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Exploring Resistance to ETS Targeting Agents in Diffuse Large B-Cell Lymphoma.

Filippo Spriano¹, Luciano Cascione^1,2, Chiara Tarantelli¹

¹Institute of Oncology Research, Faculty of Biomedical Sciences, USI, Bellinzona, Switzerland.

Cancer Medicine

|May 14, 2026

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Mechanisms of resistance to ETS inhibition in diffuse large B-cell lymphoma (DLBCL) were explored. Findings reveal diverse resistance pathways, suggesting combination therapies like venetoclax and selinexor may overcome treatment challenges.

Area of Science:

Oncology
Molecular Biology
Genetics

Background:

Diffuse large B-cell lymphoma (DLBCL) presents therapeutic challenges beyond standard immunochemotherapy.
ETS transcription factors are implicated in DLBCL pathogenesis and are targeted by TK216.
Understanding resistance mechanisms to TK216 is crucial for developing effective treatments.

Purpose of the Study:

To investigate the mechanisms of resistance to the ETS inhibitor TK216 in DLBCL.
To identify distinct patterns of resistance and potential therapeutic vulnerabilities.

Main Methods:

Generation of TK216-resistant DLBCL cell lines (U2932).
Transcriptomic and mutational analyses to characterize resistance mechanisms.
Pharmacologic screening to identify sensitivities and resistance profiles.

Keywords:

ETS MDR XPO1 diffuse large B‐cell lymphoma resistance venetoclax

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Main Results:

Resistant clones showed increased IC50 values and loss of G2-M arrest.
Three resistance patterns identified: MDR1/ABCB1 overexpression, Cluster A (proliferation/Wnt), and Cluster B (cytoskeleton/metabolism).
Resistant cells showed increased sensitivity to BCL2, MCL1, and XPO1 inhibitors (e.g., venetoclax, selinexor).

Conclusions:

Multiple, heterogeneous mechanisms contribute to TK216 resistance in DLBCL.
Targeting BCL2, MCL1, or XPO1 may overcome resistance.
Venetoclax and selinexor show promise in combination strategies against resistant DLBCL.