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Special Issue "The Immune Landscape in Solid Tumors"

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

Deadline for manuscript submissions: 31 August 2020.

Special Issue Editors

Prof. Dr. Matthias Gaida
Website
Guest Editor
Institute for Pathology, University Medical Center Mainz, Germany
Johannes Gutenberg- University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany
Prof. Dr. Wilfried Roth
Website
Guest Editor
Institute for Pathology, University Medical Center Mainz, Germany
Johannes Gutenberg- University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany

Special Issue Information

Dear Colleagues,

Although immune cells are present in nearly all types of solid tumors, there is a remarkable variation with regard to cell subpopulations, densities, activation status, and cytokine profiles. Because immune cells can orchestrate a potent anti-tumor immune reaction, immunotherapeutic approaches have been established as standard cancer therapy in recent years, including cytokine therapy or targeting signalling pathways of the infiltrating immune cells, such as immune check points. However, in some cancers the infiltrated immune cells cannot eliminate the tumor, but rather promote its progression most likely due to a massive local inflammatory response, which alters the tumor microenvironment. The Special Issue, “Immune landscape of solid tumors” of the International Journal of Molecular Sciences will address various aspects of the molecular and cellular biology of immune cells in the context of tumors, and invite experts in the field to contribute an original research article or a comprehensive review.  Topics include - but are not limited to - the characterization of tumor-infiltrating immune cells, particularly subclasses, activation status and cytokine profiles;  the analysis of signaling pathways; the interactions of tumor-infiltrating immune cells with cancer cells; the tumor microenvironment; special aspects of inflammatory carcinogenesis; establishing novel (human) cell, tissue and animal models expedient for investigating immunotherapeutic approaches, inflammatory carcinogenesis, and, finally, unraveling of potential immunotherapeutic targets and prognostic disease markers.

Prof. Dr. Matthias Gaida
Prof. Dr. Wilfried Roth
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

  • Solid tumors
  • Tumor-infiltrating immune cells
  • Immunotherapy
  • Inflammatory carcinogenesis
  • Disease models (cell culture, tissue culture, animal)
  • Tumor microenvironment
  • Fibro-inflammatory stroma
  • Signalling pathways
  • Cytokines
  • Disease markers

Published Papers (3 papers)

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Research

Open AccessArticle
Contribution of Immune Cells to Glucocorticoid Receptor Expression in Breast Cancer
Int. J. Mol. Sci. 2020, 21(13), 4635; https://doi.org/10.3390/ijms21134635 - 30 Jun 2020
Abstract
Breast cancer (BC) patients experience increased stress with elevated cortisol levels, increasing risk of cancer recurrence. Cortisol binds to a cytoplasmic receptor, glucocorticoid receptor (GR) encoded by GR gene (NR3C1). We hypothesized that not only cancer cells, but even immune cells [...] Read more.
Breast cancer (BC) patients experience increased stress with elevated cortisol levels, increasing risk of cancer recurrence. Cortisol binds to a cytoplasmic receptor, glucocorticoid receptor (GR) encoded by GR gene (NR3C1). We hypothesized that not only cancer cells, but even immune cells in the tumor microenvironment (TME) may contribute to GR expression in bulk tumor and influence prognosis. To test this, mRNA expression data was accessed from METABRIC and TCGA. “High” and “low” expression was based on highest and lowest quartiles of NR3C1 gene expression, respectively. Single-cell sequencing data were obtained from GSE75688 and GSE114725 cohorts. Computer algorithms CIBERSORT, Gene Set Enrichment Analysis and TIMER were used. GR-high BC has better median disease-free and disease-specific survival. Single cell sequencing data showed higher GR expression on immune cells compared to cancer and stromal cells. Positive correlation between GR-high BC and CD8+ T-cells was noted. In GR-high tumors, higher cytolytic activity (CYT) with decreased T-regulatory and T-follicular helper cells was observed. High GR expression was associated with lower proliferation index Ki67, enriched in IL-2_STAT5, apoptosis, KRAS, TGF-β signaling, and epithelial-to-mesenchymal transition. Immune cells significantly contribute to GR expression of bulk BC. GR-high BC has a favorable TME with higher CYT with favorable outcomes. Full article
(This article belongs to the Special Issue The Immune Landscape in Solid Tumors)
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Open AccessArticle
Intratumoral Administration of a Novel Cytotoxic Formulation with Strong Tissue Dispersive Properties Regresses Tumor Growth and Elicits Systemic Adaptive Immunity in In Vivo Models
Int. J. Mol. Sci. 2020, 21(12), 4493; https://doi.org/10.3390/ijms21124493 - 24 Jun 2020
Abstract
The recent development of immune-based therapies has improved the outcome for cancer patients; however, adjuvant therapies remain an important line of treatment for several cancer types. To maximize efficacy, checkpoint inhibitors are often combined with cytotoxic agents. While this approach often leads to [...] Read more.
The recent development of immune-based therapies has improved the outcome for cancer patients; however, adjuvant therapies remain an important line of treatment for several cancer types. To maximize efficacy, checkpoint inhibitors are often combined with cytotoxic agents. While this approach often leads to increased tumor regression, higher off target toxicity often results in certain patients. This report describes a novel formulation comprising a unique amphiphilic molecule, 8-((2-hydroxybenzoyl)amino)octanoate (SHAO), that non-covalently interacts with payloads to increase drug dispersion and diffusion when dosed intratumorally (IT) into solid tumors. SHAO is co-formulated with cisplatin and vinblastine (referred to as INT230-6). IT dosing of the novel formulation achieved greater tumor growth inhibition and improved survival in in vivo tumor models compared to the same drugs without enhancer given intravenously or IT. INT230-6 treatment increased immune infiltrating cells in injected tumors with 10% to 20% of the animals having complete responses and developing systemic immunity to the cancer. INT230-6 was also shown to be synergistic with programmed cell death protein 1 (PD-1) antibodies at improving survival and increasing complete responses. INT230-6 induced significant tumor necrosis potentially releasing antigens to induce the systemic immune-based anti-cancer attack. This research demonstrates a novel, local treatment approach for cancer that minimizes systemic toxicity while stimulating adaptive immunity. Full article
(This article belongs to the Special Issue The Immune Landscape in Solid Tumors)
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Open AccessArticle
Novel Autoantibody Signatures in Sera of Patients with Pancreatic Cancer, Chronic Pancreatitis and Autoimmune Pancreatitis: A Protein Microarray Profiling Approach
Int. J. Mol. Sci. 2020, 21(7), 2403; https://doi.org/10.3390/ijms21072403 - 31 Mar 2020
Abstract
Identification of disease-associated autoantibodies is of high importance. Their assessment could complement current diagnostic modalities and assist the clinical management of patients. We aimed at developing and validating high-throughput protein microarrays able to screen patients’ sera to determine disease-specific autoantibody-signatures for pancreatic cancer [...] Read more.
Identification of disease-associated autoantibodies is of high importance. Their assessment could complement current diagnostic modalities and assist the clinical management of patients. We aimed at developing and validating high-throughput protein microarrays able to screen patients’ sera to determine disease-specific autoantibody-signatures for pancreatic cancer (PDAC), chronic pancreatitis (CP), autoimmune pancreatitis and their subtypes (AIP-1 and AIP-2). In-house manufactured microarrays were used for autoantibody-profiling of IgG-enriched preoperative sera from PDAC-, CP-, AIP-1-, AIP-2-, other gastrointestinal disease (GID) patients and healthy controls. As a top-down strategy, three different fluorescence detection-based protein-microarrays were used: large with 6400, intermediate with 345, and small with 36 full-length human recombinant proteins. Large-scale analysis revealed 89 PDAC, 98 CP and 104 AIP immunogenic antigens. Narrowing the selection to 29 autoantigens using pooled sera first and individual sera afterwards allowed a discrimination of CP and AIP from PDAC. For validation, predictive models based on the identified antigens were generated which enabled discrimination between PDAC and AIP-1 or AIP-2 yielded high AUC values of 0.940 and 0.925, respectively. A new repertoire of autoantigens was identified and their assembly as a multiplex test will provide a fast and cost-effective tool for differential diagnosis of pancreatic diseases with high clinical relevance. Full article
(This article belongs to the Special Issue The Immune Landscape in Solid Tumors)
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