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Biomedicines
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Cancer Immunotherapy: The Multiple Impacts of Tumor Microenvironment
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Cancer Immunotherapy: The Multiple Impacts of Tumor Microenvironment

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (29 February 2024) | Viewed by 3594

Special Issue Editor

Dr. Martina Catalano

E-Mail Website
Guest Editor
Section of Clinical Pharmacology and Oncology, Department of Health Sciences, University of Florence, Florence, Italy
Interests: immunotherapy; immuno-oncology; genitourinary tumors; drugs combination; inflammation

Special Issue Information

Dear Colleagues,

Although, immunotherapy has remarkably revolutionized the field of oncology by prolonging the survival of patients with rapidly fatal cancers, strategies to improve efficacy are needed. 
Beyond approved biomarkers such as programmed death-ligan 1 (PD-L1), microsatellite instability (MSI) and tumor mutational burden (TMB), the tumor microenvironment (TME) has been recognized as a critical factor in determining the success or failure of immunotherapy treatments. It refers to the biological and cellular environment surrounding a tumor, which includes various cells and molecules that can influence the growth, invasion, and metastasis of cancer cells.
The presence of regulatory immune cells such as regulatory T cells, myeloid-derived suppressor cells, and tumor-associated macrophages, as well as other factors such as cytokines, chemokines, and metabolic products may inhibit the ability of the immune system to recognize and attack cancer cells.
To overcome this immunosuppression and enhance anti-tumor immune responses, various strategies, targeting specific cells within the TME are being developed. 

The purpose of this Special Issue is to summarize the last knowledge on TME, and the promising strategies that aim to modulate the TME and enhance anti-tumor immune responses to improve outcomes for cancer patients.

Dr. Martina Catalano
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 short 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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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 immunotherapy
  • immunotherapy strategies target therapies
  • predictive biomarkers
  • solid tumors
  • immune checkpoint inhibitors

Published Papers (3 papers)

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Research

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12 pages, 3015 KiB  
Article
Cimetidine Attenuates Therapeutic Effect of Anti-PD-1 and Anti-PD-L1 and Modulates Tumor Microenvironment in Colon Cancer
by Feng-Chi Kuo, Jerry Cheng-Yen Lai, Hui-Ru Shieh, Wan-Zu Liou, Ming-Jong Bair and Yu-Jen Chen
Biomedicines 2024, 12(3), 697; https://doi.org/10.3390/biomedicines12030697 - 21 Mar 2024
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Abstract
Histamine modulates immunity by binding to histamine receptor 2 (H2R). Cimetidine, an H2R antagonist that inhibits gastric acid secretion and treats gastrointestinal ulcers, interferes with histamine-mediated immunomodulation and may have anticancer activity. This study examined cimetidine’s effect on the anticancer effect of anti-PD-L1 [...] Read more.
Histamine modulates immunity by binding to histamine receptor 2 (H2R). Cimetidine, an H2R antagonist that inhibits gastric acid secretion and treats gastrointestinal ulcers, interferes with histamine-mediated immunomodulation and may have anticancer activity. This study examined cimetidine’s effect on the anticancer effect of anti-PD-L1 in colon cancer. The MTT assay, colony formation assay, and DNA histograms assessed cell viability, clonogenicity, and cell cycle distribution, respectively. Flow cytometry measured H2R and PD-L1 expression and estimated specific immune cell lineages. For the in vivo study, tumor cells were subcutaneously implanted into the right flank of BALB/c mice. Cimetidine had no significant effect on CT26 cell viability, clonogenicity, or cell cycle distribution. It also did not affect H2R and PD-L1 expression levels in CT26 cells. In vivo, anti-PD-1 and anti-PD-L1 suppressed CT26 tumor growth, whereas cimetidine showed mild antitumor activity. In the combined experiment, cimetidine significantly attenuated anti-PD-1 and anti-PD-L1′ antitumor effects without major toxicity. In the tumor microenvironment, anti-PD-L1 increased CD3+ T, CD4+ T, and CD8+ T cells and M1 macrophages. Combined treatment with cimetidine reversed this. Cimetidine also reversed anti-PD-1 and anti-PD-L1′s decrease in circulating and tumor-associated neutrophils. Cimetidine attenuated anti-PD-L1′s antitumor effect and modulated the tumor microenvironment in colon cancer. Full article
(This article belongs to the Special Issue Cancer Immunotherapy: The Multiple Impacts of Tumor Microenvironment)
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Review

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16 pages, 1925 KiB  
Review
Tumor-Infiltrating Lymphocytes (TILs) in Breast Cancer: Prognostic and Predictive Significance across Molecular Subtypes
by Aleksandra Ciarka, Michał Piątek, Rafał Pęksa, Michał Kunc and Elżbieta Senkus
Biomedicines 2024, 12(4), 763; https://doi.org/10.3390/biomedicines12040763 - 29 Mar 2024
Viewed by 1071
Abstract
Tumor-infiltrating lymphocytes (TILs) are pivotal in the immune response against breast cancer (BC), with their prognostic and predictive significance varying across BC subtypes. In triple-negative BC (TNBC), higher TIL levels correlate with improved prognosis and treatment response, guiding therapeutic strategies and potentially offering [...] Read more.
Tumor-infiltrating lymphocytes (TILs) are pivotal in the immune response against breast cancer (BC), with their prognostic and predictive significance varying across BC subtypes. In triple-negative BC (TNBC), higher TIL levels correlate with improved prognosis and treatment response, guiding therapeutic strategies and potentially offering avenues for treatment de-escalation. In metastatic TNBC, TILs identify patients with enhanced immunotherapy response. HER2+ BC, similar to TNBC, exhibits positive correlations between TILs and treatment response, especially in neoadjuvant settings. Luminal BC generally has low TILs, with limited prognostic impact. Single hormone receptor-positive BCs show distinct TIL associations, emphasizing subtype-specific considerations. TILs in ductal carcinoma in situ (DCIS) display ambiguous prognostic significance, necessitating further investigation. Standardizing TIL assessment methods is crucial for unlocking their full potential as biomarkers, guiding treatment decisions, and enhancing patient care in BC. Full article
(This article belongs to the Special Issue Cancer Immunotherapy: The Multiple Impacts of Tumor Microenvironment)
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19 pages, 1454 KiB  
Review
CD200/CD200R: Bidirectional Role in Cancer Progression and Immunotherapy
by Christopher Nip, Leyi Wang and Chengfei Liu
Biomedicines 2023, 11(12), 3326; https://doi.org/10.3390/biomedicines11123326 - 16 Dec 2023
Cited by 1 | Viewed by 1401
Abstract
As an immune checkpoint molecule, CD200 serves a foundational role in regulating immune homeostasis and promoting self-tolerance. While CD200 expression occurs in various immune cell subsets and normal tissues, its aberrant expression patterns in hematologic malignancies and solid tumors have been linked to [...] Read more.
As an immune checkpoint molecule, CD200 serves a foundational role in regulating immune homeostasis and promoting self-tolerance. While CD200 expression occurs in various immune cell subsets and normal tissues, its aberrant expression patterns in hematologic malignancies and solid tumors have been linked to immune evasion and cancer progression under pathological conditions, particularly through interactions with its cognate receptor, CD200R. Through this CD200/CD200R signaling pathway, CD200 exerts its immunosuppressive effects by inhibiting natural killer (NK) cell activation, cytotoxic T cell functions, and M1-polarized macrophage activity, while also facilitating expansion of myeloid-derived suppressor cells (MDSCs) and Tregs. Moreover, CD200/CD200R expression has been linked to epithelial-to-mesenchymal transition and distant metastasis, further illustrating its role in cancer progression. Conversely, CD200 has also been shown to exert anti-tumor effects in certain cancer types, such as breast carcinoma and melanoma, indicating that CD200 may exert bidirectional effects on cancer progression depending on the specific tumor microenvironment (TME). Regardless, modulating the CD200/CD200R axis has garnered clinical interest as a potential immunotherapeutic strategy for cancer therapy, as demonstrated by early-phase clinical trials. However, further research is necessary to fully understand the complex interactions of CD200 in the tumor microenvironment and to optimize its therapeutic potential in cancer immunotherapy. Full article
(This article belongs to the Special Issue Cancer Immunotherapy: The Multiple Impacts of Tumor Microenvironment)
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