ijms-logo

Journal Browser

Journal Browser

Special Issue "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: 31 December 2021.

Special Issue Editor

Prof. Dr. Luigi Racioppi
E-Mail Website
Guest Editor
1. Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università di Napoli "Federico II”Naples, Napoli, Italy
2. Department of Medicine/Hematologic Malignancies & Cell Therapy, Duke University, Durham, NC, Italy
Interests: inflammation; macrophage; dendritic cells; signal transduction; hematopoiesis; hematopoietic stem cell; tumor immunology

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

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 papers will be 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • Tumor-associated macrophages
  • Myeloid-derived suppressive cells
  • Tumor-infiltrating lymphocytes
  • Immune suppression
  • Immunotherapy
  • Precision oncology
  • Machine learning

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

Article
STAT1 Is Required for Decreasing Accumulation of Granulocytic Cells via IL-17 during Initial Steps of Colitis-Associated Cancer
Int. J. Mol. Sci. 2021, 22(14), 7695; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22147695 - 19 Jul 2021
Viewed by 732
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)
Show Figures

Figure 1

Review

Jump to: Research

Review
Cancer-Associated Fibroblasts in Conversation with Tumor Cells in Endometrial Cancers: A Partner in Crime
Int. J. Mol. Sci. 2021, 22(17), 9121; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179121 - 24 Aug 2021
Viewed by 376
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)
Show Figures

Figure 1

Back to TopTop