Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.4
5.2
Journals
Cancers
Special Issues
Immunogenic Cell Death and Associated Antitumor Immunity
share announcement

Immunogenic Cell Death and Associated Antitumor Immunity

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: 15 May 2024 | Viewed by 3942

Special Issue Editor

Prof. Dr. Steven Fiering

E-Mail Website
Guest Editor
1. Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA
2. Dartmouth Cancer Center, Geisel School of Medicine at Dartmouth and Dartmouth-Hitchcock Medical Center, Lebanon, NH 03756, USA
Interests: nanoparticles; cancer; immunology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Roughly 20 years ago, studies by Zitvogel, Kroemer, and their colleagues showed that some commonly used cytotoxic cancer drugs were stimulating antitumor immune responses against tumors, which were important in those drugs’ treatment efficacy.  This generated the concept of “immunogenic cell death” (ICD) and added “death-associated molecular patterns” (DAMPS) as additional immunogenic signals to “pathogen-associated molecular patterns” (PAMPS).  It also most importantly caused oncologists to realize that in fact, antitumor immune response had been part of their clinical practice and as a result, while it had previously been ignored and thought to be unimportant by many oncologists, it was finally taken seriously. By 2010, the concept that antitumor immunity was valid and important in cancer biology was established (after over 100 years of debate), and soon after, the first T cell checkpoint blocking antibodies were clinically approved. How ICD, caused by cytotoxic chemotherapy or other cancer treatments such as radiation or heat, interacts with the immune system is still an important topic of active research.

This Special Issue is designed to assemble important work in the area of ICD due to cancer therapy, how it interacts with natural or treatment-generated antitumor immunity, and how that response can be further strengthened to improve outcomes for patients

Prof. Dr. Steven Fiering
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. 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

  • immunogenic cell death
  • antitumor immunity
  • abscopal effect
  • cancer biology
  • cancer therapy

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

26 pages, 5613 KiB  
Article
Immunogenic Death of Hepatocellular Carcinoma Cells in Mice Expressing Caspase-Resistant ROCK1 Is Not Replicated by ROCK Inhibitors
by Gregory Naylor, Linda Julian, Steven Watson-Bryce, Margaret Mullin, Robert J. Nibbs and Michael F. Olson
Cancers 2022, 14(23), 5943; https://doi.org/10.3390/cancers14235943 - 30 Nov 2022
Cited by 1 | Viewed by 1692
Abstract
The morphological changes during apoptosis help facilitate “immunologically silent” cell death. Caspase cleavage of the ROCK1 kinase results in its activation, which drives the forceful contraction of apoptotic cells. We previously showed that when ROCK1 was mutated to render it caspase-resistant, there was [...] Read more.
The morphological changes during apoptosis help facilitate “immunologically silent” cell death. Caspase cleavage of the ROCK1 kinase results in its activation, which drives the forceful contraction of apoptotic cells. We previously showed that when ROCK1 was mutated to render it caspase-resistant, there was greater liver damage and neutrophil recruitment after treatment with the hepatotoxin diethylnitrosamine (DEN). We now show that acute DEN-induced liver damage induced higher levels of pro-inflammatory cytokines/chemokines, indicative of immunogenic cell death (ICD), in mice expressing non-cleavable ROCK1 (ROCK1nc). Hepatocellular carcinoma (HCC) tumours in ROCK1nc mice had more neutrophils and CD8+ T cells relative to mice expressing wild-type ROCK1, indicating that spontaneous tumour cell death also was more immunogenic. Since ICD induction has been proposed to be tumour-suppressive, the effects of two distinct ROCK inhibitors on HCC tumours was examined. Both fasudil and AT13148 significantly decreased tumour numbers, areas and volumes, but neither resulted in greater numbers of neutrophils or CD8+ T cells to be recruited. In the context of acute DEN-induced liver damage, AT13148 inhibited the recruitment of dendritic, natural killer and CD8+ T cells to livers. These observations indicate that there is an important role for ROCK1 cleavage to limit immunogenic cell death, which was not replicated by systemic ROCK inhibitor administration. As a result, concomitant administration of ROCK inhibitors with cancer therapeutics would be unlikely to result in therapeutic benefit by inducing ICD to increase anti-tumour immune responses. Full article
(This article belongs to the Special Issue Immunogenic Cell Death and Associated Antitumor Immunity)
►▼ Show Figures

Figure 1

23 pages, 3619 KiB  
Article
Regulatory Role of Sphingosine-1-Phosphate and C16:0 Ceramide, in Immunogenic Cell Death of Colon Cancer Cells Induced by Bak/Bax-Activation
by Jeremy A. Hengst, Asvelt J. Nduwumwami and Jong K. Yun
Cancers 2022, 14(21), 5182; https://doi.org/10.3390/cancers14215182 - 22 Oct 2022
Cited by 3 | Viewed by 1687
Abstract
We recently identified the sphingosine kinases (SphK1/2) as key intracellular regulators of immunogenic cell death (ICD) in colorectal cancer (CRC) cells. To better understand the mechanism by which SphK inhibition enhances ICD, we focused on the intracellular signaling pathways leading to cell surface [...] Read more.
We recently identified the sphingosine kinases (SphK1/2) as key intracellular regulators of immunogenic cell death (ICD) in colorectal cancer (CRC) cells. To better understand the mechanism by which SphK inhibition enhances ICD, we focused on the intracellular signaling pathways leading to cell surface exposure of calreticulin (ectoCRT). Herein, we demonstrate that ABT-263 and AZD-5991, inhibitors of Bcl-2/Bcl-XL and Mcl-1, respectively, induce the production of ectoCRT, indicative of ICD. Inhibition of SphK1 significantly enhanced ABT/AZD-induced ectoCRT production, in a caspase 8-dependent manner. Mechanistically, we demonstrate that ABT/AZD-induced Bak/Bax activation stimulates pro-survival SphK1/sphingosine-1-phosphate (S1P) signaling, which attenuates ectoCRT production. Additionally, we identified a regulatory role for ceramide synthase 6 (CerS6)/C16:0 ceramide in transporting of ectoCRT to the cell surface. Together, these results indicate that the sphingolipid metabolic regulators of the sphingolipid rheostat, S1P and C16:0 ceramide, influence survival/death decisions of CRC cells in response to ICD-inducing chemotherapeutic agents. Importantly, SphK1, which produces S1P, is a stress-responsive pro-survival lipid kinase that suppresses ICD. While ceramide, produced by the inhibition of SphK1 is required for production of the cell surface marker of ICD, ectoCRT. Thus, inhibition of SphK1 represents a means to enhance the therapeutic efficacy of ICD-inducing agents. Full article
(This article belongs to the Special Issue Immunogenic Cell Death and Associated Antitumor Immunity)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop