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Abstract Background: Although cancer immunotherapy has shown great promises, many cancers remain resistant to treatment due to tumor heterogeneity, immune tolerance, and insufficient immune activation. Bria-IMT is a therapeutic cancer vaccine composed of SV-BR-1-GM, a breast cancer cell line engineered to release GM-CSF. This therapy has completed a phase I/II clinical trial (NCT03066947) and is under evaluation in a phase III study (NCT06072612) for advance metastatic breast cancer. Mechanistically, SV-BR-1-GM cells function as antigen-presenting cells, directly activating CD4+ T cells in an antigen-specific, HLA-restricted manner (as shown in vitro). They also deliver a broad repertoire of cancer antigens to stimulate endogenous immune responses. Building on evidence that suggests changes in circulating cytokines and chemokines reflect treatment-induced immune activation, this study aims to characterize serum cytokine and chemokine profiles as potential biomarkers of immunological response and clinical outcome following cancer immunotherapy. Methods: This retrospective analysis evaluated 35 different cytokines/chemokines in serum samples collected from 30 patients enrolled in the Phase I/II trial (NCT03066947) of Bria-IMT alone or in combination with an anti-PD-1 checkpoint inhibitor (CPI). Serum was isolated from blood pre- and post-therapy. We used multiplex ELISA using meso-scale-discovery (MSD) technology to measure 35 different cytokines/chemokines known to be associated with immune regulation. Data was analyzed using MSD discovery workbench, and plotted using Origin 2025. Results: Patients were categorized by RECIST into stable disease (SD, n=13), progressive disease (PD, n=10), partial responders (PR, n=5), and non-evaluable (NE, n=2). Following three or more treatment cycles, patients with SD and PR demonstrated increased levels of proinflammatory cytokines IL-2 and IL-15 compared to baseline; by contrast, an increase was not observed in patients with PD. IL-2 is produced by activated T cells and supports their proliferation, while IL-15, typically presented by dendritic cells and monocytes, promotes NK cell and memory CD8+ T cell activation. This dual increase suggests coordinated activation of both the adaptive and innate immune compartments. MCP-1 (CCL2) and IP-10 (CXCL10), chemokines involved in the recruitment of monocytes, T cells, and dendritic cells, were also significantly elevated in patients with SD and PR. Both chemokines are known to be secreted by activated dendritic cells, further suggesting dendritic cell engagement in response to therapy. In contrast, these cytokines and chemokines did not increase in patients with PD. Importantly, immunosuppressive cytokines such as IL-10, IL-13, and IL-4 were not upregulated following treatment. This cytokine profile indicates a Th1-skewed, proinflammatory immune response associated with disease control. The absence of such changes in PD patients suggests a lack of effective immune activation in those with progressive disease. Conclusion: SV-BR1-GM induces a cytokine profile consistent with a Th1-polarized immune response, marked by elevated IL-2 and IL-15 in patients with clinical benefit (SD and PR). These cytokines, along with increased levels of MCP-1 and IP-10, reflect enhanced activation and recruitment of cytotoxic T cells, NK cells, and antigen-presenting cells. In contrast, there was no induction of Th2- or regulatory-associated cytokines such as IL-4, IL-10, or IL-13, suggesting that the vaccine does not promote an immunosuppressive or tolerogenic environment. This Th1-biased response aligns with effective anti-tumor immunity and suggests that serum cytokine profiles may serve as informative biomarkers of immunologic activity and clinical benefit following SV-BR-1-GM vaccination. Citation Format: P. Kesarwani, S. Modi, G. Woodfield, B. Bayer, V. Bhardwaj, S. Pachhal, G. D. Priore, C. L. Wiseman, W. V. Williams, M. Lopez-Lago. Th1-biased cytokine signatures as biomarkers of clinical benefit following SV-BR-1-GM cancer vaccination in 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 PS2-09-03.
Published in: Clinical Cancer Research
Volume 32, Issue 4_Supplement, pp. PS2-09