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Targeting DNA Repair, Cell Cycle, and Tumor Microenvironment in B Cell Lymphoma

Paul J Bröckelmann1,2, Mathilde R W de Jong3,4, Ron D Jachimowicz1,2,5,6

  • 1Max Planck Research Group Mechanisms of DNA Repair, Max Planck Institute for Biology of Ageing, 50931 Cologne, Germany.

Cells
|October 17, 2020
PubMed

Insights

DNA double-strand breaks (DSBs) are critical DNA damage. This review explores their role in B cell development, lymphomagenesis, and therapeutic strategies targeting DNA repair and the tumor microenvironment.

Area of Science:

  • Molecular Biology
  • Immunology
  • Oncology

Background:

  • DNA double-strand breaks (DSBs) are highly toxic DNA lesions that threaten genome stability.
  • The ATM kinase-mediated DNA damage response (DDR) is crucial for repairing DSBs and maintaining genomic integrity.
  • Programmed DSBs are essential for normal B cell development and immune responses.

Purpose of the Study:

  • To review the role of DNA repair and cell cycle control in B cell development and lymphomagenesis.
  • To explore the interplay between the DDR and the tumor microenvironment (TME).
  • To discuss therapeutic strategies for B cell lymphomas, focusing on defective DDR signaling and TME.

Main Methods:

  • Literature review of DNA repair pathways.
  • Analysis of cell cycle control mechanisms in B cells.
  • Examination of the relationship between DDR and TME in lymphomagenesis.

Main Results:

  • Disturbances in DSB repair and cell cycle control are implicated in B cell lymphomagenesis.
  • The DDR and TME are intricately linked, influencing lymphoma progression.
  • Defective DDR signaling presents therapeutic vulnerabilities in B cell lymphomas.

Conclusions:

  • Understanding DSB repair and DDR is vital for B cell development and preventing lymphomagenesis.
  • Targeting DDR and TME offers promising therapeutic avenues for B cell lymphomas.
  • Mantle cell lymphoma serves as a model for exploring these therapeutic strategies in B cell lymphomas.
Keywords:
ATMB cell developmentDNA damage responseDSB repairSTINGcell cyclecyclin D1immunotherapymantle cell lymphomatumor microenvironment

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