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Immune, Inflammatory and Metabolic Mechanisms in Cancer
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Immune, Inflammatory and Metabolic Mechanisms in Cancer

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: closed (15 February 2023) | Viewed by 8947

Special Issue Editor

Prof. Dr. Ana Caruntu

E-Mail Website
Guest Editor
1. Department of Oral and Maxillofacial Surgery, Faculty of Dental Medicine, Titu Maiorescu University, 031593 Bucharest, Romania
2. Department of Oral and Maxillofacial Surgery, Carol Davila Central Military Emergency Hospital, 010825 Bucharest, Romania
Interests: tissue regeneration; healing; head and neck cancer; biomaterials; inflammation; biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer is still a mysterious disease, acting like an “iceberg” that reveals only little of its magnitude and complexity, while continuously taking the tribute of human lives worldwide. Scientific community has achieved great progresses that led to breakthroughs in cancer therapy, however on a global scale humanity is far from winning the war against cancer. One of the most intriguing aspects about cancer is that frequently the same elements can play contrasting roles, acting as cancer protective or cancer promoting factors. Metabolic, immune and inflammatory changes have been described as “double-edged swords” in many types of malignancies, thus enhancing the complexity of the labyrinth of carcinogenesis, cancer progression and disease response to treatment. A deeper understanding of the mechanisms that interconnect inflammatory pathways, antitumor immune response, immuno-tolerance, metabolomics and cancer could open new perspectives that might represent additional steps towards revolutionizing anticancer therapies.

This Special Issue aims to bring together the most recent and relevant scientific research that could enlighten the complex universe of cancer pathogenesis, focusing on metabolic, immune and inflammatory mechanisms related to cancer. Investigators are encouraged to submit original research articles, review papers and communications covering the above mentioned subjects.

Prof. Dr. Ana Caruntu
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. 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

  • immune mechanisms in cancer
  • innane immune system
  • addaptive immune system
  • cancer immunity cycle
  • immune checkpoint inhibitors
  • immune biomarkers
  • immunotherapy
  • inflammation
  • inflammasomes
  • inflammation epigenetics
  • inflammatory signaling pathways
  • inflammatory biomarkers
  • cancer cell metabolism
  • nutrient deprivation
  • acidosis
  • metabolic cancer therapy

Published Papers (3 papers)

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Research

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12 pages, 2200 KiB  
Article
Differential Transcriptome Responses in Human THP-1 Macrophages Following Exposure to T98G and LN-18 Human Glioblastoma Secretions: A Simplified Bioinformatics Approach to Understanding Patient-Glioma-Specific Effects on Tumor-Associated Macrophages
by Micaela R. Scobie, Abdullah Abood and Charles D. Rice
Int. J. Mol. Sci. 2023, 24(6), 5115; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24065115 - 07 Mar 2023
Cited by 1 | Viewed by 1762
Abstract
A common theme in glioma disease progression is robust infiltration of immune cells within the tumor microenvironment, resulting in a state of chronic inflammation. This disease state is characterized by an abundance of CD68+ microglia and CD163+ bone marrow-derived macrophages with [...] Read more.
A common theme in glioma disease progression is robust infiltration of immune cells within the tumor microenvironment, resulting in a state of chronic inflammation. This disease state is characterized by an abundance of CD68+ microglia and CD163+ bone marrow-derived macrophages with the greater the percentage of CD163+ cells, the poorer the prognosis. These macrophages are “cold,” in that their phenotype is of an alternatively activated state (M0-M2-like) supporting tumor growth rather than being engaged with classically activated, pro-inflammatory, and anti-tumor activities, referred to as “hot”, or M1-like. Herein, we have developed an in vitro approach that uses two human glioma cell lines, T98G and LN-18, which exhibit a variety of differing mutations and characteristics, to demonstrate their disparate effects on differentiated THP-1 macrophages. We first developed an approach to differentiating THP-1 monocytes to macrophages with mixed transcriptomic phenotypes we regard as M0-like macrophages. We then found that supernatants from the two different glioma cell lines induced different gene expression profiles in THP-1 macrophages, suggesting that from patient to patient, gliomas may be considered as different diseases. This study suggests that in addition to standard glioma treatment modalities, transcriptome profiling of the effects of cultured glioma cells on a standard THP-1 macrophage in vitro model may lead to future druggable targets that aim to reprogram tumor-associated macrophages towards an anti-tumor phenotype. Full article
(This article belongs to the Special Issue Immune, Inflammatory and Metabolic Mechanisms in Cancer)
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Review

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40 pages, 3245 KiB  
Review
Diverse Neutrophil Functions in Cancer and Promising Neutrophil-Based Cancer Therapies
by Khetam Sounbuli, Nadezhda Mironova and Ludmila Alekseeva
Int. J. Mol. Sci. 2022, 23(24), 15827; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232415827 - 13 Dec 2022
Cited by 15 | Viewed by 2992
Abstract
Neutrophils represent the most abundant cell type of leukocytes in the human blood and have been considered a vital player in the innate immune system and the first line of defense against invading pathogens. Recently, several studies showed that neutrophils play an active [...] Read more.
Neutrophils represent the most abundant cell type of leukocytes in the human blood and have been considered a vital player in the innate immune system and the first line of defense against invading pathogens. Recently, several studies showed that neutrophils play an active role in the immune response during cancer development. They exhibited both pro-oncogenic and anti-tumor activities under the influence of various mediators in the tumor microenvironment. Neutrophils can be divided into several subpopulations, thus contradicting the traditional concept of neutrophils as a homogeneous population with a specific function in the innate immunity and opening new horizons for cancer therapy. Despite the promising achievements in this field, a full understanding of tumor–neutrophil interplay is currently lacking. In this review, we try to summarize the current view on neutrophil heterogeneity in cancer, discuss the different communication pathways between tumors and neutrophils, and focus on the implementation of these new findings to develop promising neutrophil-based cancer therapies. Full article
(This article belongs to the Special Issue Immune, Inflammatory and Metabolic Mechanisms in Cancer)
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19 pages, 1185 KiB  
Review
Clinical Efficacies of FLT3 Inhibitors in Patients with Acute Myeloid Leukemia
by Moo-Kon Song, Byeong-Bae Park and Ji-Eun Uhm
Int. J. Mol. Sci. 2022, 23(20), 12708; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232012708 - 21 Oct 2022
Cited by 5 | Viewed by 3453
Abstract
FLT3 mutations are the most common genomic alteration detected in acute myeloid leukemia (AML) with a worse clinical prognosis. The highly frequent FLT3 mutations, together with the side effects associated with clinical prognosis, make FLT3 promising treatment targets and have provoked the advancement [...] Read more.
FLT3 mutations are the most common genomic alteration detected in acute myeloid leukemia (AML) with a worse clinical prognosis. The highly frequent FLT3 mutations, together with the side effects associated with clinical prognosis, make FLT3 promising treatment targets and have provoked the advancement of FLT3 inhibitors. Recently, numerous FLT3 inhibitors were actively developed, and thus the outcomes of this aggressive subtype of AML were significantly improved. Recently, midostaurin and gilteritinib were approved as frontline treatment of AML and as therapeutic agents in the recurred disease by the United States Food and Drug Administration. Recently, numerous promising clinical trials attempted to seek appropriate management in frontline settings, in relapsed/refractory disease, or after stem cell transplantation in AML. This review follows numerous clinical trials about the usefulness of FLT3 inhibitors as frontline therapy, as relapsed/refractory conditioning, and as maintenance therapy of stem cell transplantation. The cumulative data of FLT3 inhibitors would be important clinical evidence for further management with FLT3 inhibitors in AML patients with FLT3 mutations. Full article
(This article belongs to the Special Issue Immune, Inflammatory and Metabolic Mechanisms in Cancer)
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