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Tumor Microenvironment of Breast Cancer—2nd Edition
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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 3025

Special Issue Editor

Dr. Masanori Oshi

E-Mail Website
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
Special Issues, Collections and Topics in MDPI journals

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.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • breast cancer
  • tumor microenvironment
  • TME
  • stromal cells

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Related Special Issue

Published Papers (3 papers)

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Research

14 pages, 4609 KB  
Article
Effect of Healthy and Tumor-Associated Breast Adipose Tissue on Breast Cancer Cell Migration and Activation
by Iris L. Holt-Kedde, Hetty Timmer-Bosscha, Frank A. E. Kruyt, Wendy Kelder, Bert van der Vegt, Mieke C. Zwager, Carolien P. Schröder and Marlous Arjaans
Cancers 2026, 18(5), 868; https://doi.org/10.3390/cancers18050868 - 8 Mar 2026
Viewed by 512
Abstract
Background: Obesity is a recognized risk factor for developing breast cancer (BC), but factors involved remain unclear. We investigated if breast adipose tissue from healthy women, BRCA1/2 mutation carriers and BC patients, can stimulate BC cell line migration and activation. Methods: adipose tissue [...] Read more.
Background: Obesity is a recognized risk factor for developing breast cancer (BC), but factors involved remain unclear. We investigated if breast adipose tissue from healthy women, BRCA1/2 mutation carriers and BC patients, can stimulate BC cell line migration and activation. Methods: adipose tissue conditioned medium (ATCM), was prepared from breast adipose tissue from healthy subjects (naïve; group 1 (n = 20)), BRCA1/2 mutation carriers (group 2 (n = 22)) and BC patients (group 3 (n = 38)). ATCM effect on migration of BC cell lines MCF-7, SK-BR-3 and MDA-MB-231 was measured with xCELLigence (ACEA Biosciences, San Diego, CA, USA) cell migration assay. Activation of migration was determined by measuring filopodia activation. Migration and filopodia activation were related to body mass index (BMI) and BC subtypes. Luminex multiplex assay was performed to examine the secretory profile of adipose tissue. Results: ATCM from group 1 induced migration and filopodia activation in MCF-7 and MDA-MB-231, but not in SK-BR-3. ATCM from group 2 induced filopodia activation but no migration. ATCM from group 3 induced less migration in MCF-7 than ATCM from group 1. Higher BMI was associated with increased ATCM-induced activation in MCF-7 (group 1) and MDA-MB-231 (group 2). ATCM from group 1 and 2 showed a metabolic secretory profile, whereas group 3 showed higher pro-angiogenic and inflammatory cytokines. Conclusions: This study shows that breast adipose tissue from healthy women, BRCA1/2 mutation carriers and BC patients, can stimulate BC cell line migration and activation. This effect is related to BC subtype and BMI. These data improve insight in adipose tissue as factor in BC development. Full article
(This article belongs to the Special Issue Tumor Microenvironment of Breast Cancer—2nd Edition)
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18 pages, 3393 KB  
Article
Metabolic Crosstalk in Triple-Negative Breast Cancer Lung Metastasis: Differential Effects of Vitamin D and E in a Co-Culture System
by Balquees Kanwal, Saranya Pounraj, Rumeza Hanif and Zaklina Kovacevic
Cancers 2026, 18(2), 294; https://doi.org/10.3390/cancers18020294 - 18 Jan 2026
Viewed by 930
Abstract
Background: Triple-negative breast cancer (TNBC) is more likely to metastasise to the lungs than other breast cancer (BrCa) types, yet the molecular interactions within the tumour microenvironment (TME) at secondary sites remain poorly understood. Methods: This pilot study aimed to explore the metabolic [...] Read more.
Background: Triple-negative breast cancer (TNBC) is more likely to metastasise to the lungs than other breast cancer (BrCa) types, yet the molecular interactions within the tumour microenvironment (TME) at secondary sites remain poorly understood. Methods: This pilot study aimed to explore the metabolic crosstalk between MDA-MB-231 TNBC cells and MRC-5 lung fibroblasts within a co-culture system to replicate the lung metastatic TME. Co-cultures were also treated with Vitamin D or Vitamin E to evaluate the effects of these nutraceuticals on the metabolic crosstalk between TNBC cells and fibroblasts. Results: Our findings demonstrate that co-culture induced the activation of fibroblasts into cancer-associated fibroblasts (CAFs), evidenced by increased α-SMA and FAP expression. Metabolic profiling revealed that TNBC cells in co-culture displayed increased expression of enzymes associated with oxidative phosphorylation (OXPHOS) and glutamine metabolism, while fibroblasts exhibited a metabolic profile consistent with glycolysis and lactate metabolism. Vitamin D inhibited lactate metabolism and HIF-1α expression in fibroblasts while suppressing TCA cycle activity in cancer cells, suggesting a potential role in disrupting oncogenic metabolic crosstalk. Conversely, Vitamin E treatment was associated with increased expression of TCA cycle and oxidative metabolism-related markers in BrCa cells without significantly affecting fibroblast glycolysis. Such differential metabolic responses may contribute to metabolic heterogeneity within the tumour microenvironment. Conclusions: These results provide valuable insights into the metabolic dynamics of TNBC metastases in the lung TME and demonstrate that Vitamins D and E exert distinct effects on metabolic crosstalk between cancer cells and fibroblasts. These findings may have significant implications for the potential supplementation of Vitamins D and E in patients with metastatic TNBC and justify further in-depth analysis. Full article
(This article belongs to the Special Issue Tumor Microenvironment of Breast Cancer—2nd Edition)
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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 1168
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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