Cutaneous T-cell lymphoma cells are sensitive to rapamycin
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Updated: Jun 11, 2026

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Published on: April 11, 2025
Melanie Kremer1, Katja Sliva, Claus-Detlev Klemke
1Paul-Ehrlich-Institut, Paul-Ehrlich, Langen, Germany.
Abstract:
Cutaneous T-cell lymphomas (CTCL) are characterised by clonal expansion of helper T lymphocytes that infiltrate the skin. Only a small number of cell lines exist to study cellular pathways leading to T-cell transformation and to identify new targets for intervention. We wanted to investigate the inhibition of mTOR as a possible therapeutic target in CTCL. Primary cells of patients with Sézary syndrome (SS) and conventional CTCL cell lines were analysed. Constitutive activation of mTOR was found, and concomitantly, we could show that rapamycin, a specific inhibitor of mTOR, inhibits CTCL cell growth in vitro by induction of cell cycle arrest. Using a previously established animal model for CTCL, we additionally observed upon rapamycin treatment tumor growth inhibition in vivo. In summary, primary cells from patients with SS as well as CTCL cell lines allowed us to identify mTOR as an important target for intervention.
Insights
Inhibition of mTOR, a key pathway in cutaneous T-cell lymphomas (CTCL), with rapamycin effectively halts CTCL cell growth and tumor progression, identifying mTOR as a promising therapeutic target.
Area of Science:
- Oncology
- Dermatology
- Immunology
Background:
- Cutaneous T-cell lymphomas (CTCL) involve skin-infiltrating T lymphocytes.
- Limited cell lines hinder research into CTCL pathogenesis and therapeutic targets.
Purpose of the Study:
- To investigate the inhibition of the mTOR pathway as a potential therapeutic strategy for CTCL.
- To analyze mTOR activation in primary Sézary syndrome (SS) cells and CTCL cell lines.
Main Methods:
- Analysis of primary SS cells and established CTCL cell lines.
- Treatment with rapamycin, a specific mTOR inhibitor.
- In vitro cell growth assays and in vivo studies using a CTCL animal model.
Main Results:
- Constitutive activation of mTOR was observed in CTCL cells.
- Rapamycin inhibited CTCL cell proliferation in vitro by inducing cell cycle arrest.
- Rapamycin treatment demonstrated tumor growth inhibition in a CTCL animal model in vivo.
Conclusions:
- The mTOR pathway is constitutively activated in CTCL.
- Inhibition of mTOR with rapamycin is a viable therapeutic approach for CTCL.
- mTOR represents a significant target for novel CTCL interventions.
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