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

Deadline for manuscript submissions: closed (30 September 2021) | Viewed by 44096

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Dr. Claire Pecqueur

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CRCI2NA (Centre de Recherche en Cancérologie et immunologie Intégré- Nantes, Angers), INSERM (Institut National en santé et de la Recherche Medicale), CNRS (Centre National de la Recherche Scientifique), Université de Nantes, 44007 Nantes, France
Interests: tumor metabolism; glioblastoma; microenvironment; cancer stem cells
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Dear Colleagues,

Inflammation is often associated with the development of cancer. Chronic inflammation has been linked to several steps involved in tumorigenesis, including cellular transformation, tumor promotion, survival, proliferation, invasion, angiogenesis, and metastasis. Tumor-extrinsic inflammation can be caused by many factors ranging from infection, chemical or pollutant exposure (Tobacco, alcohol and asbestos) to autoimmune diseases. By contrast, cancer-elicited inflammation can be caused by cancer-initiating mutations leading to the activation of oncogenes or inactivation of tumor suppressors and resulting in the secretion of pro-inflammatory cytokines and chemokines by cancer cells. Importantly, both extrinsic and intrinsic inflammation can result in immunosuppression, thereby promoting tumor development.

In this Special Issue, we would like to shed light on recent findings describing key molecular and cellular pathways linking inflammation and cancer development. To address these topics, we will welcome original publications or state-of the art review on mechanisms linking inflammation and cancer, the inflammatory cells in tumor microenvironment, the key molecular players linking inflammation and cancer, and the therapeutic strategies for prevention and treatment.

Dr. Claire Pecqueur
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

inflammation
tumor microenvironment
immune cells

Published Papers (13 papers)

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20 pages, 11785 KiB

Open AccessArticle

The Immune Microenvironment of Chordomas: An Immunohistochemical Analysis

by Maroa Dridi, Lila Krebs-Drouot, David Meyronet, Jean Marc Dumollard, François Vassal, Emmanuel Jouanneau, Timothée Jacquesson, Cédric Barrey, Sylvain Grange, Jean Boutonnat, Michel Péoc’h and Georgia Karpathiou

Cancers 2021, 13(13), 3335; https://doi.org/10.3390/cancers13133335 - 2 Jul 2021

Cited by 13 | Viewed by 2187

Abstract

Chordomas are rare sarcomas that are usually treated by surgery and/or radiotherapy since these are chemo-resistant tumors, but immunotherapy could be a possible option for chordoma patients. However, few reports investigating the composition of the chordoma immune microenvironment exist. We immunohistochemically studied 81 chordomas regarding their immune microenvironment factors and compared them with clinicopathological data. Macrophages and CD4 cells were the most prominent inflammatory cell populations, followed by CD8 T cells, while CD20 B cells and high endothelial venules (MECA-79+) were less frequently found. PD-L1 (22C3) expression by inflammatory cells was found in 21 (26%) tumors and was associated with a larger tumor size. None of the cases showed the expression of PD-L1 by tumor cells. Survival analysis showed that younger patients had a better overall survival. Considering the immunohistochemical factors studied, higher CD8, the presence of PD-L1+ immune cells, and higher vascular density were adverse prognostic factors, but in multivariate analysis, only PD-L1+ immune cells retained prognostic significance. To conclude, chordoma tumor cells do not express PD-L1, but PD-L1+ immune cells seem to play a negative prognostic role, supporting the need for further studies in this field and the possible beneficial role of immunotherapy in these patients. Full article

(This article belongs to the Special Issue Inflammation and Tumor)

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16 pages, 5684 KiB

Open AccessArticle

TLR4-Mediated Recognition of Mouse Polyomavirus Promotes Cancer-Associated Fibroblast-Like Phenotype and Cell Invasiveness

by Vaclav Janovec, Boris Ryabchenko, Aneta Škarková, Karolína Pokorná, Daniel Rösel, Jan Brábek, Jan Weber, Jitka Forstová, Ivan Hirsch and Sandra Huérfano

Cancers 2021, 13(9), 2076; https://doi.org/10.3390/cancers13092076 - 25 Apr 2021

Cited by 4 | Viewed by 2471

Abstract

The tumorigenic potential of mouse polyomavirus (MPyV) has been studied for decades in cell culture models and has been mainly attributed to nonstructural middle T antigen (MT), which acts as a scaffold signal adaptor, activates Src tyrosine kinases, and possesses transforming ability. We hypothesized that MPyV could also transform mouse cells independent of MT via a Toll-like receptor 4 (TLR4)-mediated inflammatory mechanism. To this end, we investigated the interaction of MPyV with TLR4 in mouse embryonic fibroblasts (MEFs) and 3T6 cells, resulting in secretion of interleukin 6 (IL-6), independent of active viral replication. TLR4 colocalized with MPyV capsid protein VP1 in MEFs. Neither TLR4 activation nor recombinant IL-6 inhibited MPyV replication in MEFs and 3T6 cells. MPyV induced STAT3 phosphorylation through both direct and MT-dependent and indirect and TLR4/IL-6-dependent mechanisms. We demonstrate that uninfected mouse fibroblasts exposed to the cytokine environment from MPyV-infected fibroblasts upregulated the expressions of MCP-1, CCL-5, and α-SMA. Moreover, the cytokine microenvironment increased the invasiveness of MEFs and CT26 carcinoma cells. Collectively, TLR4 recognition of MPyV induces a cytokine environment that promotes the cancer-associated fibroblast (CAF)-like phenotype in noninfected fibroblasts and increases cell invasiveness. Full article

(This article belongs to the Special Issue Inflammation and Tumor)

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14 pages, 1124 KiB

Open AccessArticle

Preoperative Inflammatory Markers as a Predictor of Three-Year Overall Survival in Older Cancer Patients Undergoing Oncologic Surgery

by Baukje Brattinga, Abraham Rutgers, Jacco J. De Haan, Anthony R. Absalom, Hanneke van der Wal-Huisman, Geertruida H. de Bock and Barbara L. van Leeuwen

Cancers 2021, 13(8), 1824; https://doi.org/10.3390/cancers13081824 - 11 Apr 2021

Cited by 8 | Viewed by 2041

Abstract

Oncologic surgery results in substantially higher morbidity and mortality rates in older patients compared to younger patients, yet little is known about the relation between the preoperative inflammatory state and postoperative outcome in the specific group of older cancer patients. The aim of this study was to examine whether preoperative inflammatory markers could be a predictor of overall survival in older patients undergoing elective surgery for a solid malignant tumor. Patients 65 years and older undergoing surgery for a solid malignant tumor were included in a prospective cohort study. Inflammatory markers C-reactive protein (CRP), interleukin-1 beta (IL-1β), IL-6, IL10, IL-12 and tumor necrosis factor-alpha (TNF-α) were measured in plasma samples preoperatively. The main outcome was overall survival three years after surgery. Between 2010 and 2016, 328 patients with a median age of 71.5 years (range 65–89) were included. A significantly higher mortality rate three years after surgery, was found in patients with high preoperative plasma levels of CRP and IL-6 (p = 0.013 and p = 0.046, respectively). In multivariate analysis, corrected for variables such as age, disease stage, frailty, comorbidities, type of surgery and complications, a preoperative plasma level of CRP ≥ 10 mg/L was an independent prognostic factor for inferior overall survival three years after surgery (multivariate hazard ratio 1.50, 95% confidence interval 1.04–2.16, p = 0.031). Also, for the specific group of patients with colorectal cancer, a preoperative plasma level of CRP ≥ 10 mg/L was a prognostic factor for inferior survival three years after surgery (multivariate hazard ratio 2.40, 95% confidence interval 1.20–4.81, p = 0.014). Preoperative elevated plasma level of CRP is an independent unfavorable prognostic factor for overall survival three years after oncologic surgery. This gives more insight into the relationship between inflammation and survival in older cancer patients, and might contribute to risk stratification for poor outcome after surgery in older cancer patients. Full article

(This article belongs to the Special Issue Inflammation and Tumor)

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17 pages, 10521 KiB

Open AccessArticle

Clinical Significance of PDCD4 in Melanoma by Subcellular Expression and in Tumor-Associated Immune Cells

by Thuy T. Tran, Chetan K. Rane, Christopher R. Zito, Sarah A. Weiss, Shlomit Jessel, Liliana Lucca, Benjamin Y. Lu, Victor O. Oria, Adebowale Adeniran, Veronica L. Chiang, Sacit Bulent Omay, David A. Hafler, Harriet M. Kluger and Lucia B. Jilaveanu

Cancers 2021, 13(5), 1049; https://doi.org/10.3390/cancers13051049 - 2 Mar 2021

Cited by 9 | Viewed by 3363

Abstract

Little is known about the subcellular localization and function of programmed cell death 4 (PDCD4) in melanoma. Our past studies suggest PDCD4 interacts with Pleckstrin Homology Domain Containing A5 (PLEKHA5) to influence melanoma brain metastasis outcomes, as high intracranial PDCD4 expression leads to improved survival. We aimed to define the subcellular distribution of PDCD4 in melanoma and in the tumor microenvironment during neoplastic progression and its impact on clinical outcomes. We analyzed multiple tissue microarrays with well-annotated clinicopathological variables using quantitative immunofluorescence and evaluated single-cell RNA-sequencing on a brain metastasis sample to characterize PDCD4+ immune cell subsets. We demonstrate differences in PDCD4 expression during neoplastic progression, with high tumor and stromal PDCD4 levels associated with improved survival in primary melanomas and in intracranial metastases, but not in extracranial metastatic disease. While the expression of PDCD4 is well-documented on CD8+ T cells and natural killer cells, we show that it is also found on B cells and mast cells. PDCD4 expression in the tumor microenvironment is associated with increased immune cell infiltration. Further studies are needed to define the interaction of PDCD4 and PLEKHA5 and to evaluate the utility of this pathway as a therapeutic target in melanoma brain metastasis. Full article

(This article belongs to the Special Issue Inflammation and Tumor)

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21 pages, 3615 KiB

Open AccessArticle

The Caspase-1/IL-18 Axis of the Inflammasome in Tumor Cells: A Modulator of the Th1/Tc1 Response of Tumor-Infiltrating T Lymphocytes in Colorectal Cancer

by Linda Bilonda Mutala, Cécile Deleine, Matilde Karakachoff, Delphine Dansette, Kathleen Ducoin, Romain Oger, Olivia Rousseau, Juliette Podevin, Emilie Duchalais, Pierre Fourquier, Wassila El Alami Thomas, Pierre-Antoine Gourraud, Jaafar Bennouna, Camille Brochier, Nadine Gervois, Céline Bossard and Anne Jarry

Cancers 2021, 13(2), 189; https://doi.org/10.3390/cancers13020189 - 7 Jan 2021

Cited by 10 | Viewed by 3414

Abstract

In colorectal cancer (CRC), a high density of T lymphocytes represents a strong prognostic marker in subtypes of CRC. Optimized immunotherapy strategies to boost this T-cell response are still needed. A good candidate is the inflammasome pathway, an emerging player in cancer immunology that bridges innate and adaptive immunity. Its effector protein caspase-1 matures IL-18 that can promote a T-helper/cytotoxic (Th1/Tc1) response. It is still unknown whether tumor cells from CRC possess a functional caspase-1/IL-18 axis that could modulate the Th1/Tc1 response. We used two independent cohorts of CRC patients to assess IL-18 and caspase-1 expression by tumor cells in relation to the density of TILs and the microsatellite status of CRC. Functional and multiparametric approaches at the protein and mRNA levels were performed on an ex vivo CRC explant culture model. We show that, in the majority of CRCs, tumor cells display an activated and functional caspase-1/IL-18 axis that contributes to drive a Th1/Tc1 response elicited by TILs expressing IL-18Rα. Furthermore, unsupervised clustering identified three clusters of CRCs according to the caspase-1/IL-18/TIL density/interferon gamma (IFNγ) axis and microsatellite status. Together, our results strongly suggest that targeting the caspase-1/IL-18 axis can improve the anti-tumor immune response in subgroups of CRC. Full article

(This article belongs to the Special Issue Inflammation and Tumor)

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18 pages, 11714 KiB

Open AccessArticle

Secreted Frizzled-Related Protein 1 as a Biomarker against Incomplete Age-Related Lobular Involution and Microcalcifications’ Development

by Alisson Clemenceau, Mirette Hanna, Kaoutar Ennour-Idrissi, Anna Burguin, Caroline Diorio and Francine Durocher

Cancers 2020, 12(9), 2693; https://doi.org/10.3390/cancers12092693 - 21 Sep 2020

Cited by 3 | Viewed by 2367

Abstract

As a downregulator of the Wnt signaling pathway, SFRP1 is involved in several components of the age-related lobular involution process such as inflammation, apoptosis, and adipogenesis. Because microcalcifications are associated with inflammation, we aimed to demystify the cross talk between SFRP1, inflammatory markers, and microcalcifications by assessing SFRP1 expression (immunohistochemistry) in a cohort of 162 women with different degrees of lobular involution. SFRP1 expression was inversely associated with the degree of lobular involution (OR = 0.84; p-value < 0.01). SFRP1 expression, age at mastectomy, and waist circumference taken together predicted the degree of lobular involution (AUC = 78.1). This predictive model was best in patients with microcalcifications (AUC = 81.1) and in parous women (AUC = 87.8). SFRP1 expression was correlated with leptin (rho = 0.32), TNF-α (rho = 0.21), and IL-6 (rho = 0.21) expression by epithelial cells (all p-values <0.001). SFRP1 expression was lower in nulliparous women with involuted breast tissue compared with parous women with involuted breast tissue (Δmean = −2.31; p-value < 0.01) and was higher in nulliparous women with microcalcifications compared with nulliparous women without microcalcifications (Δmean = 2.4; p-value < 0.05). In this study, we highlighted two SFRP1-based predictive models for incomplete lobular involution and the development of microcalcifications and identified two distinct inflammatory profiles associated with age-related lobular involution in parous and nulliparous women. Full article

(This article belongs to the Special Issue Inflammation and Tumor)

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Review

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18 pages, 1079 KiB

Open AccessReview

Does Inflammation Contribute to Cancer Incidence and Mortality during Aging? A Conceptual Review

by Florent Guerville, Isabelle Bourdel-Marchasson, Julie Déchanet-Merville, Isabelle Pellegrin, Pierre Soubeyran, Victor Appay and Maël Lemoine

Cancers 2022, 14(7), 1622; https://doi.org/10.3390/cancers14071622 - 23 Mar 2022

Cited by 6 | Viewed by 2497

Abstract

Aging is associated with chronic low-grade inflammation, cancer incidence and mortality. As inflammation contributes to cancer initiation and progression, one could hypothesize that age-associated chronic low-grade inflammation contributes to the increase in cancer incidence and/or mortality observed during aging. Here, we review the evidence supporting this hypothesis: (1) epidemiological associations between biomarkers of systemic inflammation and cancer incidence and mortality in older people, (2) therapeutic clues suggesting that targeting inflammation could reduce cancer incidence and mortality and (3) experimental evidence from animal models highlighting inflammation as a link between various mechanisms of aging and cancer initiation and progression. Despite a large body of literature linking aging, inflammation and cancer, convincing evidence for the clear implication of specific inflammatory pathways explaining cancer incidence or mortality during aging is still lacking. Further dedicated research is needed to fill these gaps in evidence and pave the way for the development of applications in clinical care. Full article

(This article belongs to the Special Issue Inflammation and Tumor)

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17 pages, 1885 KiB

Open AccessReview

The Pseudokinase TRIB1 in Immune Cells and Associated Disorders

by Richard Danger, Yodit Feseha and Sophie Brouard

Cancers 2022, 14(4), 1011; https://doi.org/10.3390/cancers14041011 - 17 Feb 2022

Cited by 5 | Viewed by 2775

Abstract

Research advances in Tribbles homolog (TRIB) genes have established the consensus that this protein family plays roles in diverse biological conditions and regulates intracellular signaling networks and several human diseases. In this review, we focus on one member of the family, TRIB1, and its role at the crossroads of immune signaling. TRIB1 directly interacts with transcription factors such as FOXP3 and C/EBPα, with several signaling molecules such as MEK1 and MALT1 and directly acts on key cell signaling pathways such as the MAPK and NF-κB pathways. Altogether, these interactions emphasize that TRIB1 is at the center of major cell signaling pathways while TRIB1 has cell-specific roles, potentially depending on the expressing cells and binding partners. In this review, we describe its roles in immune cells and highlight the interacting partners explaining these functions which suggests TRIB1 as a precise mediator of cellular homeostasis as well as in different cancers and immune-related disorders. Full article

(This article belongs to the Special Issue Inflammation and Tumor)

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28 pages, 21119 KiB

Open AccessReview

Targeting Metabolism to Control Immune Responses in Cancer and Improve Checkpoint Blockade Immunotherapy

by Angèle Luby and Marie-Clotilde Alves-Guerra

Cancers 2021, 13(23), 5912; https://doi.org/10.3390/cancers13235912 - 24 Nov 2021

Cited by 13 | Viewed by 3250

Abstract

Over the past decade, advances in cancer immunotherapy through PD1–PDL1 and CTLA4 immune checkpoint blockade have revolutionized the management of cancer treatment. However, these treatments are inefficient for many cancers, and unfortunately, few patients respond to these treatments. Indeed, altered metabolic pathways in the tumor play a pivotal role in tumor growth and immune response. Thus, the immunosuppressive tumor microenvironment (TME) reprograms the behavior of immune cells by altering their cellular machinery and nutrient availability to limit antitumor functions. Today, thanks to a better understanding of cancer metabolism, immunometabolism and immune checkpoint evasion, the development of new therapeutic approaches targeting the energy metabolism of cancer or immune cells greatly improve the efficacy of immunotherapy in different cancer models. Herein, we highlight the changes in metabolic pathways that regulate the differentiation of pro- and antitumor immune cells and how TME-induced metabolic stress impedes their antitumor activity. Finally, we propose some drug strategies to target these pathways in the context of cancer immunotherapy. Full article

(This article belongs to the Special Issue Inflammation and Tumor)

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17 pages, 1056 KiB

Open AccessReview

CAR T Cell Therapy’s Potential for Pediatric Brain Tumors

by Pauline Thomas, Natacha Galopin, Emma Bonérandi, Béatrice Clémenceau, Sophie Fougeray and Stéphane Birklé

Cancers 2021, 13(21), 5445; https://doi.org/10.3390/cancers13215445 - 29 Oct 2021

Cited by 10 | Viewed by 3263

Abstract

Malignant central nervous system tumors are the leading cause of cancer death in children. Progress in high-throughput molecular techniques has increased the molecular understanding of these tumors, but the outcomes are still poor. Even when efficacious, surgery, radiation, and chemotherapy cause neurologic and neurocognitive morbidity. Adoptive cell therapy with autologous CD19 chimeric antigen receptor T cells (CAR T) has demonstrated remarkable remission rates in patients with relapsed refractory B cell malignancies. Unfortunately, tumor heterogeneity, the identification of appropriate target antigens, and location in a growing brain behind the blood–brain barrier within a specific suppressive immune microenvironment restrict the efficacy of this strategy in pediatric neuro-oncology. In addition, the vulnerability of the brain to unrepairable tissue damage raises important safety concerns. Recent preclinical findings, however, have provided a strong rationale for clinical trials of this approach in patients. Here, we examine the most important challenges associated with the development of CAR T cell immunotherapy and further present the latest preclinical strategies intending to optimize genetically engineered T cells’ efficiency and safety in the field of pediatric neuro-oncology. Full article

(This article belongs to the Special Issue Inflammation and Tumor)

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13 pages, 1193 KiB

Open AccessReview

Host–Microbiota Interactions in Liver Inflammation and Cancer

by Julie Giraud and Maya Saleh

Cancers 2021, 13(17), 4342; https://doi.org/10.3390/cancers13174342 - 27 Aug 2021

Cited by 8 | Viewed by 3470

Abstract

Hepatocellular carcinoma (HCC) is a classical inflammation-promoted cancer that occurs in a setting of liver diseases, including nonalcoholic fatty liver disease (NAFLD) or alcoholic liver disease (ALD). These pathologies share key characteristics, notably intestinal dysbiosis, increased intestinal permeability and an imbalance in bile acids, choline, fatty acids and ethanol metabolites. Translocation of microbial- and danger-associated molecular patterns (MAMPs and DAMPs) from the gut to the liver elicits profound chronic inflammation, leading to severe hepatic injury and eventually HCC progression. In this review, we first describe how the gut and the liver communicate and discuss mechanisms by which the intestinal microbiota elicit hepatic inflammation and HCC. We focus on the role of microbial products, e.g., MAMPs, host inflammatory effectors and host–microbiome-derived metabolites in tumor-promoting mechanisms, including cell death and senescence. Last, we explore the potential of harnessing the microbiota to treat liver diseases and HCC. Full article

(This article belongs to the Special Issue Inflammation and Tumor)

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26 pages, 982 KiB

Open AccessReview

Targeting the NLRP3 Inflammasome as a New Therapeutic Option for Overcoming Cancer

by Sonia Missiroli, Mariasole Perrone, Caterina Boncompagni, Chiara Borghi, Alberto Campagnaro, Francesco Marchetti, Gabriele Anania, Pantaleo Greco, Francesco Fiorica, Paolo Pinton and Carlotta Giorgi

Cancers 2021, 13(10), 2297; https://doi.org/10.3390/cancers13102297 - 11 May 2021

Cited by 45 | Viewed by 7684

Abstract

Inflammasomes are multiprotein complexes that regulate the maturation and secretion of the proinflammatory cytokines interleukin-1beta (IL-1β and interleukin-18 (IL-18) in response to various intracellular stimuli. As a member of the inflammasomes family, NLRP3 is the most studied and best characterized inflammasome and has been shown to be involved in several pathologies. Recent findings have made it increasingly apparent that the NLRP3 inflammasome may also play a central role in tumorigenesis, and it has attracted attention as a potential anticancer therapy target. In this review, we discuss the role of NLRP3 in the development and progression of cancer, offering a detailed summary of NLRP3 inflammasome activation (and inhibition) in the pathogenesis of various forms of cancer. Moreover, we focus on the therapeutic potential of targeting NLRP3 for cancer therapy, emphasizing how understanding NLRP3 inflammasome-dependent cancer mechanisms might guide the development of new drugs that target the inflammatory response of tumor-associated cells. Full article

(This article belongs to the Special Issue Inflammation and Tumor)

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28 pages, 4636 KiB

Open AccessReview

Roles of Inflammasomes in Epstein–Barr Virus-Associated Nasopharyngeal Cancer

by Chin King Looi, Ling-Wei Hii, Felicia Fei-Lei Chung, Chun-Wai Mai, Wei-Meng Lim and Chee-Onn Leong

Cancers 2021, 13(8), 1786; https://doi.org/10.3390/cancers13081786 - 8 Apr 2021

Cited by 13 | Viewed by 3892

Abstract

Epstein–Barr virus (EBV) infection is recognised as one of the causative agents in most nasopharyngeal carcinoma (NPC) cases. Expression of EBV viral antigens can induce host’s antiviral immune response by activating the inflammasomes to produce pro-inflammatory cytokines, such as interleukin-1β (IL-1β) and IL-18. These cytokines are known to be detrimental to a wide range of virus-infected cells, in which they can activate an inflammatory cell death program, called pyroptosis. However, aberrant inflammasome activation and production of its downstream cytokines lead to chronic inflammation that may contribute to various diseases, including NPC. In this review, we summarise the roles of inflammasomes during viral infection, how EBV evades inflammasome-mediated immune response, and progress into tumourigenesis. The contrasting roles of inflammasomes in cancer, as well as the current therapeutic approaches used in targeting inflammasomes, are also discussed in this review. While the inflammasomes appear to have dual roles in carcinogenesis, there are still many questions that remain unanswered. In particular, the exact molecular mechanism responsible for the regulation of the inflammasomes during carcinogenesis of EBV-associated NPC has not been explored thoroughly. Furthermore, the current practical application of inflammasome inhibitors is limited to specific tumour types, hence, further studies are warranted to discover the potential of targeting the inflammasomes for the treatment of NPC. Full article

(This article belongs to the Special Issue Inflammation and Tumor)

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