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EDITORIAL article

Front. Vet. Sci.
Sec. Comparative and Clinical Medicine
Volume 12 - 2025 | doi: 10.3389/fvets.2025.1543814
This article is part of the Research Topic Tumor Microenvironment Complexity and its Therapeutic Implications View all 7 articles

Editorial: Tumor Microenvironment Complexity and its Therapeutic Implications

Provisionally accepted
Denner Santos Dos Anjos Denner Santos Dos Anjos 1Marxa L Figueiredo Marxa L Figueiredo 2Renee Laufer Amorim Renee Laufer Amorim 1Carlos Eduardo Fonseca-Alves Carlos Eduardo Fonseca-Alves 3*
  • 1 São Paulo State University, São Paulo, São Paulo, Brazil
  • 2 Purdue University, West Lafayette, Indiana, United States
  • 3 Paulista University, São Paulo, Brazil

The final, formatted version of the article will be published soon.

    The tumor microenvironment (TME) is a dynamic and complex system composed of cancer cells, stromal cells, immune cells, extracellular matrix components, and various signaling molecules (1). This intricate network not only supports tumor growth but also plays a pivotal role in modulating the host immune response. Understanding the interplay between the TME and the immune system is critical for unraveling tumor progression mechanisms and designing more effective therapeutic strategies (2).Cancer cells within the TME adopt numerous strategies to evade immune surveillance, including the secretion of immunosuppressive cytokines, the recruitment of regulatory immune cells, and the upregulation of immune checkpoint molecules (3). These mechanisms create an immunosuppressive environment that hinders the anti-tumor immune response, enabling the tumor to grow unchecked.Additionally, the role of stromal components, such as cancer-associated fibroblasts (CAFs) and the 31 extracellular matrix (ECM), further complicate this scenario by providing physical barriers to 32 immune cell infiltration and by influencing cellular signaling pathways (4,5). 33The immune system, on the other hand, demonstrates a dual role within the TME, acting both as a 34 tumor suppressor and a promoter (5). combination with metronomic chemotherapy. Among the inflammatory indices analyzed, the C-110 reactive-protein-albumin ratio above the cut-off of 1.9 had the worst progression-free survival (PFS) 111 and overall survival (OS) rates. In addition, blood-circulating Treg lymphocytes were correlated with 112 worse PFS and OS rates, suggesting dysfunction or loss of T cell function in the tumor 113 microenvironment, and characterizing an immunosuppressive profile. 114In summary, the articles included in this Research Topic summarize and discuss the main results 115 related to the TME, spotlight novel potential targeted therapies, and identify potential immune 116 checkpoint molecules, cancer-cancer, and cancer-T cell interactions, providing a more personalized 117 profile that we envision can guarantee, in the future, more individualized treatment regimens. 118

    Keywords: canine, immunology, Immunotherapy, immuno-oncology, Tumor-associated inflammation

    Received: 11 Dec 2024; Accepted: 09 Jan 2025.

    Copyright: © 2025 Dos Anjos, Figueiredo, Laufer Amorim and Fonseca-Alves. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Carlos Eduardo Fonseca-Alves, Paulista University, São Paulo, Brazil

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.