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. 2020 Sep 18;70(3):593–606. doi: 10.1007/s12020-020-02478-z

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — Modulation of the PitNET angiogenesis by different TME elements. Different proteins are secreted by the pituitary tumour cells into the tumour microenvironment (TME) of PitNETs, and some of these may be able to influence and modulate the pituitary tumour angiogenesis, such as CCL2, CXCL10 and CX3CL1. Proteins released by non-neoplastic infiltrating immune cells present within the TME of PitNETs, such as macrophages, CD4+ T cells, FOXP3+ T cells, B cells, may further influence the pituitary tumour neovascularisation. In addition, PitNET-associated tumour-associated fibroblasts (TAFs) are also a source of cytokines and chemokines, including CCL2, which may further modulate the angiogenesis of PitNETs [10]. CD4+ T, CD4+ T cells; CD20+ B, CD20+ B lymphocytes; FOXP3+ T, FOXP3+ T regulatory cells; M2:M1 M2 and M1 macrophage ratio, NF-PitNETs non-functioning pituitary neuroendocrine tumours, PitNET pituitary neuroendocrine tumour, TAF pituitary tumour-associated fibroblast