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Cancers
Special Issues
Immunomodulation in Cancer Treatment
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Immunomodulation in Cancer Treatment

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

Deadline for manuscript submissions: 31 August 2025 | Viewed by 992

Special Issue Editor

Dr. Samuel D. Saibil

E-Mail Website
Guest Editor
Departments of Medicine and Immunology, University of Toronto, Toronto, ON M5S 1A8, Canada
Interests: immuno-metabolism; adoptive cell therapy

Special Issue Information

Dear Colleagues,

Immune therapy has revolutionized the treatment of cancer.  Much of the impact has been achieved due to immune checkpoint inhibitor (ICI) antibodies targeting the Programmed Death 1 (PD1) axis.  It is now clear that, unfortunately, these anti-PD1 ICIs alone are not sufficient to achieve durable tumor control in most patients with cancer. Fortunately, tremendous progress has been made in developing novel approaches to manipulate the immune system to fight cancer.  These include cellular therapies, bi-specific T-cell engagers (BiTES) and therapies aimed at targeting immunometabolism, the microbiome or non-T cell populations of immune cells.  We are pleased to invite you to contribute to this Special Issue of Cancers entitled “Immunomodulation in Cancer Treatment”.  This Special Issue will focus on novel approaches to manipulating the immune response against cancer that demonstrate the potential to translate to improved clinical outcomes. For this Special Issue, original research articles and reviews are welcome.  Research areas may include (but are not limited to) the following:

  • Cell therapies utilizing tumor-infiltrating lymphocytes (TILs), T-cell receptor transgenic T-cells (TCR-T) or chimeric antigen receptor T-cells (CAR-T);
  • Bispecific antibodies or T-cell engagers;
  • Novel cytokine therapies;
  • Microbiome-targeted therapies;
  • Immuno-metabolic treatments;
  • Therapies targeting innate lymphoid cells (ILCs), macrophages or other innate immune cells.

We look forward to receiving your contributions.

Dr. Samuel D. Saibil
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 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. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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

  • adoptive cell therapy
  • TILs
  • TCT-T
  • BiTes
  • CAR-T
  • immuno-metabolism
  • immune therapy

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Published Papers (1 paper)

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Research

20 pages, 7803 KiB  
Article
Impact of Hyaluronic Acid on the Cutaneous T-Cell Lymphoma Microenvironment: A Novel Anti-Tumor Mechanism of Bexarotene
by Tetsuya Ikawa, Emi Yamazaki, Ryo Amagai, Yumi Kambayashi, Mana Sekine, Takuya Takahashi, Yoshihide Asano and Taku Fujimura
Cancers 2025, 17(2), 324; https://doi.org/10.3390/cancers17020324 - 20 Jan 2025
Viewed by 583
Abstract
Background: Cutaneous T-cell lymphoma (CTCL) is a type of non-Hodgkin’s lymphoma that primarily affects the skin, rich in hyaluronic acid (HA). HA is a component of the extracellular matrix in the dermis and likely affects the development of CTCL, but the mechanism is [...] Read more.
Background: Cutaneous T-cell lymphoma (CTCL) is a type of non-Hodgkin’s lymphoma that primarily affects the skin, rich in hyaluronic acid (HA). HA is a component of the extracellular matrix in the dermis and likely affects the development of CTCL, but the mechanism is poorly understood. Here we show that low-molecular-weight HA (LMWHA) possibly exacerbates CTCL, and bexarotene, already used in CTCL treatment, decreases HA production. Methods: We conducted immunohistochemistry, qRT-PCR, immunoblotting, and HA quantification using both mouse and human specimens to evaluate the impact of HA on CTCL. Additionally, we assessed the effect of bexarotene, which is already used for CTCL treatment, on HA metabolism. Results: HA expression was higher in patients’ serum and skin sections than in healthy controls. HA extracted from the skin of mice inoculated with tumors showed an increase in LMWHA. LMWHA increased lymphoma cell proliferation in vitro and accelerated tumor formation in mice in vivo. LMWHA also created a favorable environment for tumor cells by affecting fibroblasts, vascular endothelial cells, and tumor-associated macrophages. Thus, increased levels of HA, mainly LMWHA, exacerbate CTCL progression by affecting tumor cells and their microenvironment. Bexarotene treatment reduced the amount of total HA in murine tumor-inoculated skin, as well as the supernatant of cultured normal human dermal fibroblasts (NHDFs) and HuT78 cells. Detailed in vitro analyses showed that bexarotene treatment decreased HA synthase (HAS)1 and HAS2 expression in NHDFs and HAS1 and HAS3, and CEMIP expression in HuT78 cells. Chromatin immunoprecipitation assays revealed that bexarotene reduced retinoid X receptor-α binding to the HAS1 and HAS2 promoters in NHDFs. Conclusions: Bexarotene potentially exerts its anti-tumor effect by reducing HA levels through decreased expression of HAS. These findings provide new insights into the process of CTCL development and additional insights regarding bexarotene treatment. Full article
(This article belongs to the Special Issue Immunomodulation in Cancer Treatment)
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