The Tumor Microenvironment and Molecular Aberrations Convey Immune Evasion (Volume II)

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Immunology and Immunotherapy".

Deadline for manuscript submissions: 1 June 2024 | Viewed by 1935

Special Issue Editor


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Guest Editor
Department of Medical and Molecular Sciences, College of Health Sciences, University of Delaware, Newark, DE 19716, USA
Interests: DNA methylation; cancer invasion and metastasis in breast and pancreatic cancers; carcinoma-associated fibroblasts; epithelial–mesenchymal transition; AKT signaling pathway; tumor microenvironment and immune evasion
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Special Issue Information

Dear Colleagues,

This Special Issue is the second edition of the Special Issue "The Tumor Microenvironment and Molecular Aberrations Convey Immune Evasion" (https://www.mdpi.com/journal/cancers/special_issues/TMMIE).

It has been widely recognized that the complex interplay between immunity and cancer determines whether cancer cells will survive or be destroyed. The battle between tumoricidal and tumor-promoting activity relies on the extent to which the antitumor immune response is exerted. In general, immune evasive mechanisms adapted by cancers encompass the downregulation of antigen presentations or recognition, a lack of immune effector cells, the obstruction of antitumor immune cell maturation, the accumulation of immunosuppressive cells, the production of inhibitory cytokines, chemokines or ligands/receptors, the establishment of a hypoxic tumor microenvironment, the development of cancer-promoting metabolisms, and the upregulation of immune checkpoint modulators. As such, restoring or stimulating tumoricidal effects, in conjunction with surgical resection and chemo- or radiation-mediated, hormone-based, kinase-targeted, DNA repair-disrupted, small molecule inhibitor-mediated, signal transduction pathway-modified, aberrant epigenome-reverted, and cytokine-involved treatments, may spark promising therapeutic regimens to eradicate fatal cancers. This Special Issue welcomes papers outlining mechanisms of immune escape or depicting strategies for boosting immune surveillance, compatible with additional non-immune interventions to eradicate human cancers.

Dr. Huey-Jen Lin
Guest Editor

Manuscript Submission Information

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Keywords

  • CD8+ tumor-infiltrating lymphocytes
  • cytotoxic T lymphocytes -associated protein 4
  • dendritic cells
  • immune evasion
  • hypoxia-inducible factors
  • myeloid-derived suppressor cells
  • natural killer
  • programmed death receptor and ligand
  • regulatory T cells
  • tumor-associated macrophages
  • tumor microenvironment

Published Papers (2 papers)

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Research

12 pages, 2684 KiB  
Article
TIM-3 Expression on Dendritic Cells in Colorectal Cancer
by Mei Sakuma, Masanori Katagata, Hirokazu Okayama, Shotaro Nakajima, Katsuharu Saito, Takahiro Sato, Satoshi Fukai, Hideaki Tsumuraya, Hisashi Onozawa, Wataru Sakamoto, Motonobu Saito, Zenichiro Saze, Tomoyuki Momma, Kosaku Mimura and Koji Kono
Cancers 2024, 16(10), 1888; https://doi.org/10.3390/cancers16101888 - 15 May 2024
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Abstract
TIM-3 was originally identified as a negative regulator of helper T cells and is expressed on dendritic cells (DCs). Since the inhibition of TIM-3 on DCs has been suggested to enhance T cell-mediated anti-tumor immunity, we examined its expression on DCs within the [...] Read more.
TIM-3 was originally identified as a negative regulator of helper T cells and is expressed on dendritic cells (DCs). Since the inhibition of TIM-3 on DCs has been suggested to enhance T cell-mediated anti-tumor immunity, we examined its expression on DCs within the tumor microenvironment (TME) in colorectal cancer (CRC) using transcriptomic data from a public database (n = 592) and immunohistochemical evaluations from our cohorts of CRC (n = 115). The expression of TIM-3 on DCs in vitro was examined by flow cytometry, while the expression of its related molecules, cGAS and STING, on immature and mature DCs was assessed by Western blotting. The expression of HAVCR2 (TIM-3) was strongly associated with the infiltration of DCs within the TME of CRC. Immunohistochemical staining of clinical tissue samples revealed that tumor-infiltrating DCs expressed TIM-3; however, their number at the tumor-invasive front significantly decreased with stage progression. TIM-3 expression was higher on immature DCs than on mature DCs from several different donors (n = 6). Western blot analyses showed that the expression of STING was higher on mature DCs than on immature DCs, which was opposite to that of TIM-3. We demonstrated that TIM-3 was highly expressed on tumor-infiltrating DCs of CRC and that its expression was higher on immature DCs than on mature DCs. Full article
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17 pages, 4564 KiB  
Article
Differential Immune Infiltration Profiles in Colitis-Associated Colorectal Cancer versus Sporadic Colorectal Cancer
by Josefine Schardey, Can Lu, Jens Neumann, Ulrich Wirth, Qiang Li, Tianxiao Jiang, Petra Zimmermann, Joachim Andrassy, Alexandr V. Bazhin, Jens Werner and Florian Kühn
Cancers 2023, 15(19), 4743; https://doi.org/10.3390/cancers15194743 - 27 Sep 2023
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Abstract
Background: Chronic inflammation is a significant factor in colorectal cancer (CRC) development, especially in colitis-associated CRC (CAC). T-cell exhaustion is known to influence inflammatory bowel disease (IBD) progression and antitumor immunity in IBD patients. This study aimed to identify unique immune infiltration characteristics [...] Read more.
Background: Chronic inflammation is a significant factor in colorectal cancer (CRC) development, especially in colitis-associated CRC (CAC). T-cell exhaustion is known to influence inflammatory bowel disease (IBD) progression and antitumor immunity in IBD patients. This study aimed to identify unique immune infiltration characteristics in CAC patients. Methods: We studied 20 CAC and 20 sporadic CRC (sCRC) patients, who were matched by tumor stage, grade, and location. Immunohistochemical staining targeted various T-cell markers (CD3, CD4, CD8, and FOXP3), T-cell exhaustion markers (TOX and TIGIT), a B-cell marker (CD20), and a neutrophil marker (CD66b) in tumor and tumor-free mucosa from both groups. The quantification of the tumor immune stroma algorithm assessed immune-infiltrating cells. Results: CAC patients had significantly lower TOX+ cell infiltration than sCRC in tumors (p = 0.02) and paracancerous tissues (p < 0.01). Right-sided CAC showed increased infiltration of TOX+ cells (p = 0.01), FOXP3+ regulatory T-cells (p < 0.01), and CD20+ B-cells (p < 0.01) compared to left-sided CAC. In sCRC, higher tumor stages (III and IV) had significantly lower TIGIT+ infiltrate than stages I and II. In CAC, high CD3+ (p < 0.01) and CD20+ (p < 0.01) infiltrates correlated with improved overall survival. In sCRC, better survival was associated with decreased TIGIT+ cells (p < 0.038) and reduced CD8+ infiltrates (p = 0.02). Conclusion: In CAC, high CD3+ and CD20+ infiltrates relate to improved survival, while this association is absent in sCRC. The study revealed marked differences in TIGIT and TOX expression, emphasizing distinctions between CAC and sCRC. T-cell exhaustion appears to have a different role in CAC development. Full article
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