Abstract B086: Disease-critical macrophage populations interact with stroma to modulate the tumor microenvironment

Abstract Myeloid cells in the tumor microenvironment (TME) exhibit diverse functions, from pro-tumor to anti-tumor. To elucidate myeloid heterogeneity, we developed a deep-learning model to annotate 20 myeloid subtypes in single-cell data. We identified two macrophage populations, macro_SPP1 and macro_C1QC, which were pan-cancer, enriched in tumors compared to normal tissues, and linked to clinical outcomes. Higher macro_SPP1 abundance correlated with IO non-responders, pre-IO treatment, and lower inflammation, while macro_C1QC showed the opposite trends. We developed and validated gene signatures to quantify these macrophages in bulk RNAseq. Applying these signatures to TCGA and real-world data, we confirmed that macro_SPP1 was associated with worse survival and poor IO response, whereas macro_C1QC was linked to better outcomes. Tumors with chromosome 9p21 deletions had higher macro_SPP1 and fibroblast signatures, suggesting a TME influence on macrophage heterogeneity. Cell-cell communication analysis in single-cell data revealed that fibroblasts sent the strongest signals to macrophages in lung and pancreatic cancers. Fibroblast-derived ligands such as FN1 and collagens exhibited stronger signaling to macro_SPP1 than macro_C1QC, and colocalized with macro_SPP1 spatially. Conversely, macro_SPP1 sent higher total signals to other cells in the TME than macro_C1QC, with SPP1 to fibroblasts and endothelial cells being the most differentiating signal. In summary, we identified two disease-critical macrophage populations: pro-tumor macro_SPP1 and anti-tumor macro_C1QC. We found interactions between macrophages and fibroblasts as key modulators of the TME. Citation Format: Weiwei Zhong, Mitra Ansariola, Micaela Tatman, Rachel Wester, Kim Van Naarden Braun, Shameek Biswas. Disease-critical macrophage populations interact with stroma to modulate the tumor microenvironment [abstract]. In: Proceedings of the AACR IO Conference: Discovery and Innovation in Cancer Immunology: Revolutionizing Treatment through Immunotherapy; 2025 Feb 23-26; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Immunol Res 2025;13(2 Suppl):Abstract nr B086.

Authors

Institutions

Publication Details

Journal
Cancer Immunology Research
Published
2025-02-23
DOI
https://doi.org/10.1158/2326-6074.io2025-b086
Primary Topic
Immune cells in cancer
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Abstract B086: Disease-critical macrophage populations interact with stroma to modulate the tumor microenvironment

Kim Van Naarden Braun, Weiwei Zhong, Rachel Wester, Shameek Biswas et al.
Cancer Immunology Research
Immune cells in cancer
article

Abstract B086: Disease-critical macrophage populations interact with stroma to modulate the tumor microenvironment

Kim Van Naarden Braun, Weiwei Zhong, Rachel Wester, Shameek Biswas, Mitra Ansariola, Micaela Tatman
article en

Abstract

Abstract Myeloid cells in the tumor microenvironment (TME) exhibit diverse functions, from pro-tumor to anti-tumor. To elucidate myeloid heterogeneity, we developed a deep-learning model to annotate 20 myeloid subtypes in single-cell data. We identified two macrophage populations, macro_SPP1 and macro_C1QC, which were pan-cancer, enriched in tumors compared to normal tissues, and linked to clinical outcomes. Higher macro_SPP1 abundance correlated with IO non-responders, pre-IO treatment, and lower inflammation, while macro_C1QC showed the opposite trends. We developed and validated gene signatures to quantify these macrophages in bulk RNAseq. Applying these signatures to TCGA and real-world data, we confirmed that macro_SPP1 was associated with worse survival and poor IO response, whereas macro_C1QC was linked to better outcomes. Tumors with chromosome 9p21 deletions had higher macro_SPP1 and fibroblast signatures, suggesting a TME influence on macrophage heterogeneity. Cell-cell communication analysis in single-cell data revealed that fibroblasts sent the strongest signals to macrophages in lung and pancreatic cancers. Fibroblast-derived ligands such as FN1 and collagens exhibited stronger signaling to macro_SPP1 than macro_C1QC, and colocalized with macro_SPP1 spatially. Conversely, macro_SPP1 sent higher total signals to other cells in the TME than macro_C1QC, with SPP1 to fibroblasts and endothelial cells being the most differentiating signal. In summary, we identified two disease-critical macrophage populations: pro-tumor macro_SPP1 and anti-tumor macro_C1QC. We found interactions between macrophages and fibroblasts as key modulators of the TME. Citation Format: Weiwei Zhong, Mitra Ansariola, Micaela Tatman, Rachel Wester, Kim Van Naarden Braun, Shameek Biswas. Disease-critical macrophage populations interact with stroma to modulate the tumor microenvironment [abstract]. In: Proceedings of the AACR IO Conference: Discovery and Innovation in Cancer Immunology: Revolutionizing Treatment through Immunotherapy; 2025 Feb 23-26; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Immunol Res 2025;13(2 Suppl):Abstract nr B086.

Cancer Immunology ResearchVol. 13(2_Supplement)
Bristol-Myers Squibb (United States) (US)
Openalex Percentile: Top 96%
Immune cells in cancer
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.