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June 20, 2026Current Cancer Drug Targets

Therapy-Induced Cellular Senescence in Non-Hodgkin Lymphomas, with Emphasis on Aggressive B-Cell Subtypes: Molecular Mechanisms and Emerging Drug Targets

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Authors

VTVictor TomacinschiiACAndreea CasianMRMaria Robu

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Overview

Narrative review synthesizes molecular mechanisms of therapy-induced senescence in non-Hodgkin lymphomas, suggesting novel therapeutic strategies.

Key Points

  • This article aims to synthesize the molecular mechanisms of therapy-induced senescence in non-Hodgkin lymphomas and identify potential drug targets.
  • Narrative review of mechanistic and translational literature
  • Focus on DNA damage response signaling and key cellular pathways
  • Searches conducted in databases like PubMed, Scopus, and Google Scholar
  • TIS is initiated by persistent DNA damage response signaling leading to growth arrest, connected to p53 and p16^INK4a pathways.
  • Senescent lymphoma cells develop a SASP that alters the tumor microenvironment and immune responses.
  • Epigenetic changes promote stem-like features and may lead to disease persistence and relapse.

Cite This Study

Tomacinschii et al. (2026) studied this question.

synapsesocial.com/papers/6a362f63db0793dc1a536deahttps://doi.org/10.2174/0115680096479876260608105824
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Cancer therapy-induced senescence: A critical yet overlooked aspect2026
  2. 2Therapy-induced cellular senescence: Potentiating tumor elimination or driving cancer resistance and recurrence?2024 · 12 citations
  3. 3Persistent accumulation of therapy-induced senescent cells: an obstacle to long-term cancer treatment efficacy2025 · 42 citations
  4. 4Therapy induced senescence promotes immunogenicity in acute myeloid Leukemia through reduced EZH2 activity2026
  5. 5Abstract LB150: Senescence as an immune tolerance breaker: Inhibitors of mitotic kinases TTK (Mps1) and AURKA induce pro-immunogenic senescence that primes the tumor microenvironment for immunotherapy via cGAS-STING signaling2026