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Cancers
Special Issues
Molecular Immunotherapy of Solid Tumors
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Molecular Immunotherapy of Solid Tumors

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

Deadline for manuscript submissions: closed (15 August 2023) | Viewed by 5678

Special Issue Editor

Dr. Raheleh Roudi

E-Mail Website
Guest Editor
Molecular Imaging Program at Stanford, Department of Radiology, Stanford University, Stanford, CA 94305, USA
Interests: molecular oncology; immunotherapy; solid tumors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer immunotherapy is transforming multidisciplinary cancer care and opening new therapeutic avenues. The current types of immunotherapies that have been explored include monoclonal antibodies (mAb), immune-checkpoint inhibitors (ICIs), oncolytic viral platforms (OV), cancer vaccines, adoptive cell therapy (ACT), and various combinatorial approaches. The purpose of this Special Issue is to define the role of molecular immunotherapies in solid tumors, including (1) mAb in cancer treatment; (2) the contribution of ICIs in the progress of cancer therapies; (3) cancer vaccines in solid tumors; (4) predictive biomarkers for checkpoint-inhibitor-based immunotherapy; (5) drug resistance and immunotherapies; and (6) the combination of immunotherapies with conventional cancer treatments. This Special Issue welcomes both original research articles and reviews.

Dr. Raheleh Roudi
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

  • immunotherapy
  • immune-checkpoint inhibitors
  • dendritic cell/cytokine-induced killer-cell-based immunotherapy
  • CTLA-4 inhibitors
  • PD-1/ PD-L1 inhibitors
  • LAG-3 inhibitors
  • solid tumors
  • adverse events
  • randomized trials
  • survival

Published Papers (3 papers)

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Research

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15 pages, 2508 KiB  
Article
Directed Evolution of Seneca Valley Virus in Tumorsphere and Monolayer Cell Cultures of a Small-Cell Lung Cancer Model
by Shakeel Waqqar, Kai Lee, Blair Lawley, Timothy Bilton, Miguel E. Quiñones-Mateu, Mihnea Bostina and Laura N. Burga
Cancers 2023, 15(9), 2541; https://doi.org/10.3390/cancers15092541 - 28 Apr 2023
Cited by 1 | Viewed by 1672
Abstract
The Seneca Valley virus (SVV) is an oncolytic virus from the picornavirus family, characterized by a 7.3-kilobase RNA genome encoding for all the structural and functional viral proteins. Directed evolution by serial passaging has been employed for oncolytic virus adaptation to increase the [...] Read more.
The Seneca Valley virus (SVV) is an oncolytic virus from the picornavirus family, characterized by a 7.3-kilobase RNA genome encoding for all the structural and functional viral proteins. Directed evolution by serial passaging has been employed for oncolytic virus adaptation to increase the killing efficacy towards certain types of tumors. We propagated the SVV in a small-cell lung cancer model under two culture conditions: conventional cell monolayer and tumorspheres, with the latter resembling more closely the cellular structure of the tumor of origin. We observed an increase of the virus-killing efficacy after ten passages in the tumorspheres. Deep sequencing analyses showed genomic changes in two SVV populations comprising 150 single nucleotides variants and 72 amino acid substitutions. Major differences observed in the tumorsphere-passaged virus population, compared to the cell monolayer, were identified in the conserved structural protein VP2 and in the highly variable P2 region, suggesting that the increase in the ability of the SVV to kill cells over time in the tumorspheres is acquired by capsid conservation and positively selecting mutations to counter the host innate immune responses. Full article
(This article belongs to the Special Issue Molecular Immunotherapy of Solid Tumors)
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24 pages, 7156 KiB  
Article
LncRNA ERVH48-1 Contributes to the Drug Resistance of Prostate Cancer and Proliferation through Sponging of miR-4784 to the Activation of the Wnt/β-Catenin Pathway
by Binshen Chen, Kai Xu, Yiming Zhang, Peng Xu, Chaoming Li, Jun Liu and Yawen Xu
Cancers 2023, 15(6), 1902; https://doi.org/10.3390/cancers15061902 - 22 Mar 2023
Cited by 2 | Viewed by 1758
Abstract
Long noncoding RNAs (LncRNAs) are very important in the way that docetaxel resistance (DR) happens in prostate cancer (PCa) patients. ImmuneScore and StromalScore were calculated using PCa-related expression data from TCGA and the ESTIMATE algorithm. We finally found the DEGs that were related [...] Read more.
Long noncoding RNAs (LncRNAs) are very important in the way that docetaxel resistance (DR) happens in prostate cancer (PCa) patients. ImmuneScore and StromalScore were calculated using PCa-related expression data from TCGA and the ESTIMATE algorithm. We finally found the DEGs that were related to the immune system and the stroma of the patients by making profiles of the DEGs in ImmuneScore and StromalScore. The CancerSubtypes algorithm identified prognosis-related PCa subtypes, and the GSVA assessed their pathway activity. A UniCox regression analysis was used to identify a prognosis-related differential gene set. We then used intersection analysis to identify immunological and prognostic (IP)-related genes (IPGs). The coexpression of long noncoding RNAs (lncRNAs) and IPGs was used to identify IP-related lncRNAs (IPLs). Three methods (SVM-RFE, random forest, and LASSO) were used to find genes that overlap in the GEO database. A gene signature was then validated by building an ROC curve. CIBERSORT technology was used to look at the possibility of a link between the gene signature and immune cells. LncRNA–miRNA pairs and miRNA–mRNA pairs from the miRDB and TargetScan databases were used to construct the ERVH48-1-miR-4784-WNT2B ceRNA regulation network. The concentration of docetaxel elevated the expression of ERVH48-1. Overexpression of ERVH48-1 increased PCa-DR cell proliferation, invasion, and migration while inhibiting apoptosis. ERVH48-1 increased the tumorigenicity of PCa-DR cells in nude mice. ERVH48-1, acting as a ceRNA, targeted miR-4784 to increase WNT2B expression. ICG001 therapy increased Wnt/-catenin signaling activity in PCa-DR cells by inhibiting ERVH48-1. Finally, ERVH48-1 increased docetaxel resistance in a WNT2B-dependent manner via the miR-4784/Wnt/-catenin pathway. Full article
(This article belongs to the Special Issue Molecular Immunotherapy of Solid Tumors)
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Other

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25 pages, 956 KiB  
Systematic Review
Immune Checkpoint Inhibitors Targeting the PD-1/PD-L1 Pathway in Advanced, Recurrent Endometrial Cancer: A Scoping Review with SWOT Analysis
by Racheal Louise Johnson, Subhasheenee Ganesan, Amudha Thangavelu, Georgios Theophilou, Diederick de Jong, Richard Hutson, David Nugent, Timothy Broadhead, Alexandros Laios, Michele Cummings and Nicolas Michel Orsi
Cancers 2023, 15(18), 4632; https://doi.org/10.3390/cancers15184632 - 19 Sep 2023
Cited by 1 | Viewed by 1629
Abstract
Results of recent clinical trials using the immune check point inhibitors (ICI) pembrolizumab or dostarlimab with/without lenvatinib has led to their approval for specific molecular subgroups of advanced recurrent endometrial cancer (EC). Herein, we summarise the clinical data leading to this first tissue-agnostic [...] Read more.
Results of recent clinical trials using the immune check point inhibitors (ICI) pembrolizumab or dostarlimab with/without lenvatinib has led to their approval for specific molecular subgroups of advanced recurrent endometrial cancer (EC). Herein, we summarise the clinical data leading to this first tissue-agnostic approval. As this novel therapy is not yet available in the United Kingdom standard care setting, we explore the strengths, weaknesses, opportunities, and threats (SWOT) of ICI treatment in EC. Major databases were searched focusing on clinical trials using programmed cell death protein 1 (PD-1) and its ligand (PD-L1) ICI which ultimately contributed to anti-PD-1 approval in EC. We performed a data quality assessment, reviewing survival and safety analysis. We included 15 studies involving 1609 EC patients: 458 with mismatch repair deficiency (MMRd)/microsatellite instability-high (MSI-H) status and 1084 with mismatch repair proficiency/microsatellite stable (MMRp/MSS) status. Pembrolizumab/dostarlimab have been approved for MMRd ECs, with the addition of lenvatinib for MMRp cases in the recurrent setting. Future efforts will focus on the pathological assessment of biomarkers to determine molecular phenotypes that correlate with response or resistance to ICI in order to identify patients most likely to benefit from this treatment. Full article
(This article belongs to the Special Issue Molecular Immunotherapy of Solid Tumors)
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