primary brain, 8 systemic) and 8 human immunodeficiency virus-negative atypical lymphoproliferations expressing large amounts of the latent membrane protein 1 (LMP1) of Epstein-Barr virus was performed to characterize the carboxy terminal NF-kappa B activation domain of LMP1 at the molecular level in an immunocompromised host. In-frame deletions within the NF-kappa B activation domain were identified in all but… 
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Deletion variants within the NF-kappaB activation domain of the LMP1 oncogene in acquired immunodeficiency syndrome-related large cell lymphomas, in prelymphomas and atypical lymphoproliferations.

The prevalence of the same mutational pattern in AIDS-related lymphoma as well as in hyperplastic reactive states and prelymphomas supports the hypothesis that these variants confer a growth advantage manifested under impaired cellular immunity.

High frequency of a 30‐bp deletion of Epstein–Barr virus latent membrane protein 1 gene in primary HIV non‐Hodgkin's brain lymphomas

Its high incidence suggests that the oncogenic mechanism of LMP1 in the brain might differ significantly from that in systemic lymphoid proliferations, and might be enhanced by HIV infection.

Mutations in the Epstein-Barr virus latent membrane protein-I (BNLF-

Genetic changes described previously in the C-terminus of the LMP-1 gene in various malignancy derivedEBV strains are also presetit frequently in wild type viruses and do not simply define tumour specific EBV strains, which may play a role in EBV oncogenesis.

Selective outgrowth of a posttransplant B-immunoblastic lymphoma expressing a latent membrane protein-1 deletion variant.

A B-immunoblastic lymphoma that developed in a pretransplantation EBV-seronegative woman 4 months after kidney transplant from her HLA-haploidentical brother is reported and has been in remission for 36 months.

Carboxy‐terminal sequence variation of LMP1 gene in Epstein–Barr‐virus‐associated mononucleosis and tumors from Serbian patients

This study demonstrated noticeable geographical‐associated characteristics in the LMP1 C terminus of investigated isolates of patients with mononucleosis syndrome, renal transplantation, and tumors, mostly nasopharyngeal carcinoma.

Deletion of Epstein-Barr virus latent membrane protein 1 gene in United States and Brazilian Hodgkin's disease and reactive lymphoid tissue: high frequency of a 30-bp deletion.

Ethnic differences in the expression of Epstein-Barr virus latent membrane protein-1 mutations in nasopharyngeal carcinoma.

Mutations in the Epstein-Barr virus latent membrane protein-1 (BNLF-1) gene in spontaneous lymphoblastoid cell lines: effect on in vitro transformation associated parameters and tumorigenicity in SCID and nude mice

Genetic changes described previously in the C-terminus of the LMP-1 gene in various malignancy derivedEBV strains are also present frequently in wild type viruses and do not simply define tumour specific EBV strains, and may play a role in EBV oncogenesis.

Epstein‐Barr virus in Hodgkin's disease: frequency of a 30‐bp deletion in the latent membrane protein (LMP‐1) oncogene in South African patients

  • M. Fadiel EssopM. EngelP. CloseColin Sinclair‐SmithGorm Pallesen
  • Biology, Medicine
    International journal of cancer
  • 1999
The aim was to determine the frequency of del-LMP-1 in EBV-positive HD in South African patients, and to assess whether this deletion might be associated with aggressive clinical behaviour.

Deletion of Epstein-Barr virus latent membrane protein 1 gene in Japanese and Brazilian gastric carcinomas, metastatic lesions, and reactive lymphocytes.

The similar high incidence of 30-bp deletion in LMP1 gene in both carcinoma cells and reactive lymphocytes in EBVaGC cases suggests that this deletion may not be relevant to the pathogenesis of EB VaGC.

References

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A deletion mutant of the LMP1 oncogene of Epstein-Barr virus is associated with evolution of angioimmunoblastic lymphadenopathy into B immunoblastic lymphoma.

Two patients with AILD that subsequently progressed into immunoblastic lymphoma (IBL) were studied to investigate whether the LMP1 deletion mutant was implicated in progression of AILD into IBL, and identical deletions and point mutations were revealed.

High expression of latent membrane protein 1 of Epstein-Barr virus and BCL-2 oncoprotein in acquired immunodeficiency syndrome-related primary brain lymphomas.

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Mutational hot spots within the carboxy terminal region of the LMP1 oncogene of Epstein-Barr virus are frequent in lymphoproliferative disorders.

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The Epstein-Barr virus latent membrane protein-1 (LMP1) mediates activation of NF-kappa B and cell surface phenotype via two effector regions in its carboxy-terminal cytoplasmic domain.

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Expression of Epstein-Barr virus latent gene products in tumour cells of Hodgkin's disease

Deletions within the LMP1 oncogene of Epstein-Barr virus are clustered in Hodgkin's disease and identical to those observed in nasopharyngeal carcinoma.

It is suggested that partial deletions of the LMP1 oncogene occur at a particular localization and confer a proliferative phenotype to lymphoid cells in HD.

LMP-1 activates NF-kappa B by targeting the inhibitory molecule I kappa B alpha

Results indicate that LMP-1 activates NF-kappa B in B-cell lines by targeting I kappa B alpha, a transcription factor controlling the expression of genes involved in cell activation and growth control, has been shown to be activated by L MP-1.