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ePoster Display

24P - The STAT3 phosphorylation status discriminates tumor associated populations in myeloid cell tumor-infiltrating model


16 Sep 2021


ePoster Display


Basic Science

Tumour Site


Ester Palmeiro


Annals of Oncology (2021) 32 (suppl_5): S361-S375. 10.1016/annonc/annonc684


E.B. Palmeiro1, M. Ibañez2, C. Hernández3, L. Chocarro4, H. Arasanz5, A. Bocanegra6, J. Fernandez7, E. Santamaria7, R. Vera5, C. Smerdou3, D. Escors6, G. Kochan6

Author affiliations

  • 1 Oncoimmunlogy, Departamento de Salud de Navarra Servicio Navarro de Salud Osasunbidea SNS O Conde Oliveto, 31003 - Pamplona/ES
  • 2 Agronomy And Biotecnhology, UPNA, Pamplona/ES
  • 3 Gene Therapy, CIMA, Pamplona/ES
  • 4 Oncoimmunology Unit, Navarrabiomed, 31008 - Pamplona/ES
  • 5 Dept. Medical Oncology, Complejo Hospitalario de Navarra - Royal Navarre Hospital, 31008 - Pamplona/ES
  • 6 Oncoimmunology, Navarrabiomed, 31008 - Pamplona/ES
  • 7 Clinical Neuroproteomics, Navarrabiomed, Pamplona/ES


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Abstract 24P


Tumor associated myeloid cells are major promoters of progression and metastasis. Monocytic and granulocytic myeloid-derived suppressor cells (M-MDSC and G-MDSC) together with tumor associated macrophages (TAM) are among the main contributors to tumor-induced immunosuppression. The influence of the tumor microenvironment on their differentiation is well-accepted but the specific molecular changes leading towards MDSC subsets and TAM are not well-characterized. Here, we describe the main differences between MDSC subsets and TAMs, focused on differential pathways by high-throughput proteomics.


We used an ex vivo differentiation system for MDSCs and TAM by modelling the tumor microenvironment from C57BL/6J mouse bone marrow cells in conditioning medium (1). We also differentiated resting macrophages (M0) as controls using standard techniques. Flow cytometry and microscopy confirmed their phenotype by assessing their morphology and presence of characteristic lineage markers. Three global experiment of mass spectrometry-based quantitative (shotgun) proteomics were performed. Construction of functional interactomes from up- or down-regulated proteins was conducted with the Ingenuity Pathway Analysis (IPA) Tool from Quiagen. Targeted proteins were evaluated using western blot. Bibliography: 1) Liechtenstein T, Perez-Janices N, Gato M, et al. Oncotarget. 2014;5(17):7843-7857.


We observed morphological differences in ex vivo differentiated myeloid populations. High-throughput proteomics uncovered protein expression patterns characteristic of populations modelling tumor-infiltrating subsets, result of the tumor microenvironment pressure. MAPK1 was identified as upstream regulator using IPA tool. We identified upregulation of STAT3 phosphorylation in all tumor-associated subsets. Both TAM and MDSC have strongly upregulated phosphorylation on S727. Moreover, strong increase in STAT3 Y705 phosphorylation was observed in TAM versus both monocytic and granulocytic MDSC.


In the present study, we identified differences in proteomic signatures between myeloid cells modelling M-MDSCs, G-MDSC and TAMs related to lineage, and cancer-driven polarization.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.


Has not received any funding.


All authors have declared no conflicts of interest.

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