Immunotherapy for Cancers

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

Deadline for manuscript submissions: 31 May 2024 | Viewed by 2825

Special Issue Editors

1. Laboratory of Immunology and General Pathology, University of Insubria, Varese, Italy
2. Laboratory of Innate Immunity, IRCCS MultiMedica, Milan, Italy
Interests: natural killer cells; innate lymphoid cells; tumor microenvironment; tumor angiogenesis; tumor immunology; immunotherapy
Special Issues, Collections and Topics in MDPI journals
Dr. Barbara Bassani
E-Mail Website
Guest Editor
Laboratory of Innate Immunity, IRCCS MultiMedica, Milan, Italy
Interests: natural killer cells; neutrophils; myeloid-derived suppressor cells; T cells; tumor immunology; mesenchymal cells; ZEB1; angiogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer immunotherapy is a revolutionary tool to fight against cancer, restoring/re-awakening the immune host response by different approaches including vaccines (including nano-vaccines), cell therapies (including CAR-T and, more recently, CAR-NK), modified antibodies, immunocytokines, etc.

Although immunotherapy has emerged as the “next generation” of cancer treatment, it has not yet been shown to be successful in the treatment of all cancer types, for whom the preferential therapeutic options still remain radiotherapy, chemotherapy, and target therapy. This strongly suggests that a deeper examination of the interactions between immune cells in the micro- and macro-environment, which are currently poorly characterized, is still crucial for the clinical outcome and success of immunotherapy.

From this perspective, the immune-tumor microenvironment (TIME), as a key element in the new era of immunotherapy, has become a major challenge, and reverting this in the case of resistance to immunotherapy is still a major challenge. During this time, the roles of tissue-residing cells in promoting or suppressing tumor growth, metastasis and resistance to therapy have been gradually elucidated. Immunotherapy presents an opportunity to fight against cancer; several strategies have been employed but not all are successful. It is therefore clear that in the “window of unsuccessful immunotherapy”, a deeper knowledge of cellular and molecular mechanisms regulating immune suppression and angiogenesis is still required. It is also now clear that immunotherapy alone is not sufficient to eliminate cancer, thus opening new windows for therapeutic approaches based on combinations (in term of molecules and timing/sequences of their administration).

For this Special Issue, we aim to collect original research, reviews, mini-reviews, and perspective articles reviewing/discussing the state of the art and/or proposing novel insights in basic and translational research of cancer immunotherapy. Areas of interest include but are not limited to:

  • High-throughput (“omics” and bioinformatic) approaches followed by experimental validation to dissect (novel) molecular targets for cancer immunotherapy;
  • TME/TIME-oriented molecular and cellular mechanisms/targets as potential candidates for immunotherapy;
  • The role of chronic inflammation and fibrosis in permitting immune-escape and/or resistance to immunotherapy;
  • Metabolic and immunometabolic drivers of immunosuppression, tumor progression/metastasis and resistance to cancer immunotherapy;
  • Combination approaches, including drug repurposing, in cancer immunotherapy;
  • Novel diagnostic or prognostic tools for cancer immunotherapy;
  • Stromal–immune cell interactions driving tumor progression, immunoescape and resistance to immunotherapy;
  • Epigenetics and immunotherapy;
  • Marine drugs and phytochemicals able to potentiate the immune response against cancers.

You may choose our Joint Special Issue in Vaccines.

Dr. Antonino Bruno
Dr. Barbara Bassani
Guest Editors

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

  • cancer immunotherapy
  • innate immunity
  • adaptive immunity
  • tumor immune microenvironment
  • tumor microenvironment
  • combination therapies
  • drug repurposing

Published Papers (2 papers)

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Research

18 pages, 7854 KiB  
Article
The Defined TLR3 Agonist, Nexavant, Exhibits Anti-Cancer Efficacy and Potentiates Anti-PD-1 Antibody Therapy by Enhancing Immune Cell Infiltration
Cancers 2023, 15(24), 5752; https://doi.org/10.3390/cancers15245752 - 08 Dec 2023
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Abstract
Nexavant was reported as an alternative to the TLR3 agonist of Poly(I:C) and its derivatives. The physicochemical properties, signaling pathways, anti-cancer effects, and mechanisms of Nexavant were investigated. The distinctive characteristics of Nexavant compared to that of Poly(I:C) were demonstrated by precise quantification, [...] Read more.
Nexavant was reported as an alternative to the TLR3 agonist of Poly(I:C) and its derivatives. The physicochemical properties, signaling pathways, anti-cancer effects, and mechanisms of Nexavant were investigated. The distinctive characteristics of Nexavant compared to that of Poly(I:C) were demonstrated by precise quantification, enhanced thermostability, and increased resistance to RNase A. Unlike Poly(I:C), which activates TLR3, RIG-I, and MDA5, Nexavant stimulates signaling through TLR3 and RIG-I but not through MDA5. Compared to Poly(I:C), an intratumoral Nexavant treatment led to a unique immune response, immune cell infiltration, and suppression of tumor growth in various animal cancer models. Nexavant therapy outperformed anti-PD-1 antibody treatment in all the tested models and showed a synergistic effect in combinational therapy, especially in well-defined cold tumor models. The effect was similar to that of nivolumab in a humanized mouse model. Intranasal instillation of Nexavant led to the recruitment of immune cells (NK, CD4+ T, and CD8+ T) to the lungs, suppressing lung metastasis and improving animal survival. Our study highlighted Nexavant’s defined nature for clinical use and unique signaling pathways and its potential as a standalone anti-cancer agent or in combination with anti-PD-1 antibodies. Full article
(This article belongs to the Special Issue Immunotherapy for Cancers)
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45 pages, 8055 KiB  
Article
HIV-1 Protease as DNA Immunogen against Drug Resistance in HIV-1 Infection: DNA Immunization with Drug Resistant HIV-1 Protease Protects Mice from Challenge with Protease-Expressing Cells
Cancers 2023, 15(1), 238; https://doi.org/10.3390/cancers15010238 - 30 Dec 2022
Cited by 2 | Viewed by 1588
Abstract
DNA immunization with HIV-1 protease (PR) is advanced for immunotherapy of HIV-1 infection to reduce the number of infected cells producing drug-resistant virus. A consensus PR of the HIV-1 FSU_A strain was designed, expression-optimized, inactivated (D25N), and supplemented with drug resistance (DR) mutations [...] Read more.
DNA immunization with HIV-1 protease (PR) is advanced for immunotherapy of HIV-1 infection to reduce the number of infected cells producing drug-resistant virus. A consensus PR of the HIV-1 FSU_A strain was designed, expression-optimized, inactivated (D25N), and supplemented with drug resistance (DR) mutations M46I, I54V, and V82A common for FSU_A. PR variants with D25N/M46I/I54V (PR_Ai2mut) and with D25N/M46I/I54V/V82A (PR_Ai3mut) were cloned into the DNA vaccine vector pVAX1, and PR_Ai3mut, into a lentiviral vector for the transduction of murine mammary adenocarcinoma cells expressing luciferase 4T1luc2. BALB/c mice were DNA-immunized by intradermal injections of PR_Ai, PR_Ai2mut, PR_Ai3mut, vector pVAX1, or PBS with electroporation. All PR variants induced specific CD8+ T-cell responses revealed after splenocyte stimulation with PR-derived peptides. Splenocytes of mice DNA-immunized with PR_Ai and PR_Ai2mut were not activated by peptides carrying V82A, whereas splenocytes of PR_Ai3mut-immunized mice recognized both peptides with and without V82A mutation. Mutations M46I and I54V were immunologically silent. In the challenge study, DNA immunization with PR_Ai3mut protected mice from the outgrowth of subcutaneously implanted adenocarcinoma 4T1luc2 cells expressing PR_Ai3mut; a tumor was formed only in 1/10 implantation sites and no metastases were detected. Immunizations with other PR variants were not protective; all mice formed tumors and multiple metastasis in the lungs, liver, and spleen. CD8+ cells of PR_Ai3mut DNA-immunized mice exhibited strong IFN-γ/IL-2 responses against PR peptides, while the splenocytes of mice in other groups were nonresponsive. Thus, immunization with a DNA plasmid encoding inactive HIV-1 protease with DR mutations suppressed the growth and metastatic activity of tumor cells expressing PR identical to the one encoded by the immunogen. This demonstrates the capacity of T-cell response induced by DNA immunization to recognize single DR mutations, and supports the concept of the development of immunotherapies against drug resistance in HIV-1 infection. It also suggests that HIV-1-infected patients developing drug resistance may have a reduced natural immune response against DR HIV-1 mutations causing an immune escape. Full article
(This article belongs to the Special Issue Immunotherapy for Cancers)
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