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Molecular Immunology of Solid Tumors
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Molecular Immunology of Solid Tumors

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (31 March 2022) | Viewed by 19855

Special Issue Editor

Prof. Dr. Steven Fiering

E-Mail Website
Guest Editor
Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA
Interests: immunology; cancer and tumor immunology; in situ vaccination; cancer nanotechnology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The pro- and anti-tumor importance of immune cells of many types is now well established in solid tumor biology, as is the potential to treat cancer using immune-based therapies.  This has opened a major new area of intellectual and clinical research in cancer and promises to lead to broadly improved outcomes.  Despite clear progress in cancer immunotherapy that has benefited many patients, the majority of patients do not respond to current immunotherapies. The field requires a deeper and broader understanding of how immune cells support or oppose cancer development and the molecular pathways involved in order to create the intellectual foundation for the next generation of cancer immune therapies. This Special Issue on the molecular immunology of solid tumors provides a venue for publishing research that increases our understanding of immune cell interactions with tumors and the molecular pathways that mediate those interactions. Submissions should have a focus on the molecular pathways that impact immune cell interactions with tumors.

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. 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
  • solid tumors
  • anti-tumor
  • molecular pathways

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Published Papers (6 papers)

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Research

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16 pages, 3305 KiB  
Article
Pharmacologic Tumor PDL1 Depletion with Cefepime or Ceftazidime Promotes DNA Damage and Sensitivity to DNA-Damaging Agents
by Clare Murray, Eva Galvan, Carlos Ontiveros, Yilun Deng, Haiyan Bai, Alvaro Souto Padron, Kathryn Hinchee-Rodriguez, Myrna G. Garcia, Anand Kornepati, Jose Conejo-Garcia and Tyler J. Curiel
Int. J. Mol. Sci. 2022, 23(9), 5129; https://doi.org/10.3390/ijms23095129 - 4 May 2022
Cited by 5 | Viewed by 2757
Abstract
The interaction between tumor surface-expressed PDL1 and immune cell PD1 for the evasion of antitumor immunity is well established and is targeted by FDA-approved anti-PDL1 and anti-PD1 antibodies. Nonetheless, recent studies highlight the immunopathogenicity of tumor-intrinsic PDL1 signals that can contribute to the [...] Read more.
The interaction between tumor surface-expressed PDL1 and immune cell PD1 for the evasion of antitumor immunity is well established and is targeted by FDA-approved anti-PDL1 and anti-PD1 antibodies. Nonetheless, recent studies highlight the immunopathogenicity of tumor-intrinsic PDL1 signals that can contribute to the resistance to targeted small molecules, cytotoxic chemotherapy, and αPD1 immunotherapy. As genetic PDL1 depletion is not currently clinically tractable, we screened FDA-approved drugs to identify those that significantly deplete tumor PDL1. Among the candidates, we identified the β-lactam cephalosporin antibiotic cefepime as a tumor PDL1-depleting drug (PDD) that increases tumor DNA damage and sensitivity to DNA-damaging agents in vitro in distinct aggressive mouse and human cancer lines, including glioblastoma multiforme, ovarian cancer, bladder cancer, and melanoma. Cefepime reduced tumor PDL1 post-translationally through ubiquitination, improved DNA-damaging-agent treatment efficacy in vivo in immune-deficient and -proficient mice, activated immunogenic tumor STING signals, and phenocopied specific genetic PDL1 depletion effects. The β-lactam ring and its antibiotic properties did not appear contributory to PDL1 depletion or to these treatment effects, and the related cephalosporin ceftazidime produced similar effects. Our findings highlight the rapidly translated potential for PDDs to inhibit tumor-intrinsic PDL1 signals and improve DNA-damaging agents and immunotherapy efficacy. Full article
(This article belongs to the Special Issue Molecular Immunology of Solid Tumors)
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16 pages, 6125 KiB  
Article
TRIM37 Promotes Pancreatic Cancer Progression through Modulation of Cell Growth, Migration, Invasion, and Tumor Immune Microenvironment
by Tuyen Thi Do, Chun-Chieh Yeh, Guo-Wei Wu, Chia-Chen Hsu, Hung-Chih Chang and Hui-Chen Chen
Int. J. Mol. Sci. 2022, 23(3), 1176; https://doi.org/10.3390/ijms23031176 - 21 Jan 2022
Cited by 3 | Viewed by 2031
Abstract
TRIM37 dysregulation has been observed in several cancer types, implicating its possible role in tumorigenesis. However, the role of TRIM37 in pancreatic cancer progression remains unclear. In the present study, we observed that TRIM37 knockdown resulted in reduced proliferation, clonogenicity, migration, and invasion [...] Read more.
TRIM37 dysregulation has been observed in several cancer types, implicating its possible role in tumorigenesis. However, the role of TRIM37 in pancreatic cancer progression remains unclear. In the present study, we observed that TRIM37 knockdown resulted in reduced proliferation, clonogenicity, migration, and invasion ability of pancreatic cancer cells. Furthermore, an in vivo study using an orthotopic syngeneic animal model further confirmed that reduced expression of TRIM37 in cancer cells suppressed tumor growth in vivo. Moreover, in mice bearing TRIM37 knockdown pancreatic cancer cells, the proportion of CD11b+F4/80+MHCIIlow immunosuppressive macrophages was significantly reduced in tumor milieu, which might be due to the regulatory role of TRIM37 in cytokine production by pancreatic cancer cells. Collectively, these findings suggest a key role of TRIM37 in promoting pancreatic cancer progression. Full article
(This article belongs to the Special Issue Molecular Immunology of Solid Tumors)
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16 pages, 5285 KiB  
Article
Deciphering Repertoire of B16 Melanoma Reactive TCRs by Immunization, In Vitro Restimulation and Sequencing of IFNγ-Secreting T Cells
by Anna V. Izosimova, Diana V. Yuzhakova, Valeria D. Skatova, Lilia N. Volchkova, Elena V. Zagainova, Dmitry M. Chudakov and George V. Sharonov
Int. J. Mol. Sci. 2021, 22(18), 9859; https://doi.org/10.3390/ijms22189859 - 12 Sep 2021
Cited by 3 | Viewed by 2789
Abstract
Recent advances in cancer immunotherapy have great promise for the treatment of solid tumors. One of the key limiting factors that hamper the decoding of physiological responses to these therapies is the inability to distinguish between specific and nonspecific responses. The identification of [...] Read more.
Recent advances in cancer immunotherapy have great promise for the treatment of solid tumors. One of the key limiting factors that hamper the decoding of physiological responses to these therapies is the inability to distinguish between specific and nonspecific responses. The identification of tumor-specific lymphocytes is also the most challenging step in cancer cell therapies such as adoptive cell transfer and T cell receptor (TCR) cloning. Here, we have elaborated a protocol for the identification of tumor-specific T lymphocytes and the deciphering of their repertoires. B16 melanoma engraftment following anti-PD1 checkpoint therapy provides better antitumor immunity compared to repetitive immunization with heat-shocked tumor cells. We have also revealed that the most error-prone part of dendritic cell (DC) generation, i.e., their maturation step, can be omitted if DCs are cultured at a sufficiently high density. Using this optimized protocol, we have achieved a robust IFNγ response to B16F0 antigens, but only within CD4+ T helper cells. A comparison of the repertoires of IFNγ-positive and -negative cells shows a prominent enrichment of certain clones with putative tumor specificity among the IFNγ+ fraction. In summary, our optimized protocol and the data provided here will aid in the acquisition of broad statistical data and the creation of a meaningful database of B16-specific TCRs. Full article
(This article belongs to the Special Issue Molecular Immunology of Solid Tumors)
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Review

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18 pages, 677 KiB  
Review
Future Prospects of Immunotherapy in Non-Small-Cell Lung Cancer Patients: Is There Hope in Other Immune Checkpoints Targeting Molecules?
by Natalia Krzyżanowska, Kamila Wojas-Krawczyk, Janusz Milanowski and Paweł Krawczyk
Int. J. Mol. Sci. 2022, 23(6), 3087; https://doi.org/10.3390/ijms23063087 - 13 Mar 2022
Cited by 5 | Viewed by 2541
Abstract
Currently, one of the leading treatments for non-small-cell lung cancer is immunotherapy involving immune checkpoint inhibitors. These monoclonal antibodies restore the anti-tumour immune response altered by negative immune checkpoint interactions. The most commonly used immunotherapeutics in monotherapy are anti-PD-1 and anti-PD-L1 antibodies. The [...] Read more.
Currently, one of the leading treatments for non-small-cell lung cancer is immunotherapy involving immune checkpoint inhibitors. These monoclonal antibodies restore the anti-tumour immune response altered by negative immune checkpoint interactions. The most commonly used immunotherapeutics in monotherapy are anti-PD-1 and anti-PD-L1 antibodies. The effectiveness of both groups of antibodies has been proven in many clinical trials, which have translated into positive immunotherapeutic registrations for cancer patients worldwide. These antibodies are generally well tolerated, and certain patients achieve durable responses. However, given the resistance of some patients to this form of therapy, along with its other drawbacks, such as adverse events, alternatives are constantly being sought. Specifically, new drugs targeting already known molecules are being tested, and new potential targets are being explored. The aim of this paper is to provide an overview of the latest developments in this area. Full article
(This article belongs to the Special Issue Molecular Immunology of Solid Tumors)
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18 pages, 2392 KiB  
Review
Granzymes: The Molecular Executors of Immune-Mediated Cytotoxicity
by Zachary L. Z. Hay and Jill E. Slansky
Int. J. Mol. Sci. 2022, 23(3), 1833; https://doi.org/10.3390/ijms23031833 - 6 Feb 2022
Cited by 32 | Viewed by 4060
Abstract
Cytotoxic T lymphocytes, differentiated CD8+ T cells, use multiple mechanisms to mediate their function, including release of granules containing perforin and granzymes at target cells. Granzymes are a family of cytotoxic proteases that each act on unique sets of biological substrates within target [...] Read more.
Cytotoxic T lymphocytes, differentiated CD8+ T cells, use multiple mechanisms to mediate their function, including release of granules containing perforin and granzymes at target cells. Granzymes are a family of cytotoxic proteases that each act on unique sets of biological substrates within target cells, usually to induce cell death. Granzymes are differentially expressed within T cells, depending on their environment and activation state, making the granzyme cytotoxic pathway dynamic and responsive to individual circumstances. In this review, we describe what is currently known about granzyme structure, processing, and granzyme-induced cell death in the context of cancer and in some other inflammatory diseases. Full article
(This article belongs to the Special Issue Molecular Immunology of Solid Tumors)
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25 pages, 2559 KiB  
Review
Cancer-Homing CAR-T Cells and Endogenous Immune Population Dynamics
by Emanuela Guerra, Roberta Di Pietro, Mariangela Basile, Marco Trerotola and Saverio Alberti
Int. J. Mol. Sci. 2022, 23(1), 405; https://doi.org/10.3390/ijms23010405 - 30 Dec 2021
Cited by 11 | Viewed by 4684
Abstract
Chimeric antigen receptor (CAR) therapy is based on patient blood-derived T cells and natural killer cells, which are engineered in vitro to recognize a target antigen in cancer cells. Most CAR-T recognize target antigens through immunoglobulin antigen-binding regions. Hence, CAR-T cells do not [...] Read more.
Chimeric antigen receptor (CAR) therapy is based on patient blood-derived T cells and natural killer cells, which are engineered in vitro to recognize a target antigen in cancer cells. Most CAR-T recognize target antigens through immunoglobulin antigen-binding regions. Hence, CAR-T cells do not require the major histocompatibility complex presentation of a target peptide. CAR-T therapy has been tremendously successful in the treatment of leukemias. On the other hand, the clinical efficacy of CAR-T cells is rarely detected against solid tumors. CAR-T-cell therapy of cancer faces many hurdles, starting from the administration of engineered cells, wherein CAR-T cells must encounter the correct chemotactic signals to traffic to the tumor in sufficient numbers. Additional obstacles arise from the hostile environment that cancers provide to CAR-T cells. Intense efforts have gone into tackling these pitfalls. However, we argue that some CAR-engineering strategies may risk missing the bigger picture, i.e., that a successful CAR-T-cell therapy must efficiently intertwine with the complex and heterogeneous responses that the body has already mounted against the tumor. Recent findings lend support to this model. Full article
(This article belongs to the Special Issue Molecular Immunology of Solid Tumors)
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