3D-Q-FISH/Telomere/TRF2 Nanotechnology Identifies a Progressively Disturbed Telomere/Shelterin/Lamin AC Complex as the Common Pathogenic, Molecular/Spatial Denominator of Classical Hodgkin Lymphoma

Cells. 2024 Oct 23;13(21):1748. doi: 10.3390/cells13211748.

Abstract

The bi- or multinucleated Reed-Sternberg cell (RS) is the diagnostic cornerstone of Epstein-Barr Virus (EBV)-positive and EBV-negative classical Hodgkin lymphoma (cHL). cHL is a germinal center (GC)-derived B-cell disease. Hodgkin cells (H) are the mononuclear precursors of RS. An experimental model has to fulfill three conditions to qualify as common pathogenic denominator: (i) to be of GC-derived B-cell origin, (ii) to be EBV-negative to avoid EBV latency III expression and (iii) to support permanent EBV-encoded oncogenic latent membrane protein (LMP1) expression upon induction. These conditions are unified in the EBV-, diffuse large B-Cell lymphoma (DLBCL) cell line BJAB-tTA-LMP1. 3D reconstructive nanotechnology revealed spatial, quantitative and qualitative disturbance of telomere/shelterin interactions in mononuclear H-like cells, with further progression during transition to RS-like cells, including progressive complexity of the karyotype with every mitotic cycle, due to BBF (breakage/bridge/fusion) events. The findings of this model were confirmed in diagnostic patient samples and correlate with clinical outcomes. Moreover, in vitro, significant disturbance of the lamin AC/telomere interaction progressively occurred. In summary, our research over the past three decades identified cHL as the first lymphoid malignancy driven by a disturbed telomere/shelterin/lamin AC interaction, generating the diagnostic RS. Our findings may act as trailblazer for tailored therapies in refractory cHL.

Keywords: 3D Q-FISH; Hodgkin lymphoma; LMP1 oncogene; Reed–Sternberg cell; TRF2; breakage–bridge–fusion (BBF) cycles; lamin A/C; nanotechnology; t-stumps; telomere/shelterin.

Publication types

  • Review

MeSH terms

  • Cell Line, Tumor
  • Hodgkin Disease* / diagnosis
  • Hodgkin Disease* / genetics
  • Hodgkin Disease* / metabolism
  • Hodgkin Disease* / pathology
  • Hodgkin Disease* / virology
  • Humans
  • In Situ Hybridization, Fluorescence
  • Nanotechnology / methods
  • Reed-Sternberg Cells / metabolism
  • Reed-Sternberg Cells / pathology
  • Shelterin Complex / metabolism
  • Telomere* / metabolism

Substances

  • Shelterin Complex

Grants and funding

This research received no external funding.