Claudia Bossen
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Claudia Bossen has a total of 143 co-authors. Here are the top co-authors by number of shared publications:
- Jincheng Wu
Novartis Biomedical Research, Oncology
54 shared publications - Lexiang Ji
University of Georgia
53 shared publications - Marc R. Pelletier
Novartis Institutes for Biomedical Research, Cambridge, Massachusetts
53 shared publications - Alexander Savchenko
Novartis, Cambridge, MA, USA
33 shared publications - Andrew A. Butler
10Novartis Pharmaceuticals Corporation, East Hanover, New Jersey
33 shared publications - Benjamin J. Solomon
Peter MacCallum Cancer Centre, Melbourne, VIC, Australia
33 shared publications
Latest Publications
- Open Access
- 22 April 2026
- Published by National Academy of Sciences in Proceedings of the National Academy of Sciences
- Vol. 123 (17)
Targeting CRTC2 reverses STK11 mutant NSCLC tumor resistance to immunotherapy
Non–small cell lung cancer (NSCLC) patients with tumors harboring STK11 mutations are resistant to standard of care anti-PD-1/PD-L1 blockade. For this patient population there are no currently available tailored treatments, underlying the critical need to discover effective therapeutic strategies. In this study, we dissected the molecular mechanisms responsible for STK11 -mediated resistance to immune checkpoint blockade (ICB) and identified CRTC2, a coactivator of the transcription factor cAMP response element-binding protein (CREB), as a key signaling node regulating Stk11 -dependent cell-extrinsic functions. CRTC2 deletion remodeled the immune profiles of Stk11 -KO tumors and resensitized them to anti-PD-1 treatment, comparably to Stk11 -proficient tumors. Mechanistically, the abrogation of the binding between CRTC2 and CREB was sufficient to restore sensitivity to immunotherapy. These findings provide critical insights into the central role of CRTC2 in modulating response to ICB and identify the disruption of CRTC2–CREB interaction as a potential therapeutic approach for this patient population.
- 22 April 2026
- Published by National Academy of Sciences in Proceedings of the National Academy of Sciences
- Vol. 123 (17)
Open AccessTargeting CRTC2 reverses STK11 mutant NSCLC tumor resistance to immunotherapy
Non–small cell lung cancer (NSCLC) patients with tumors harboring STK11 mutations are resistant to standard of care anti-PD-1/PD-L1 blockade. For this patient population there are no currently available tailored treatments, underlying the critical need to discover effective therapeutic strategies. In this study, we dissected the molecular mechanisms responsible for STK11 -mediated resistance to immune checkpoint blockade (ICB) and identified CRTC2, a coactivator of the transcription factor cAMP response element-binding protein (CREB), as a key signaling node regulating Stk11 -dependent cell-extrinsic functions. CRTC2 deletion remodeled the immune profiles of Stk11 -KO tumors and resensitized them to anti-PD-1 treatment, comparably to Stk11 -proficient tumors. Mechanistically, the abrogation of the binding between CRTC2 and CREB was sufficient to restore sensitivity to immunotherapy. These findings provide critical insights into the central role of CRTC2 in modulating response to ICB and identify the disruption of CRTC2–CREB interaction as a potential therapeutic approach for this patient population.
- Open Access
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table S4 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
Baseline gene expression with significant association with ICI treatment outcome (OS) in PD-L1 negative in both CANOPY-1 and Tempus cohort 1 patients
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S4 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
Baseline gene expression with significant association with ICI treatment outcome (OS) in PD-L1 negative in both CANOPY-1 and Tempus cohort 1 patients
- Open Access
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S2 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
Criteria to define post-ICI patients (n = 326) into acquired (n = 75) and primary resistance (n = 59) in Tempus cohort
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S2 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
Criteria to define post-ICI patients (n = 326) into acquired (n = 75) and primary resistance (n = 59) in Tempus cohort
- Open Access
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table S6 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
Table of differentially expressed gene table in acquired resistance compared to treatment naïve cohort
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S6 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
Table of differentially expressed gene table in acquired resistance compared to treatment naïve cohort
- Open Access
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S3 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
Distribution of biopsy tissue sites comparing the treatment-naïve group (cohort 1) with the post-ICI group (cohort 2) in the left two panels and contrasting primary resistance with acquired resistance within cohort 2 in the right two panels
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S3 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
Distribution of biopsy tissue sites comparing the treatment-naïve group (cohort 1) with the post-ICI group (cohort 2) in the left two panels and contrasting primary resistance with acquired resistance within cohort 2 in the right two panels
- Open Access
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table S1 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
List of gene expression signatured
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S1 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
List of gene expression signatured
- Open Access
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Table 1 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
Key patient characteristics of the five cohorts in the study
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessTable 1 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
Key patient characteristics of the five cohorts in the study
- Open Access
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S6 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
Analysis of TME between pre- and post-ICI samples in patients with paired biopsies (Tempus cohort 3).
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S6 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
Analysis of TME between pre- and post-ICI samples in patients with paired biopsies (Tempus cohort 3).
- Open Access
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Figure 4 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
Analysis of the TME after monochemotherapy in the Tempus cohort 3 and SU2C-NSCLC cohorts. A, Volcano plot of differential expression analysis for 12 patients treated with platinum-based chemotherapy within Tempus cohort 3. B, Box plot of IFNγ signature expression before and after platinum therapy in 12 patients with paired biopsies. C, Box plot of the IFNγ signature by prior platinum-based therapy history in the SU2C-NSCLC cohort. D, Schematic of PD-L1 IHC class switching observed in Tempus cohort 3 by treatment class (ICI vs. non-ICI).
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessFigure 4 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
Analysis of the TME after monochemotherapy in the Tempus cohort 3 and SU2C-NSCLC cohorts. A, Volcano plot of differential expression analysis for 12 patients treated with platinum-based chemotherapy within Tempus cohort 3. B, Box plot of IFNγ signature expression before and after platinum therapy in 12 patients with paired biopsies. C, Box plot of the IFNγ signature by prior platinum-based therapy history in the SU2C-NSCLC cohort. D, Schematic of PD-L1 IHC class switching observed in Tempus cohort 3 by treatment class (ICI vs. non-ICI).
- Open Access
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table S2 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
Patient characteristics of three Tempus cohorts for age, gender, race and PD-L1 class
- 30 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S2 from Defining Non–small Cell Lung Cancer Tumor Microenvironment Changes at Primary and Acquired Immune Checkpoint Inhibitor Resistance Using Clinical and Real-World Data
Patient characteristics of three Tempus cohorts for age, gender, race and PD-L1 class