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.

The 30-bp deletion variant of Epstein-Barr virus-encoded latent membrane protein-1 prevails in acute infectious mononucleosis.

A hypervariable region within the C-terminus of LMP-1 is identified, in a domain required for maximal stimulation of NF-kappaB activity, that is identical to those observed in Epstein-Barr virus-associated AIDS-related lymphoma.

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.

MOLECULAR PATHOGENESIS OF EPSTEIN-BARR VIRUS ASSOCIATED POSTTRANSPLANT LYMPHOMAS: NEW INSIGHTS THROUGH LATENT MEMBRANE PROTEIN 1 FINGERPRINTING1

The results show that highly selected CD34+ PBSCT does not protect against transfer of EBV positive founder cells of donor type PTL and that, after allo-SCT, recipient types PTLs are not uncommon and may be favoured by LMP1 deletion variant strains present in recipient lymphocytes.

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.

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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.

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

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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.

Epstein-Barr virus burden in Hodgkin's disease is related to latent membrane protein gene expression but not to active viral replication.

Viral burden in Hodgkin's disease is not primarily related to active viral replication, but is associated with LMP gene expression, as shown in cases containing many copies of viral DNA and of mixed cellularity histological subtype.