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Tumor Microenvironment of Breast Cancer—2nd Edition

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: 15 July 2026 | Viewed by 824

Special Issue Editor


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Guest Editor
1. Department of Surgical Oncology, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14263, USA
2. Department of Gastroenterological Surgery, Graduate School of Medicine, Yokohama City University, Yokohama 236-0004, Japan
Interests: breast cancer; tumor microenvironment; surgical oncology
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Special Issue Information

Dear Colleagues,

This Special Issue is the second edition entitled “Tumor Microenvironment of Breast Cancer–2nd Edition”. The original can be found at https://www.mdpi.com/journal/cancers/special_issues/617378FN2S.

The tumor microenvironment (TME) consists of cancer cells, but also many other types of cells, including stromal and immune cells that play critical roles in cancer biology. The interactions that occur within the TME include fundamental mechanisms that affect tumor progression and treatment outcomes. Recently developed cancer therapeutics are targeting these interactions within the TME, including immune- and stroma-targeted approaches. The tumor immune microenvironment significantly influences patient survival, and neoadjuvant therapy with immune checkpoint inhibitors is now considered the standard of care for some triple-negative breast cancers. Despite these recent advancements, many breast cancer patients still encounter resistance to treatment, the progression of disease, and poor outcomes. In this Special Issue of Cancers, we hope to gather the latest findings (original articles), as well as summary reports (review articles), that discuss breast cancer TME, with the aim of aiding the next generation of researchers.

Dr. Masanori Oshi
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • breast cancer
  • tumor microenvironment
  • TME
  • stromal cells

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Published Papers (1 paper)

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Research

26 pages, 3699 KB  
Article
Tumor–Immune Cell Crosstalk Drives Immune Cell Reprogramming Towards a Pro-Tumor Proliferative State Involving STAT3 Activation
by Karen Norek, Jacob Kennard, Kenneth Fuh, Robert D. Shepherd, Kristina D. Rinker and Olesya A. Kharenko
Cancers 2026, 18(1), 116; https://doi.org/10.3390/cancers18010116 - 30 Dec 2025
Viewed by 603
Abstract
Background/Objectives: Tumor-induced immune reprogramming is increasingly recognized as a key mechanism by which cancers evade surveillance and promote disease progression. The interaction between cancer and immune cells within the tumor microenvironment (TME) can drive phenotypic and functional changes in immune populations, facilitating [...] Read more.
Background/Objectives: Tumor-induced immune reprogramming is increasingly recognized as a key mechanism by which cancers evade surveillance and promote disease progression. The interaction between cancer and immune cells within the tumor microenvironment (TME) can drive phenotypic and functional changes in immune populations, facilitating metastasis and immune evasion. Methods: In this study, we used co-culture models to expose THP1 monocytes to triple-negative breast cancer (TNBC) cells, MDA-MB-231 and BT-549, either directly or indirectly via tumor-conditioned media, to mimic tumor–immune cell communication. Transcriptomic and pathway analyses revealed that cancer-exposed monocytes adopt a reprogrammed phenotype marked by activation of pro-tumorigenic signaling pathways, enhanced proliferative capacity, and elevated expression of pro-inflammatory cytokines such as IL6. Results: Functional assays confirmed a significant increase in monocyte proliferation under both direct and indirect tumor exposure. Importantly, we demonstrated that this tumor-driven proliferation of THP1 cells could be suppressed by the STAT3 inhibitor STAT3-IN-12. This highlights the critical role of STAT3 signaling in mediating immune cell transformation and supporting a novel immunomodulatory approach for therapeutic intervention. Conclusions: These findings support the potential for targeting tumor-educated transcriptional programs as a novel immunomodulatory strategy in cancer treatment. Restoring immune cell homeostasis and suppressing pro-tumor phenotypes through pharmacological inhibition of the key signaling nodes such as STAT3 may complement existing cancer therapies. This study provides new insights into immune cell plasticity in cancer and identifies actionable strategies to counteract tumor-driven immune dysregulation. Full article
(This article belongs to the Special Issue Tumor Microenvironment of Breast Cancer—2nd Edition)
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