Ablation of CDK6 and STAT5B rewires T cell developmental dynamics and prevents ALK+ lymphoma formation

Abstract CDK6 and STAT5B are well-established oncogenic drivers, but their interplay during transformation remains poorly understood. Here, we demonstrate that simultaneous genetic deletion of Cdk6 and Stat5b in an NPM-ALK Tg/+ mouse model completely prevents tumor formation. Immature DN2/3 thymocytes are identified as the cellular origin of ALK-driven malignancy. Single-cell transcriptomics reveals a tumor-specific differentiation trajectory that is fully disrupted by combined Cdk6/Stat5b loss, coinciding with a developmental shift. We uncover shared transcriptional targets of CDK6 and STAT5B involved in cell-cycle regulation and apoptosis at the tumor initiation stage. In human ALCL cells, dual deletion of CDK6 and STAT5B induces context-dependent synthetic lethality, exposing a potential therapeutic vulnerability. A transcriptional signature derived from CDK6/STAT5B-dependent tumor initiation genes identifies a high-risk subgroup of ALCL patients with worse survival. Together, these findings establish a molecular link between thymocyte development, the crosstalk of CDK6 and STAT5B, oncogenic signaling, and clinical outcome in ALCL.

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Publication Details

Journal
Nature Communications
Published
2026-09-15
DOI
https://doi.org/10.1038/s41467-026-77466-4
Primary Topic
Lymphoma Diagnosis and Treatment
Type
article
Field-Weighted Citation Impact
0.00

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article

Ablation of CDK6 and STAT5B rewires T cell developmental dynamics and prevents ALK+ lymphoma formation

Tania Brandstoetter, Richard Moriggl, Alessia Schirripa, Jonatan Kendler et al.
Nature Communications
Lymphoma Diagnosis and Treatment
article

Ablation of CDK6 and STAT5B rewires T cell developmental dynamics and prevents ALK+ lymphoma formation

Tania Brandstoetter, Richard Moriggl, Alessia Schirripa, Jonatan Kendler, Karoline Kollmann, Elisabeth Gamper, Klavdija Bastl, Lukas Kenner, Thorsten Klampfl, Reinhard Grausenburger, A. G. Pichler, Michaela Prchal‐Murphy, Veronika Sexl, Barbara Maurer, Sebastian Kollmann, Sabine Lagger, Dua Shahid, Maximilian Sexl, Giorgia Damonte, Philipp B. Staber, Stefania Massari, Hager El Kersh
article en

Abstract

Abstract CDK6 and STAT5B are well-established oncogenic drivers, but their interplay during transformation remains poorly understood. Here, we demonstrate that simultaneous genetic deletion of Cdk6 and Stat5b in an NPM-ALK Tg/+ mouse model completely prevents tumor formation. Immature DN2/3 thymocytes are identified as the cellular origin of ALK-driven malignancy. Single-cell transcriptomics reveals a tumor-specific differentiation trajectory that is fully disrupted by combined Cdk6/Stat5b loss, coinciding with a developmental shift. We uncover shared transcriptional targets of CDK6 and STAT5B involved in cell-cycle regulation and apoptosis at the tumor initiation stage. In human ALCL cells, dual deletion of CDK6 and STAT5B induces context-dependent synthetic lethality, exposing a potential therapeutic vulnerability. A transcriptional signature derived from CDK6/STAT5B-dependent tumor initiation genes identifies a high-risk subgroup of ALCL patients with worse survival. Together, these findings establish a molecular link between thymocyte development, the crosstalk of CDK6 and STAT5B, oncogenic signaling, and clinical outcome in ALCL.

Nature Communications
University of Veterinary Medicine Vienna (AT), University of Salzburg (AT), Universität Innsbruck (AT), Comprehensive Cancer Center Vienna (AT), Medical University of Vienna (AT), University of Genoa (IT), Saarland University (DE)
Österreichischen Akademie der Wissenschaften, Austrian Science Fund, Veterinärmedizinische Universität Wien
Good health and well-being
Openalex Percentile: Top 12%
Lymphoma Diagnosis and Treatment
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