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

Deadline for manuscript submissions: closed (31 May 2024) | Viewed by 24687

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Special Issue Editors

Dr. Deepak Parashar

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Guest Editor

Division of Hematology & Oncology, Department of Medicine, Medical College of Wisconsin, Milwaukee, WI 53226, USA
Interests: animal health; diagnosis; immunology; parasitology; animal nutrition
Special Issues, Collections and Topics in MDPI journals

Dr. Vivek K. Kashyap

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Guest Editor

Department of Immunology and Microbiology, South Texas Center of Excellence in Cancer Research, School of Medicine, University of Texas Rio Grande Valley, Edinburg, TX, USA
Interests: basic mechanisms of cancer progression, health disparities, pre-clinical drug development; miRNA; lncRNAs; snoRNAs; nano-technology therapies; antibody-drug conjugates, and exosome-mediated drug delivery
Special Issues, Collections and Topics in MDPI journals

Dr. Subhash Tripathi

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Seattle Children’s Research Institute, Seattle, CA, USA
Interests: cancer immunology; inflammation and autoimmunity; molecular immunology; developmental immunology; gene editing and cell therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chronic inflammation plays a significant role in cancer initiation, progression, metastasis, and chemoresistance. Additionally, cancer-related inflammation is the seventh hallmark of cancer and is associated with genetic instability. Genomic and epigenomic mechanisms are essential to establishing cellular programs in cancer and immune cells. The dysregulation of these mechanisms contributes to tumor growth. Transcriptional and epigenetic changes during inflammatory conditions have revealed histone modifications and transcriptional signatures that define dysregulation of cellular function in cancer and immune cells. Eventually, discovering a core set of regulators, such as transcription factors, epigenetic regulatory molecules, and signaling molecules, that can regulate functions in these cells may be sufficient to help reprogram terminally differentiated immune cells. Such findings are certainly having an impact on immune cell-based therapies.

Recent advances in cancer and immune cell genomics and immune cell engineering have therapeutic implications and provide discourse on the challenges, perspectives, and outstanding questions for the emerging role of transcriptional, epigenetic, and metabolic regulation in cancer and immunity.

This Special Issue will highlight the latest experimental advances and technical developments in genomics and epigenomics, gene editing, gene delivery, and therapeutic approaches for studying immune regulation in immune-mediated diseases, including autoimmunity and cancer. The goal is to cover this broad field through a series of high-quality, multidisciplinary research articles discussing overlapping subjects in transcriptional and epigenetic regulation of inflammation during cancer and immunity. We will consider original research, methodology, review articles, and short reports.

Manuscript submissions presenting outstanding contributions to cancer and immunity fields, including, but not limited to, the following topics:

Inflammation in cancer immunity;
Transcriptional and epigenetic regulations in cancer cells and immune cell differentiation and development;
Transcriptomics and epigenomics of immune-mediated diseases;
Immunometabolism;
Pharmacogenomic of diseases;
Integration of Bioinformatics Data.

Dr. Deepak Parashar
Dr. Vivek K. Kashyap
Dr. Subhash Tripathi
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 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

inflammation
cancer immunity
transcriptomics
epigenomics
immunometabolism
pharmacogenomic
bioinformatics data
immunopharmacogenomics

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Published Papers (11 papers)

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Research

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19 pages, 2065 KiB

Open AccessArticle

Plasma IL-1 and IL-6 Family Cytokines with Soluble Receptor Levels at Diagnosis in Head and Neck Squamous Cell Carcinoma: High Levels Predict Decreased Five-Year Disease-Specific and Overall Survival

by Helene Hersvik Aarstad, Svein Erik Emblem Moe, Stein Lybak, Øystein Bruserud, Tor Henrik Anderson Tvedt and Hans Jørgen Aarstad

Cancers 2024, 16(8), 1484; https://doi.org/10.3390/cancers16081484 - 12 Apr 2024

Viewed by 1319

Abstract

Activation of the acute-phase cascade (APC) has been correlated with outcomes in various cancers, including head and neck squamous cell carcinoma (HNSCC). Primary drivers of the APC are the cytokines within the interleukin-6 (IL-6) and IL-1 families. Plasma levels of IL-6 family cytokines/soluble receptors (IL-6, IL-27, IL-31, OSM, CNTF, soluble (s-)gp130, s-IL-6Rα) and IL-1 family members (IL-1RA, s-IL-33Rα) were determined at diagnosis for 87 human papillomavirus (HPV)-negative (−) HNSCC patients. We then studied the 5-year Disease-Specific Survival (DSS) and Overall Survival (OS). Increased plasma levels of IL-6 (p < 0.001/p < 0.001) (DSS/OS), IL-31 (p = 0.044/p = 0.07), IL-1RA (p = 0.004/p = 0.035), soluble (s)-IL-6Rα p = 0.022/p = 0.035), and s-gp130 (p = 0.007/p = 0.003) at diagnosis were predictors of both OS and DSS from HPV(−) HNSCC patients. The cytokine DSS/OS predictions were associated with TNM stage and smoking history, whereas the soluble receptors IL-6Rα, gp130, and IL33Rα more uniquely predicted DSS/OS. Clinically, IL-6 levels above 2.5 pg/mL yielded 75% specificity and 70% sensitivity for DSS. In conclusion, high plasma levels of IL-6, IL-31, and IL-1RA, as well as the soluble receptors IL-6Rα, gp130, and IL33Rα, predicted clinical outcome. This shows their potential as candidates for both general therapy and immune therapy stratification, as well as being future platforms for the development of new immunotherapy. Full article

(This article belongs to the Special Issue Inflammation, Immunity, and Cancer Progression)

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15 pages, 661 KiB

Open AccessArticle

The Prognostic Value of the Novel Global Immune-Nutrition-Inflammation Index (GINI) in Stage IIIC Non-Small Cell Lung Cancer Patients Treated with Concurrent Chemoradiotherapy

by Erkan Topkan, Ugur Selek, Berrin Pehlivan, Ahmet Kucuk, Duriye Ozturk, Beyza Sirin Ozdemir, Ali Ayberk Besen and Huseyin Mertsoylu

Cancers 2023, 15(18), 4512; https://doi.org/10.3390/cancers15184512 - 11 Sep 2023

Cited by 3 | Viewed by 1219

Abstract

Background: We sought to determine the prognostic value of the newly developed Global Immune-Nutrition-Inflammation Index (GINI) in patients with stage IIIC non-small cell lung cancer (NSCLC) who underwent definitive concurrent chemoradiotherapy (CCRT). Methods: This study was conducted on a cohort of 802 newly diagnosed stage IIIC NSCLC patients who underwent CCRT. The novel GINI created first here was defined as follows: GINI = [C-reactive protein × Platelets × Monocytes × Neutrophils] ÷ [Albumin × Lymphocytes]. The receiver operating characteristic (ROC) curve analysis was used to determine the optimal pre-CCRT GINI cut-off value that substantially interacts with the locoregional progression-free (LRPFS), progression-free (PFS), and overall survival (OS). Results: The optimal pre-CCRT GINI cutoff was 1562 (AUC: 76.1%; sensitivity: 72.4%; specificity: 68.2%; Youden index: 0.406). Patients presenting with a GINI ≥ 1562 had substantially shorter median LRPFS (13.3 vs. 18.4 months; p < 0.001), PFS (10.2 vs. 14.3 months; p < 0.001), and OS (19.1 vs. 37.8 months; p < 0.001) durations than those with a GINI < 1562. Results of the multivariate analysis revealed that the pre-CCRT GINI ≥ 1562 (vs. <1562), T4 tumor (vs. T3), and receiving only 1 cycle of concurrent chemotherapy (vs. 2–3 cycles) were the factors independently associated with poorer LRPS (p < 0.05 for each), PFS (p < 0.05 for each), and OS (p < 0.05 for each). Conclusion: The newly developed GINI index efficiently divided the stage IIIC NSCLSC patients into two subgroups with substantially different median and long-term survival outcomes. Full article

(This article belongs to the Special Issue Inflammation, Immunity, and Cancer Progression)

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20 pages, 3931 KiB

Open AccessArticle

Contribution of Mesenchymal Stem Cells from Obese Adipose Tissue to PD-L1 Over-Expression and Breast Cancer Progression through Pathogenic Th17 Cell Activation

by Ferdinand Blangero, Maud Robert, Thomas Andraud, Charles Dumontet, Hubert Vidal and Assia Eljaafari

Cancers 2023, 15(11), 2963; https://doi.org/10.3390/cancers15112963 - 29 May 2023

Viewed by 1799

Abstract

Background: Obesity is a well-known risk factor for cancer. We have previously reported the role of adipose-tissue-derived mesenchymal stem cells from obese individuals (ob-ASC) in the promotion of pathogenic Th17 cells and immune check point (ICP) upregulation. Thus, we postulated herein that this mechanism could contribute to breast cancer (BC) aggressiveness. Methods: Conditioning medium (CM) from mitogen-activated ob-ASC and immune cell co-cultures were added to two human breast cancer cell line (BCCL) cultures. Expressions of pro-inflammatory cytokines, angiogenesis markers, metalloproteinases, and PD-L1 (a major ICP) were measured at the mRNA and/or protein levels. BCCL migration was explored in wound healing assays. Anti-cytokine neutralizing antibodies (Ab) were added to co-cultures. Results: CM from ob-ASC/MNC co-cultures increased IL-1β, IL-8, IL-6, VEGF-A, MMP-9, and PD-L1 expressions in both BCCLs and accelerated their migration. The use of Abs demonstrated differential effects for IL-17A and IFNγ on BCCL pro-inflammatory cytokine over-expression or PD-L1 upregulation, respectively, but potentiating effects on BCCL migration. Finally, co-cultures with ob-ASC, but not lean ASC, enhanced PD-L1 expression. Conclusions: Our results demonstrate increased inflammation and ICP markers and accelerated BCCL migration following the activation of pathogenic Th17 cells by ob-ASC, which could represent a new mechanism linking obesity with BC progression. Full article

(This article belongs to the Special Issue Inflammation, Immunity, and Cancer Progression)

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16 pages, 3315 KiB

Open AccessArticle

Complement Activation and Up-Regulated Expression of Anaphylatoxin C3a/C3aR in Glioblastoma: Deciphering the Links with TGF-β and VEGF

by Franck Ah-Pine, Axelle Malaterre-Septembre, Yosra Bedoui, Mohamed Khettab, James W. Neal, Sébastien Freppel and Philippe Gasque

Cancers 2023, 15(9), 2647; https://doi.org/10.3390/cancers15092647 - 7 May 2023

Cited by 6 | Viewed by 3099

Abstract

The complement (C) innate immune system has been shown to be activated in the tumor microenvironment of various cancers. The C may support tumor growth by modulating the immune response and promoting angiogenesis through the actions of C anaphylatoxins (e.g., C5a, C3a). The C has important double-edged sword functions in the brain, but little is known about its role in brain tumors. Hence, we analyzed the distribution and the regulated expression of C3a and its receptor C3aR in various primary and secondary brain tumors. We found that C3aR was dramatically upregulated in Grade 4 diffuse gliomas, i.e., glioblastoma multiforme, IDH-wildtype (GBM) and astrocytoma, IDH-mutant, Grade 4, and was much less expressed in other brain tumors. C3aR was observed in tumor-associated macrophages (TAM) expressing CD68, CD18, CD163, and the proangiogenic VEGF. Robust levels of C3a were detected in the parenchyma of GBM as a possible result of Bb-dependent C activation of the alternative C pathway. Interestingly, in vitro models identified TGF-β1 as one of the most potent growth factors that upregulate VEGF, C3, and C3aR in TAM (PMA-differentiated THP1) cell lines. Further studies should help to delineate the functions of C3a/C3aR on TAMs that promote chemotaxis/angiogenesis in gliomas and to explore the therapeutic applications of C3aR antagonists for brain tumors. Full article

(This article belongs to the Special Issue Inflammation, Immunity, and Cancer Progression)

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10 pages, 682 KiB

Open AccessArticle

Inflammation and Prostate Cancer: Pathological Analysis from Pros-IT CNR 2

by Francesco Sessa, Rossella Nicoletti, Cosimo De Nunzio, Angelo Porreca, Stefano Maria Magrini, Vincenzo Mirone, Andrea Tubaro, Sergio Serni, Paolo Gontero, Marianna Noale, Stefania Maggi, Mauro Gacci and on behalf of the Pros-IT2 Study Group

Cancers 2023, 15(3), 630; https://doi.org/10.3390/cancers15030630 - 19 Jan 2023

Cited by 2 | Viewed by 1971

Abstract

Background: Extensive research effort has been devoted to investigating the link between inflammation and PCa. However, this relationship remains unclear and controversial. The aim of our multi-center study was to investigate this association by histologically evaluating the distribution of PI and PCA in prostate biopsy cores from patients of eight referral centers in Italy. Results: We evaluated 2220 cores from 197 patients; all the frustules were re-evaluated by dedicated pathologists retrospectively. Pathologists assigned IRANI scores and determined the positions of PIs; pathologists also re-evaluated the presence of PCa and relative ISUP grade. PCa was recorded in 749/2220 (33.7%). We divided this sample into a PCa PI group (634/749 cores [84.7%]) and a non-PCa + PI group (1157/1471 cores [78.7%]). We observed a statistically significant difference in the presence of inflammation among cores with cancer (p < 0.01). Moreover, periglandular inflammation was higher in the cores with neoplasia, while stromal inflammation was higher in cores without neoplasia (38.5% vs. 31.1% and 55.4% vs. 63.5% p < 0.01). Conclusions: In our experience, there is evidence of an association between PI and PCa at a tissue level. Further studies are needed to confirm our findings and to identify patients who might benefit from target therapies to prevent PCa occurrence and/or progression. Full article

(This article belongs to the Special Issue Inflammation, Immunity, and Cancer Progression)

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22 pages, 6109 KiB

Open AccessArticle

Caerin 1.1/1.9 Enhances Antitumour Immunity by Activating the IFN-α Response Signalling Pathway of Tumour Macrophages

by Xiaodan Yang, Xiaosong Liu, Junjie Li, Pingping Zhang, Hejie Li, Guoqiang Chen, Wei Zhang, Tianfang Wang, Ian Frazer and Guoying Ni

Cancers 2022, 14(23), 5785; https://doi.org/10.3390/cancers14235785 - 24 Nov 2022

Cited by 5 | Viewed by 2071

Abstract

Macrophages are one of the essential components of the tumour microenvironment (TME) of many cancers and show complex heterogeneity and functions. More recent research has been focusing on the characterisation of tumour-associated macrophages (TAMs). Previously, our study demonstrated that caerin 1.1/1.9 peptides significantly improve the therapeutic efficacy of combined specific immunotherapy and immune checkpoint blockade in a murine transplantable tumour model (TC-1). In this study, the mice inoculated with TC-1 tumour were immunised differently. The TAMs were isolated using flow cytometry and characterised by cytokine ELISA. The survival rates of mice with different treatments containing caerin 1.1/19 were assessed comparatively, including those with/without macrophage depletion. The single-cell RNA sequencing (scRNA-seq) data of previous studies were integrated to further reveal the functions of TAMs with the treatments containing caerin 1.1/1.9. As a comparison, the TAMs of stage I and II cervical cancer patients were analysed using scRNA-seq analysis. We demonstrate that caerin induced tumour clearance is associated with infiltration of tumours by IL-12 secreting Ly6C+F4/80+ macrophages exhibiting enhanced IFN-α response signalling, renders animals resistant to further tumour challenge, which is lost after macrophage depletion. Our results indicate that caerin 1.1/1.9 treatment has great potential in improving current immunotherapy efficacy. Full article

(This article belongs to the Special Issue Inflammation, Immunity, and Cancer Progression)

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23 pages, 1243 KiB

Open AccessReview

The Various Roles of PEDF in Cancer

by Mitra Elmi, Joshua H. Dass and Crispin R. Dass

Cancers 2024, 16(3), 510; https://doi.org/10.3390/cancers16030510 - 24 Jan 2024

Cited by 1 | Viewed by 1538

Abstract

Pigment epithelium-derived factor (PEDF) is a natural immunomodulator, anti-inflammatory, anti-angiogenic, anti-tumour growth and anti-metastasis factor, which can enhance tumour response to PEDF but can also conversely have pro-cancerous effects. Inflammation is a major cause of cancer, and it has been proven that PEDF has anti-inflammatory properties. PEDF’s functional activity can be investigated through measuring metastatic and metabolic biomarkers that will be discussed in this review. Full article

(This article belongs to the Special Issue Inflammation, Immunity, and Cancer Progression)

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38 pages, 3975 KiB

Open AccessReview

Inflammation-Associated Cytotoxic Agents in Tumorigenesis

by Jürgen Arnhold

Cancers 2024, 16(1), 81; https://doi.org/10.3390/cancers16010081 - 22 Dec 2023

Cited by 1 | Viewed by 1466

Abstract

Chronic inflammatory processes are related to all stages of tumorigenesis. As inflammation is closely associated with the activation and release of different cytotoxic agents, the interplay between cytotoxic agents and antagonizing principles is highlighted in this review to address the question of how tumor cells overcome the enhanced values of cytotoxic agents in tumors. In tumor cells, the enhanced formation of mitochondrial-derived reactive species and elevated values of iron ions and free heme are antagonized by an overexpression of enzymes and proteins, contributing to the antioxidative defense and maintenance of redox homeostasis. Through these mechanisms, tumor cells can even survive additional stress caused by radio- and chemotherapy. Through the secretion of active agents from tumor cells, immune cells are suppressed in the tumor microenvironment and an enhanced formation of extracellular matrix components is induced. Different oxidant- and protease-based cytotoxic agents are involved in tumor-mediated immunosuppression, tumor growth, tumor cell invasion, and metastasis. Considering the special metabolic conditions in tumors, the main focus here was directed on the disturbed balance between the cytotoxic agents and protective mechanisms in late-stage tumors. This knowledge is mandatory for the implementation of novel anti-cancerous therapeutic approaches. Full article

(This article belongs to the Special Issue Inflammation, Immunity, and Cancer Progression)

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20 pages, 2725 KiB

Open AccessEditor’s ChoiceReview

Targeting Proteasomes and the MHC Class I Antigen Presentation Machinery to Treat Cancer, Infections and Age-Related Diseases

by Priyanka S. Rana, James J. Ignatz-Hoover and James J. Driscoll

Cancers 2023, 15(23), 5632; https://doi.org/10.3390/cancers15235632 - 29 Nov 2023

Cited by 2 | Viewed by 3005

Abstract

The majority of T-cell responses involve proteasome-dependent protein degradation and the downstream presentation of oligopeptide products complexed with major histocompatibility complex (MHC) class I (MHC-I) molecules to peptide-restricted CD8⁺ T-cells. However, evasion of host immunity is a cancer hallmark that is achieved by disruption of host antigen processing and presentation machinery (APM). Consequently, mechanisms of immune evasion promote cancer growth and survival as well as de novo and acquired resistance to immunotherapy. A multitude of cell signaling pathways modulate the APM and MHC-I-dependent antigen presentation. Pharmacologics that specifically target and modulate proteasome structure and activity represent a novel emerging strategy to improve the treatment of cancers and other diseases characterized by aberrant protein accumulation. FDA-approved pharmacologics that selectively activate proteasomes and/or immunoproteasomes can be repositioned to overcome the current bottlenecks that hinder drug development to enhance antigen presentation, modulate the immunopeptidome, and enhance the cytotoxic activity of endogenous or engineered T-cells. Strategies to enhance antigen presentation may also improve the antitumor activity of T-cell immunotherapies, checkpoint inhibitors, and cancer vaccines. Proteasomes represent actionable therapeutic targets to treat difficult-to-treat infectious processes and neurodegenerative diseases that are characterized by the unwanted accrual of insoluble, deleterious, and potentially toxic proteins. Taken together, we highlight the breadth and magnitude of the proteasome and the immense potential to amplify and unmask the immunopeptidomic landscape to improve the treatment of a spectrum of human diseases. Full article

(This article belongs to the Special Issue Inflammation, Immunity, and Cancer Progression)

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15 pages, 1196 KiB

Open AccessReview

Role of Oxidative Stress in Metabolic Reprogramming of Brain Cancer

by Kirti Agrawal, Shailendra Asthana and Dhruv Kumar

Cancers 2023, 15(20), 4920; https://doi.org/10.3390/cancers15204920 - 10 Oct 2023

Cited by 8 | Viewed by 2480

Abstract

Brain cancer is known as one of the deadliest cancers globally. One of the causative factors is the imbalance between oxidative and antioxidant activities in the body, which is referred to as oxidative stress (OS). As part of regular metabolism, oxygen is reduced by electrons, resulting in the creation of numerous reactive oxygen species (ROS). Inflammation is intricately associated with the generation of OS, leading to the increased production and accumulation of reactive oxygen and nitrogen species (RONS). Glioma stands out as one of the most common malignant tumors affecting the central nervous system (CNS), characterized by changes in the redox balance. Brain cancer cells exhibit inherent resistance to most conventional treatments, primarily due to the distinctive tumor microenvironment. Oxidative stress (OS) plays a crucial role in the development of various brain-related malignancies, such as glioblastoma multiforme (GBM) and medulloblastoma, where OS significantly disrupts the normal homeostasis of the brain. In this review, we provide in-depth descriptions of prospective targets and therapeutics, along with an assessment of OS and its impact on brain cancer metabolism. We also discuss targeted therapies. Full article

(This article belongs to the Special Issue Inflammation, Immunity, and Cancer Progression)

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23 pages, 2863 KiB

Open AccessReview

Decoding Immune Signature to Detect the Risk for Early-Stage HCC Recurrence

by Aswathy R. Devan, Bhagyalakshmi Nair, Manu Kanjoormana Aryan, Vijayastelar B. Liju, Joel Joy Koshy, Bijo Mathew, Arun Valsan, Hoon Kim and Lekshmi R. Nath

Cancers 2023, 15(10), 2729; https://doi.org/10.3390/cancers15102729 - 12 May 2023

Cited by 2 | Viewed by 2829

Abstract

Hepatocellular carcinoma (HCC) is often recognized as an inflammation-linked cancer, which possesses an immunosuppressive tumor microenvironment. Curative treatments such as surgical resection, liver transplantation, and percutaneous ablation are mainly applicable in the early stage and demonstrate significant improvement of survival rate in most patients. However, 70–80% of patients report HCC recurrence within 5 years of curative treatment, representing an important clinical issue. However, there is no effective recurrence marker after surgical and locoregional therapies, thus, tumor size, number, and histological features such as cancer cell differentiation are often considered as risk factors for HCC recurrence. Host immunity plays a critical role in regulating carcinogenesis, and the immune microenvironment characterized by its composition, functional status, and density undergoes significant alterations in each stage of cancer progression. Recent studies reported that analysis of immune contexture could yield valuable information regarding the treatment response, prognosis and recurrence. This review emphasizes the prognostic value of tumors associated with immune factors in HCC recurrence after curative treatment. In particular, we review the immune landscape and immunological factors contributing to early-stage HCC recurrence, and discuss the immunotherapeutic interventions to prevent tumor recurrence following curative treatments. Full article

(This article belongs to the Special Issue Inflammation, Immunity, and Cancer Progression)

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