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Poster display session

3077 - Effect of neoadjuvant chemotherapy on correlation of tumor-associated macrophages with angiogenesis and lymphangiogenesis in human breast cancer


11 Sep 2017


Poster display session


Translational Research;  Breast Cancer


Irina Mitrofanova


Annals of Oncology (2017) 28 (suppl_5): v573-v594. 10.1093/annonc/mdx390


I. Mitrofanova1, M. Zavyalova2, M. Buldakov3, N. Cherdyntseva3, J. Kzhyshkowska4

Author affiliations

  • 1 Laboratory Of Translational Cellular And Molecular Biomedicine, Tomsk State University, 634050 - Tomsk/RU
  • 2 Department Of Pathological Anatomy, Siberian State Medical University, Tomsk/RU
  • 3 Laboratory Of Molecular Oncology And Immunology, Tomsk National Research Medical Center of the Russian Academy of Sciences, Tomsk/RU
  • 4 Medical Faculty Mannheim,institute Of Transfusion Medicine And Immunology, University of Heidelberg, Mannheim/DE


Abstract 3077


Promoting role of tumor-associated macrophages (TAM) in angiogenesis and lymphangiogenesis was demonstrated in mouse tumor model sand human cancers. However, our latest studies revealed that amount of TAM in patients with breast cancer before as well after neoadjuvant chemotherapy (NAC) reversely correlated with lymphatic metastasis. Our aim was to analyse the effect of NAC on correlation of TAM in intratumoral compartments with angiogenesis and lymphangiogenesis.


115 female patients with breast cancer T1-4N0-3M0 were included in the study. 36 patients did not receive NAC, 79 received NAC. Expression levels of CD68 (general macrophage marker), stabilin-1 (marker of М2 macrophages), CD31 (marker of blood vessels) and LYVE1 (marker of lymphatic vessels) were identified by immunohistochemistry in 5 distinct areas of tumors: 1) soft fibrous stroma; 2) coarse fibrous stroma; 3) areas of maximum stromal-and-parenchyma lrelationship; 4) parenchymal elements; 5) gaps of ductal tumor structures.


In breast cancer samples of patient who did not receive NAC direct correlation of CD68 expression in soft fibrous stroma and CD31 expression in coarse fibrous stroma (r = 0,87;р=0,02) was identified. However, reverse correlation was found between CD68 expression in gaps of ductal tumor structures and LYVE1 expression in soft fibrous stroma (r=-0,89;р=0,04). In contrast, in patients after NAC we identified a direct correlation between expression of CD68 and LYVE1 expression in the gaps of ductal tumor structures (r = 0,80;р=0,02). Expression of stabilin-1 in coarse fibrous stroma directly correlated with amount of LYVE1+ cells in areas with maximum stromal-and-parenchymal relationship (r = 0,76;р=0,04), but reversely correlated with the amount of CD31+ vessels in soft fibrous stroma (r= - 0,52;р=0,001).


Our data suggest that TAM before treatment support tumor angiogenesis however protect against lymphangiogenesis. After NAC TAM can switch their functional phenotype, do not support angiogenesis anymore but support lymphangiogenesis. The mechanism of chemotherapeutic programming of TAM remains to be identified.

This study was supported by grant RNF №14-15-00350.

Clinical trial identification

Legal entity responsible for the study

Tomsk State University, Tomsk, Russian Federation


Tomsk State University, Tomsk, Russian Federation. This study was supported by grant RNF №14-15-00350.


All authors have declared no conflicts of interest.

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