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Cancers
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Feature Papers in Section "Tumor Microenvironment"
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Feature Papers in Section "Tumor Microenvironment"

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

Deadline for manuscript submissions: 31 December 2025 | Viewed by 2511

Special Issue Editor

Dr. Sanjay Gupta

E-Mail Website
Guest Editor
Department of Urology, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA
Interests: biomarkers; prostate cancer; cancer chemoprevention; cancer metabolism; metabolic imaging; drug resistance; castration-resistance; tumor microenvironment; drug repurposing; cancer stem cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are excited to introduce a Special Issue of Cancers focused on Feature Papers in the Section "Tumor Microenvironment." This Special Issue aims to highlight the latest advancements and discoveries in understanding the complex interactions within the tumor microenvironment and their implications for cancer progression and treatment.

The tumor microenvironment plays a crucial role in tumor development, growth, and metastasis. It consists of various components, including immune cells, stromal cells, extracellular matrix, and signaling molecules. Recent advances in computational analysis and modeling utilizing single-cell transcriptomic data, bulk tumor expression profiles, and spatial transcriptomics have uncovered a wide array of intercellular signaling networks within the tumor microenvironment. The intricate interaction among tumor cell-intrinsic factors, cell-extrinsic influences, and systemic mediators of disease progression is essential for developing effective therapeutic strategies and improving patient outcomes.

We invite researchers and clinicians to submit their original research articles and reviews that delve into the diverse aspects of the tumor microenvironment. Some of the key topics of interest for this Special Issue include, but are not limited to, the following:

Cellular and molecular interactions within the tumor microenvironment;

Immune cell infiltration and immune response modulation;

Stromal cell contributions to tumor growth and metastasis;

Angiogenesis and vascularization in the tumor microenvironment;

Extracellular matrix remodeling and its impact on cancer progression;

Signaling pathways and molecular mechanisms involved in tumor–stroma crosstalk;

Therapeutic targeting of the tumor microenvironment for improved treatment outcomes.

All submitted articles will undergo a rigorous peer review process to ensure that the highest scientific quality and relevance to the field are ensured. We encourage contributions from experts in the field of tumor microenvironment research, as well as clinicians with valuable insights from patient care.

By bringing together cutting-edge research and clinical experiences, this Special Issue aims to advance our understanding of the tumor microenvironment and pave the way for novel therapeutic approaches to be used. We believe that your contributions will greatly contribute to the success of this Special Issue and have a significant impact on the field of cancer research.

If you have any questions or require further information, please do not hesitate to contact us. We are here to provide support and facilitate your participation in this Special Issue.

Thank you for your attention, and we eagerly anticipate receiving your valuable submissions.

Dr. Sanjay Gupta
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 100 words) can be sent to the Editorial Office for announcement on this website.

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

  • tumor microenvironment
  • cancer progression
  • interactions
  • therapeutic targeting
  • immune response

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Research

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18 pages, 6313 KiB  
Article
Differential Response to Local Stimulator of Interferon Genes Agonist Administration in Tumors with Various Stimulator of Interferon Genes Statuses
by Alina Drzyzga, Justyna Czapla, Sybilla Matuszczak, Barbara Łasut-Szyszka, Tomasz Cichoń, Ewelina Pilny, Magdalena Jarosz-Biej and Ryszard Smolarczyk
Cancers 2025, 17(2), 175; https://doi.org/10.3390/cancers17020175 - 8 Jan 2025
Viewed by 727
Abstract
Background/Objectives: The stimulator of interferon genes (STING) is currently accepted as a relevant target for anti-cancer therapies. Besides encouraging results showing STING agonist-induced tumor growth inhibition, in some types of tumors the effect is less prominent. We hypothesized that higher STING levels [...] Read more.
Background/Objectives: The stimulator of interferon genes (STING) is currently accepted as a relevant target for anti-cancer therapies. Besides encouraging results showing STING agonist-induced tumor growth inhibition, in some types of tumors the effect is less prominent. We hypothesized that higher STING levels in cancer cells and the possibility of its activation determine a greater anti-cancer response. As the local administration of STING agonists induces a systemic reaction, we emphasized the importance of host tumor-induced hematological disruption in the efficiency of the therapeutic response. Methods: We investigated the response to STING stimulation in murine cancer cell lines—melanoma (B16-F10) and breast carcinoma (4T1)—and murine normal cell lines: fibroblast cells (NIH/3T3), endothelial cells (H5V), and macrophages (J774A.1). We assessed STING agonist-induced tumor growth inhibition and the therapy’s impact on the hematological system parameters and systemic cytokine release. Results: Our results underlined the improved therapeutic effect of STING activation in melanoma (B16-F10) over breast carcinoma (4T1) tumors. The outcomes reflected a high dysregulation of the hematological system in mice with developed 4T1 tumors, which may support persistent inflammation and impede STING-induced therapeutic effects. Moreover, among typical cytokines produced following STING activation, CCL2 fold change was the one that increased the most in the serum of B16-F10-bearing mice and differentiated the observed response to the STING agonist between investigated tumor models. Conclusions: The current study provides new evidence of the different responses to STING activation among two poorly immunogenic tumor models. The high abundance of STING in B16-F10 cells and the possibility of its activation is linked with improved therapeutic response in vivo compared to 4T1. The effect also seems to be connected with a less dysregulated hematological system in mice with B16-F10 tumors over mice with 4T1 tumors. This highlighted the need for general insight into tumor-induced local and systemic responses to the efficiency of the proposed therapy. Full article
(This article belongs to the Special Issue Feature Papers in Section "Tumor Microenvironment")
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19 pages, 8622 KiB  
Article
Richness for Tumor-Infiltrating B-Cells in the Oral Cancer Tumor Microenvironment Is a Prognostic Factor in Early-Stage Disease and Improves Outcome in Advanced-Stage Disease
by Irene H. Nauta, Dennis N. L. M. Nijenhuis, Sonja H. Ganzevles, Pamela I. Raaff, Jan Kloosterman, Elisabeth Bloemena, Ruud H. Brakenhoff, C. René Leemans and Rieneke van de Ven
Cancers 2025, 17(1), 113; https://doi.org/10.3390/cancers17010113 - 1 Jan 2025
Viewed by 1099
Abstract
Background/Objectives: Most studies on the interaction between the immune system and cancer focus on T-cells, whereas studies on tumor-infiltrating B-lymphocytes (TIL-Bs) are still underrepresented. The aim of this study was to assess the prognostic impact of TIL-Bs in early- and advanced-stage oral cavity [...] Read more.
Background/Objectives: Most studies on the interaction between the immune system and cancer focus on T-cells, whereas studies on tumor-infiltrating B-lymphocytes (TIL-Bs) are still underrepresented. The aim of this study was to assess the prognostic impact of TIL-Bs in early- and advanced-stage oral cavity squamous cell carcinoma (OCSCC). Methods: In total, 222 OCSCCs were studied. Consecutive sections were stained for CD45 and CD19. OCSCCs were categorized as either “TIL-B-rich” or “TIL-B-poor”, and the survival of both groups was analyzed. Similar analyses were performed for CD45+ TILs and the CD19/CD45 ratio. Matched subgroups of twelve TIL-B-rich and TIL-B-poor tumors were stained for CD3 and CD8 to determine differences in T-cell infiltration, and further spatial interaction between T- and B-cells was evaluated in six samples. Results: Five-year OS was 75.0% for TIL-B-rich and 54.2% for TIL-B-poor OCSCCs (p < 0.001). The survival benefit of TIL-B-rich OCSCCs remained significant after correction for the histopathological characteristics (p = 0.033). While for early-stage tumors, TIL-B richness benefited OS independent of demographic-, clinical, or histopathological features, for advanced-stage disease, this was not the case, although a clear benefit of a TIL-B-rich status was observed, specifically up until 36 months after diagnosis. TIL-B-rich tumors contained more CD3+ TILs (p = 0.007), but not CD8+ TILs. Spatial characterization suggested that TIL-Bs mostly co-localized with CD3+CD8− TILs and that this interaction was increased in TIL-B-rich OCSCC. Conclusions: The presence of TIL-Bs is associated with a more favorable prognosis in OCSCC, in particular for early-stage disease. Full article
(This article belongs to the Special Issue Feature Papers in Section "Tumor Microenvironment")
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Review

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11 pages, 658 KiB  
Review
Thyroid Cancer—The Tumor Immune Microenvironment (TIME) over Time and Space
by Juan Carlos Jaume
Cancers 2025, 17(5), 794; https://doi.org/10.3390/cancers17050794 - 26 Feb 2025
Viewed by 261
Abstract
In thyroid cancer, the tumor immune microenvironment (TIME) plays a crucial role in cancer development, progression and response to treatment. Like many other cancers, thyroid cancer creates a complex network of interactions with immune cells directly (cell-to-cell) and via humoral mediators (i.e., cytokines). [...] Read more.
In thyroid cancer, the tumor immune microenvironment (TIME) plays a crucial role in cancer development, progression and response to treatment. Like many other cancers, thyroid cancer creates a complex network of interactions with immune cells directly (cell-to-cell) and via humoral mediators (i.e., cytokines). This dynamic microenvironment undergoes constant modification, which can lead to changes in the immunophenotype that might explain cancer progression, dedifferentiation and resistance to treatment. According to the cancer immunoediting hypothesis, cancerous tumors can shape their immune microenvironment to create an immunosuppressive milieu that allows them to evade classic immune surveillance. One mechanism by which this occurs is through the reprogramming of immune cells, often shifting their phenotypes from cytotoxic to regulatory. Recent research has shed light on cellular components and molecular interactions within the thyroid cancer TIME. Immune cells such as Tumor-Associated Lymphocytes (TALs), myeloid-derived suppressor cells (MDSCs), Tumor-Associated Macrophages (TAMs) and Double-Negative (DN) T cells seem to play key roles in shaping the immune response to thyroid cancer. Additionally, cytokines, chemokines and other signaling molecules contribute to the communication and regulation of immune cells within that microenvironment. By studying these interactions, researchers aim to uncover not just potential therapeutic targets but also biomarkers of thyroid cancer that could provide clues on severity and progression. Based on that knowledge, strategies such as the use of immune checkpoint inhibitors, antigen-specific targeted immunotherapies, and immunomodulatory agents are being explored to enhance the anti-tumor immune response and overcome cancer immunosuppressive mechanisms. In this review, we analyze the available literature and provide our own experience to unravel the complexity of the thyroid immune microenvironment. Continued research in this area holds promise for improving outcomes through the identification of immune markers of severity/progression of thyroid cancer and the development of innovative immunotherapeutic approaches. Full article
(This article belongs to the Special Issue Feature Papers in Section "Tumor Microenvironment")
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