Association between Epstein-Barr virus LMP-1 and Hodgkin lymphoma LMP-1 mechanisms in Hodgkin lymphoma development.
Leonam Oliver Durval OliveiraIgor Brasil CostaJuarez Antonio Simões QuaresmaPublished in: Reviews in medical virology (2024)
Hodgkin lymphoma is histologically characterised by the presence of Hodgkin (H) and Reed-Sternberg (RS) cells originating from germinal centre B-cells rearranged in the IgV gene. The formation of multinucleated RS cells is a product of telomere organisation in a process initiated by telomere aggregate accumulation in mononuclear H cells and may be mediated by latent membrane protein 1 (LMP-1) expression. LMP-1 is the main oncoprotein of EBV and supports several tumourigenic processes. LMP-1 may rescue proapoptotic B-cells through downregulation of B-cell receptor (BCR) components, mimicking and inducing multiple distinct B-cell signalling pathways to promote proliferation and survival, such as Janus kinase-signal transducer and activator of transcription (JAK-STAT), nuclear factor-kappa b (NF-кB), and cellular MYC (c-MYC), and inducing telomere instability mainly through Telomere repeat binding factor 2 (TRF2) downregulation to promote the formation of multinucleated RS cells. This review presents recent discoveries regarding the influence of LMP-1 on the surviving cellular signalling, genomic instability and mecanical formation of HRS cells.
Keyphrases
- epstein barr virus
- hodgkin lymphoma
- induced apoptosis
- nuclear factor
- cell cycle arrest
- signaling pathway
- diffuse large b cell lymphoma
- endoplasmic reticulum stress
- toll like receptor
- gene expression
- cell proliferation
- cell death
- acute lymphoblastic leukemia
- pi k akt
- copy number
- tyrosine kinase
- dna methylation
- peripheral blood
- long non coding rna
- dna binding