Abstract PS3-12-29: Trop2 remodeling of the immune microenvironment in triple negative breast cancer

Abstract Immune exclusion inhibits anti-tumor immunity and response to immunotherapy, but its mechanisms remain poorly defined. In triple-negative breast cancer (TNBC), an aggressive and generally immune-rich subtype, an immune-cold microenvironment predicts poor prognosis due to a limited response to chemotherapy and immune checkpoint inhibitors. To identify mechanisms regulating immune infiltration in TNBC, we performed spatial transcriptomic analysis comparing immune-enriched versus immune-cold tumors. We reveal that Trophoblast Cell-Surface Antigen 2 (TROP2), a key target of anti-cancer Antibody Drug Conjugates (ADCs), controls barrier-mediated immune exclusion in TNBC through Claudin 7 association and tight junction regulation. TROP2 expression is inversely correlated with T cell infiltration and predicts poor outcomes in TNBC. Loss-of-function and reconstitution experiments demonstrate TROP2 is sufficient to drive tumor progression in vivo in a CD8 T cell-dependent manner, while its loss deregulates expression and localization of multiple tight junction proteins, enabling T cell infiltration. Employing a humanized TROP2 syngeneic TNBC model, we show that TROP2 targeting via hRS7, the antibody component of the ADC Sacituzumab govitecan (SG), enhances the anti-PD1 response and improves T cell accessibility and effector function. Correspondingly, TROP2 expression is highly associated with lack of response to anti-PD1 therapy in human breast cancer. Thus, TROP2 controls an immune exclusion program that can be targeted to enhance immunotherapy response. Citation Format: B. Wu, W. Thant, E. Bitman, T. Liu, J. Liu, E. Paschalis, B. Patel, C. Nawrocki, K. Xu, L. Nieman, D. Ting, N. Thimmiah, S. Sun, R. Abelman, V. Bossuyt, S. Isakoff, L. Spring, A. Bardia, L. Ellisen. Trop2 remodeling of the immune microenvironment in triple negative breast cancer [abstract]. In: Proceedings of the San Antonio Breast Cancer Symposium 2025; 2025 Dec 9-12; San Antonio, TX. Philadelphia (PA): AACR; Clin Cancer Res 2026;32(4 Suppl):Abstract nr PS3-12-29.

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Publication Details

Journal
Clinical Cancer Research
Published
2026-02-17
DOI
https://doi.org/10.1158/1557-3265.sabcs25-ps3-12-29
Primary Topic
HER2/EGFR in Cancer Research
Type
article
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0.00
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article

Abstract PS3-12-29: Trop2 remodeling of the immune microenvironment in triple negative breast cancer

Rachel O. Abelman, Veerle Bossuyt, Elena Bitman, Win Thant et al.
Clinical Cancer Research
HER2/EGFR in Cancer Research
article

Abstract PS3-12-29: Trop2 remodeling of the immune microenvironment in triple negative breast cancer

Rachel O. Abelman, Veerle Bossuyt, Elena Bitman, Win Thant, Nayana Thimmiah, Cole Nawrocki, David Ting, Linda T. Nieman, E. Paschalis, S. Isakoff, T. Liu, L. Ellisen, B. Patel, K. Xu, S. Sun, B. Wu, A. Bardia, J. Liu, L. Spring
article en

Abstract

Abstract Immune exclusion inhibits anti-tumor immunity and response to immunotherapy, but its mechanisms remain poorly defined. In triple-negative breast cancer (TNBC), an aggressive and generally immune-rich subtype, an immune-cold microenvironment predicts poor prognosis due to a limited response to chemotherapy and immune checkpoint inhibitors. To identify mechanisms regulating immune infiltration in TNBC, we performed spatial transcriptomic analysis comparing immune-enriched versus immune-cold tumors. We reveal that Trophoblast Cell-Surface Antigen 2 (TROP2), a key target of anti-cancer Antibody Drug Conjugates (ADCs), controls barrier-mediated immune exclusion in TNBC through Claudin 7 association and tight junction regulation. TROP2 expression is inversely correlated with T cell infiltration and predicts poor outcomes in TNBC. Loss-of-function and reconstitution experiments demonstrate TROP2 is sufficient to drive tumor progression in vivo in a CD8 T cell-dependent manner, while its loss deregulates expression and localization of multiple tight junction proteins, enabling T cell infiltration. Employing a humanized TROP2 syngeneic TNBC model, we show that TROP2 targeting via hRS7, the antibody component of the ADC Sacituzumab govitecan (SG), enhances the anti-PD1 response and improves T cell accessibility and effector function. Correspondingly, TROP2 expression is highly associated with lack of response to anti-PD1 therapy in human breast cancer. Thus, TROP2 controls an immune exclusion program that can be targeted to enhance immunotherapy response. Citation Format: B. Wu, W. Thant, E. Bitman, T. Liu, J. Liu, E. Paschalis, B. Patel, C. Nawrocki, K. Xu, L. Nieman, D. Ting, N. Thimmiah, S. Sun, R. Abelman, V. Bossuyt, S. Isakoff, L. Spring, A. Bardia, L. Ellisen. Trop2 remodeling of the immune microenvironment in triple negative breast cancer [abstract]. In: Proceedings of the San Antonio Breast Cancer Symposium 2025; 2025 Dec 9-12; San Antonio, TX. Philadelphia (PA): AACR; Clin Cancer Res 2026;32(4 Suppl):Abstract nr PS3-12-29.

Clinical Cancer ResearchVol. 32(4_Supplement)
Massachusetts Eye and Ear Infirmary (US), Massachusetts General Hospital (US)
Openalex Percentile: Top 51%
HER2/EGFR in Cancer Research
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