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Tumor Microenvironment and Immune Response
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Tumor Microenvironment and Immune Response

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 12396

Special Issue Editor

Dr. Luigi Racioppi

E-Mail Website
Guest Editor
Department of Medicine, Duke University, Research Drive, 245 Carl Building, Durham, NC 27707, USA
Interests: immune response; inflammation; macrophages; dendritic cells; stem cells; signaling; calcium; tumor microenvironment; hematopoiesis; radiation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

More than 150 years ago, Rudolf Ludwig Carl Virchow noted that tumors were often infiltrated by leukocytes, proposing for the first time a link between inflammation and cancer. A few years later, Stephen Paget incorporated these pioneering observations into a more structured theory, elaborating the concept of “seed and soil” to explain the mechanisms supporting the spreading of the primary cancer cells to the metastatic niche. In 1889, the scientific community was largely unprepared to explore the biological significance of the “seed and soil” concept, spending the following century on “seed”-oriented studies and leaving the “soil” component largely unexplored.

In the last 30 years, a large body of evidence has demonstrated that the landscape of immune cells infiltrating cancer tissue has a key role in the mechanism of tumor initiation, growth, invasion, and metastasis. After more than a century from the seminal observations of Virchow and Paget, the “soil” has become an important therapeutic target, such as immunotherapy, and is a valuable therapeutic option for an increasing number of advanced cancers.

This collection hosts review articles from scientists that have been studying the tumor microenvironment using animal models, microfluidic on-chip models, and translational immunotherapeutic studies, all alongside the most advanced approaches which exploit big data analysis and machine learning to dissect the complexity of the tumor microenvironment in human cancer.

Prof. Dr. Luigi Racioppi
Guest Editor

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Keywords

  • Tumor microenvironment
  • Tumor-associated macrophages
  • Myeloid-derived suppressive cells
  • Tumor-infiltrating lymphocytes
  • Immune suppression
  • Immunotherapy
  • Precision oncology
  • Machine learning

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Published Papers (4 papers)

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Research

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25 pages, 12214 KiB  
Article
The Ferroptosis Molecular Subtype Reveals Characteristics of the Tumor Microenvironment, Immunotherapeutic Response, and Prognosis in Gastric Cancer
by Xiao Xu, Na Zhou, Hongwei Lan, Fangfang Yang, Bowen Dong and Xiaochun Zhang
Int. J. Mol. Sci. 2022, 23(17), 9767; https://doi.org/10.3390/ijms23179767 - 29 Aug 2022
Cited by 4 | Viewed by 2647
Abstract
Ferroptosis is a relatively new form of programmed cell death, which can enhance the efficacy of tumor immunotherapy by regulating the tumor microenvironment (TME). In the face of the dilemma of a great difference in the efficacy of immunotherapy for gastric cancer (GC) [...] Read more.
Ferroptosis is a relatively new form of programmed cell death, which can enhance the efficacy of tumor immunotherapy by regulating the tumor microenvironment (TME). In the face of the dilemma of a great difference in the efficacy of immunotherapy for gastric cancer (GC) patients, the exploration of ferroptosis may assist us in predicting immunotherapy efficacy prior to treatment. The potential role of ferroptosis in TME still needs further elucidation. Based on ferroptosis-related genes (FRGs), we systematically evaluated ferroptosis molecular subtypes in gastric cancer. Additionally, the association between these molecular subtypes and the characteristics of TME was examined. A ferroptosis score was constructed to further explore the predictive efficacy of ferroptosis on the immunotherapy response in gastric cancer. There were also 32 other cancers that were evaluated. Three molecular subtypes of ferroptosis in gastric cancer were identified. The three immunophenotypes of tumor immune inflamed, immune excluded, as well as immune desert were mostly in agreement with the TME features of these three subtypes. The individual tumor genetic variation, TME characteristics, immunotherapy response, and prognosis could be assessed by a ferroptosis score. High ferroptosis scores in gastric cancer suggest stromal activation and immunosuppression. It is noted that tumors with a low ferroptosis score are characterized by extensive tumor mutations as well as an immune activation, which are associated with an enhanced immunotherapy response and an improved prognosis. This study reveals that ferroptosis plays an integral role in the regulation of the tumor immune microenvironment. The ferroptosis score may serve as an independent prognostic factor for GC and will deepen our understanding of the TME infiltration mechanisms as well as lead to more rational immunotherapy regimens. Full article
(This article belongs to the Special Issue Tumor Microenvironment and Immune Response)
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15 pages, 3062 KiB  
Article
Regulatory T Cells with Additional COX-2 Expression Are Independent Negative Prognosticators for Vulvar Cancer Patients
by Nadine Ansorge, Christian Dannecker, Udo Jeschke, Elisa Schmoeckel, Helene Hildegard Heidegger, Aurelia Vattai, Maximiliane Burgmann, Bastian Czogalla, Sven Mahner and Sophie Fuerst
Int. J. Mol. Sci. 2022, 23(9), 4662; https://doi.org/10.3390/ijms23094662 - 22 Apr 2022
Cited by 2 | Viewed by 2220
Abstract
Vulvar cancer incidence numbers have been steadily rising over the past decades. In particular, the number of young patients with vulvar cancer has recently increased. Therefore, the need to identify new prognostic factors and, in addition, therapeutic options for vulvar carcinoma is more [...] Read more.
Vulvar cancer incidence numbers have been steadily rising over the past decades. In particular, the number of young patients with vulvar cancer has recently increased. Therefore, the need to identify new prognostic factors and, in addition, therapeutic options for vulvar carcinoma is more apparent. The aim of this study was to analyze the influx of COX-2 positive tumor-infiltrating lymphocytes and monocytes and their influence on prognosis. Using subtyping by immunofluorescence, the majority of COX-2 expressing immune cells were identified as FOXP3-positive regulatory T cells. In addition, peri- and intra-tumoral macrophages in the same tumor tissue were detected simultaneously as M2-polarized macrophages. COX-2 positive immune cells were independent negative prognostic markers in long-term overall survival of patients with vulvar cancer. These results show an influence of immune cell infiltration for vulvar carcinoma patients. Immune cell infiltration and immune checkpoint expression may, therefore, become interesting targets for further research on new vulvar cancer treatment strategies. Full article
(This article belongs to the Special Issue Tumor Microenvironment and Immune Response)
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16 pages, 6015 KiB  
Article
STAT1 Is Required for Decreasing Accumulation of Granulocytic Cells via IL-17 during Initial Steps of Colitis-Associated Cancer
by Yael Delgado-Ramirez, Itzel Baltazar-Perez, Yamileth Martinez, Blanca E. Callejas, Itzel Medina-Andrade, Jonadab E. Olguín, Norma L. Delgado-Buenrostro, Yolanda I. Chirino, Luis I. Terrazas and Sonia Leon-Cabrera
Int. J. Mol. Sci. 2021, 22(14), 7695; https://doi.org/10.3390/ijms22147695 - 19 Jul 2021
Cited by 11 | Viewed by 3392
Abstract
Signal transducer and activator of transcription 1 (STAT1) acts as a tumor suppressor molecule in colitis-associated colorectal cancer (CAC), particularly during the very early stages, modulating immune responses and controlling mechanisms such as apoptosis and cell proliferation. Previously, using an experimental model of [...] Read more.
Signal transducer and activator of transcription 1 (STAT1) acts as a tumor suppressor molecule in colitis-associated colorectal cancer (CAC), particularly during the very early stages, modulating immune responses and controlling mechanisms such as apoptosis and cell proliferation. Previously, using an experimental model of CAC, we reported increased intestinal cell proliferation and faster tumor development, which were consistent with more signs of disease and damage, and reduced survival in STAT1-/- mice, compared with WT counterparts. However, the mechanisms through which STAT1 might prevent colorectal cancer progression preceded by chronic inflammation are still unclear. Here, we demonstrate that increased tumorigenicity related to STAT1 deficiency could be suppressed by IL-17 neutralization. The blockade of IL-17 in STAT1-/- mice reduced the accumulation of CD11b+Ly6ClowLy6G+ cells resembling granulocytic myeloid-derived suppressor cells (MDSCs) in both spleen and circulation. Additionally, IL-17 blockade reduced the recruitment of neutrophils into intestinal tissue, the expression and production of inflammatory cytokines, and the expression of intestinal STAT3. In addition, the anti-IL-17 treatment also reduced the expression of Arginase-1 and inducible nitric oxide synthase (iNOS) in the colon, both associated with the main suppressive activity of MDSCs. Thus, a lack of STAT1 signaling induces a significant change in the colonic microenvironment that supports inflammation and tumor formation. Anti-IL-17 treatment throughout the initial stages of CAC related to STAT1 deficiency abrogates the tumor formation possibly caused by myeloid cells. Full article
(This article belongs to the Special Issue Tumor Microenvironment and Immune Response)
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Review

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17 pages, 844 KiB  
Review
Cancer-Associated Fibroblasts in Conversation with Tumor Cells in Endometrial Cancers: A Partner in Crime
by De Pradip, Aske Jennifer and Dey Nandini
Int. J. Mol. Sci. 2021, 22(17), 9121; https://doi.org/10.3390/ijms22179121 - 24 Aug 2021
Cited by 16 | Viewed by 3380
Abstract
A tumor cell carrying characteristic genomic alteration(s) exists within its host’s microenvironment. The tumor microenvironment (TME) renders holistic support to the tumor via cross-talk between tumor cells and three components of TME, immune components, vascular components, and fibroblast components. The tempero-spatial interaction of [...] Read more.
A tumor cell carrying characteristic genomic alteration(s) exists within its host’s microenvironment. The tumor microenvironment (TME) renders holistic support to the tumor via cross-talk between tumor cells and three components of TME, immune components, vascular components, and fibroblast components. The tempero-spatial interaction of tumor cells with its microenvironment is the deterministic factor for tumor growth, progression, resistance to therapy, and its outcome in clinics. TME (1) facilitates proliferation, and the ensuing metastasis-associated phenotypes, (2) perturbs immune surveillance and supports tumor cells in their effort to evade immune recognition, and (3) actively participates in developing drug-induced resistance in cancer cells. Cancer-Associated Fibroblast (CAF) is a unique component of TME. CAF is the host mesenchyme immediately surrounding the tumor cells in solid tumors. It facilitates tumor growth and progression and participates in developing drug resistance in tumor cells by playing a critical role in all the ways mentioned above. The clinical outcome of a disease is thus critically contributed to by the CAF component of TME. Although CAFs have been identified historically, the functional relevance of CAF-tumor cell cross-talk and their influence on angiogenic and immune-components of TME are yet to be characterized in solid tumors, especially in endometrial cancers. Currently, the standard of care for the treatment of endometrial cancers is primarily guided by therapies directed towards the disease’s tumor compartment and immune compartments. Unfortunately, in the current state of therapies, a complete response (CR) to the therapy is still limited despite a more commonly achieved partial response (PR) and stable disease (SD) in patients. Acknowledging the limitations of the current sets of therapies based on only the tumor and immune compartments of the disease, we sought to put forward this review based on the importance of the cross-talk between CAF of the tumor microenvironment and tumor cells. The premise of the review is to recognize the critical role of CAF in disease progression. This manuscript presents a systemic review of the role of CAF in endometrial cancers. We critically interrogated the active involvement of CAF in the tumor compartment of endometrial cancers. Here we present the functional characteristics of CAF in the context of endometrial cancers. We review (1) the characteristics of CAF, (2) their evolution from being anti-tumor to pro-tumor, (3) their involvement in regulating growth and several metastasis-associated phenotypes of tumor cells, (4) their participation in perturbing immune defense and evading immune surveillance, and (5) their role in mediating drug resistance via tumor-CAF cross-talk with particular reference to endometrial cancers. We interrogate the functional characteristics of CAF in the light of its dialogue with tumor cells and other components of TME towards developing a CAF-based strategy for precision therapy to supplement tumor-based therapy. The purpose of the review is to present a new vision and initiate a thought process which recognizes the importance of CAF in a tumor, thereby resulting in a novel approach to the design and management of the disease in endometrial cancers. Full article
(This article belongs to the Special Issue Tumor Microenvironment and Immune Response)
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