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14 pages, 2481 KiB

Open AccessArticle

Sulforaphane Attenuates Neutrophil ROS Production, MPO Degranulation and Phagocytosis, but Does Not Affect NET Formation Ex Vivo and In Vitro

by Shiori Wakasugi-Onogi, Sihui Ma, Ruheea Taskin Ruhee, Yishan Tong, Yasuhiro Seki and Katsuhiko Suzuki

Int. J. Mol. Sci. 2023, 24(10), 8479; https://doi.org/10.3390/ijms24108479 - 9 May 2023

Cited by 6 | Viewed by 2418

Abstract

Sulforaphane has several effects on the human body, including anti-inflammation, antioxidation, antimicrobial and anti-obesity effects. In this study, we examined the effect of sulforaphane on several neutrophil functions: reactive oxygen species (ROS) production, degranulation, phagocytosis, and neutrophil extracellular trap (NET) formation. We also [...] Read more.

Sulforaphane has several effects on the human body, including anti-inflammation, antioxidation, antimicrobial and anti-obesity effects. In this study, we examined the effect of sulforaphane on several neutrophil functions: reactive oxygen species (ROS) production, degranulation, phagocytosis, and neutrophil extracellular trap (NET) formation. We also examined the direct antioxidant effect of sulforaphane. First, we measured neutrophil ROS production induced by zymosan in whole blood in the presence of 0 to 560 µM sulforaphane. Second, we examined the direct antioxidant activity of sulforaphane using a HOCl removal test. In addition, inflammation-related proteins, including an azurophilic granule component, were measured by collecting supernatants following ROS measurements. Finally, neutrophils were isolated from blood, and phagocytosis and NET formation were measured. Sulforaphane reduced neutrophil ROS production in a concentration-dependent manner. The ability of sulforaphane to remove HOCl is stronger than that of ascorbic acid. Sulforaphane at 280 µM significantly reduced the release of myeloperoxidase from azurophilic granules, as well as that of the inflammatory cytokines TNF-α and IL-6. Sulforaphane also suppressed phagocytosis but did not affect NET formation. These results suggest that sulforaphane attenuates neutrophil ROS production, degranulation, and phagocytosis, but does not affect NET formation. Moreover, sulforaphane directly removes ROS, including HOCl. Full article

(This article belongs to the Special Issue Cytokines: From Cancer to Autoimmunity)

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17 pages, 2366 KiB

Open AccessArticle

Trametinib-Resistant Melanoma Cells Displaying MITF^high/NGFR^low/IL-8^low Phenotype Are Highly Responsive to Alternating Periods of Drug Withdrawal and Drug Rechallenge

by Paulina Koziej, Katarzyna Kluszczynska, Mariusz L. Hartman and Malgorzata Czyz

Int. J. Mol. Sci. 2023, 24(9), 7891; https://doi.org/10.3390/ijms24097891 - 26 Apr 2023

Cited by 3 | Viewed by 2255

Abstract

Despite significant advances in targeted therapies against the hyperactivated BRAF^V600/MEK pathway for patients with unresectable metastatic melanoma, acquired resistance remains an unsolved clinical problem. In this study, we focused on melanoma cells resistant to trametinib, an agent broadly used in combination [...] Read more.

Despite significant advances in targeted therapies against the hyperactivated BRAF^V600/MEK pathway for patients with unresectable metastatic melanoma, acquired resistance remains an unsolved clinical problem. In this study, we focused on melanoma cells resistant to trametinib, an agent broadly used in combination therapies. Molecular and cellular changes were assessed during alternating periods of trametinib withdrawal and rechallenge in trametinib-resistant cell lines displaying either a differentiation phenotype (MITF^high/NGFR^low) or neural crest stem-like dedifferentiation phenotype (NGFR^high/MITF^low). Neither drug withdrawal nor drug rechallenge induced cell death, and instead of loss of fitness, trametinib-resistant melanoma cells adapted to altered conditions by phenotype switching. In resistant cells displaying a differentiation phenotype, trametinib withdrawal markedly decreased MITF level and activity, which was associated with reduced cell proliferation capacity, and induced stemness assessed as NGFR-positive cells and senescence features, including IL-8 expression and secretion. All these changes could be reversed by trametinib re-exposure, which emphasizes melanoma cell plasticity. Trametinib-resistant cells displaying a dedifferentiation phenotype were less responsive presumably due to the already low level of MITF, a master regulator of the melanoma phenotype. Considering new directions of the development of anti-melanoma treatment, our study suggests that the phenotype of melanomas resistant to targeted therapy might be a crucial determinant of the selection of second-line therapy for melanoma patients. Full article

(This article belongs to the Special Issue Cytokines: From Cancer to Autoimmunity)

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13 pages, 294 KiB

Open AccessArticle

Influence of IL10 and TGFB1 Promoter Polymorphisms on Serum Cytokine Levels in Development and Severity of RA

by Georgi Vasilev, Mariana Ivanova, Iskren Stanilov, Lyuba Miteva, Spaska Stanilova and Irena Manolova

Int. J. Mol. Sci. 2022, 23(19), 11955; https://doi.org/10.3390/ijms231911955 - 8 Oct 2022

Cited by 4 | Viewed by 1657

Abstract

In our study, we focused on the role of the immunosuppressive cytokines TGF-β1 and IL-10 in RA and, in particular, the influence of the IL10-1082 A/G (rs1800896) and TGFB1-509C/T (rs1800469) promoter polymorphisms on their levels as a prerequisite for RA and [...] Read more.

In our study, we focused on the role of the immunosuppressive cytokines TGF-β1 and IL-10 in RA and, in particular, the influence of the IL10-1082 A/G (rs1800896) and TGFB1-509C/T (rs1800469) promoter polymorphisms on their levels as a prerequisite for RA and disease activity clinical features. We found significantly higher IL-10 and lower TGF-β1 serum levels in women with RA than in controls. Patients who carried the -1082AA and AG genotypes had significantly higher levels of lnIL-10 compared to GG in contrast to healthy women carrying the same genotypes. The heterozygous -1082AG genotype was less frequent in RA cases (45.4%) than in healthy women (56.1%) and could be a protective factor for RA development (over-dominant model, OR = 0.66 95% CI 0.38–1.57). In addition, RA patients carrying the heterozygous -1082AG genotype were less likely to be anti-CCP positive than those carrying the homozygous AA/GG genotypes (37.1% vs. 62.9%; OR = 0.495. 95% CI 0.238–1.029, p = 0.058). There was no association between TGFB1 -509C/T SNP and susceptibility to RA and no relation between systemic TGF-β1 levels and rs1800469 genotypes. In conclusion, the IL10-1082 genotypes affect the serum levels of IL-10 in women with RA in a different way from that in healthy women and appear to play a role in the genetic predisposition and autoantibody production in the Bulgarian population. Full article

(This article belongs to the Special Issue Cytokines: From Cancer to Autoimmunity)

12 pages, 1105 KiB

Open AccessCommunication

Inflammatory Biomarkers Associated with In-Hospital Mortality in Critical COVID-19 Patients

by Krisztina Pál, Anca Alexandra Molnar, Adina Huțanu, János Szederjesi, Ionuț Branea, Ágota Timár and Minodora Dobreanu

Int. J. Mol. Sci. 2022, 23(18), 10423; https://doi.org/10.3390/ijms231810423 - 9 Sep 2022

Cited by 13 | Viewed by 2335

Abstract

The COVID-19 pandemic poses global healthcare challenges due to its unpredictable clinical course. The aim of this study is to identify inflammatory biomarkers and other routine laboratory parameters associated with in-hospital mortality in critical COVID-19 patients. We performed a retrospective observational study on [...] Read more.

The COVID-19 pandemic poses global healthcare challenges due to its unpredictable clinical course. The aim of this study is to identify inflammatory biomarkers and other routine laboratory parameters associated with in-hospital mortality in critical COVID-19 patients. We performed a retrospective observational study on 117 critical COVID-19 patients. Following descriptive statistical analysis of the survivor and non-survivor groups, optimal cut-off levels for the statistically significant parameters were determined using the ROC method, and the corresponding Kaplan-Meier survival curves were calculated. The inflammatory parameters that present statistically significant differences between survivors and non-survivors are IL-6 (p = 0.0004, cut-off = 27.68 pg/mL), CRP (p = 0.027, cut-off = 68.15 mg/L) and IL-6/Ly ratio (p = 0.0003, cut-off = 50.39). Additionally, other statistically significant markers are creatinine (p = 0.031, cut-off = 0.83 mg/dL), urea (p = 0.0002, cut-off = 55.85 mg/dL), AST (p = 0.0209, cut-off = 44.15 U/L), INR (p = 0.0055, cut-off = 1.075), WBC (p = 0.0223, cut-off = 11.68 × 10⁹/L) and pH (p = 0.0055, cut-off = 7.455). A survival analysis demonstrated significantly higher in-hospital mortality rates of patients with values of IL-6, IL-6/Ly, AST, INR, and pH exceeding previously mentioned thresholds. In our study, IL-6 and IL-6/Ly have a predictive value for the mortality of critically-ill patients diagnosed with COVID-19. The integration of these parameters with AST, INR and pH could contribute to a prognostic score for the risk stratification of critical patients, reducing healthcare costs and facilitating clinical decision-making. Full article

(This article belongs to the Special Issue Cytokines: From Cancer to Autoimmunity)

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17 pages, 4338 KiB

Open AccessArticle

Antheraea pernyi Suppressor of Cytokine Signaling 2 Negatively Modulates the JAK/STAT Pathway to Attenuate Microbial Infection

by Saima Kausar, Isma Gul, Ruochen Liu, Xiao-Xue Ke, Zhen Dong, Muhammad Nadeem Abbas and Hongjuan Cui

Int. J. Mol. Sci. 2022, 23(18), 10389; https://doi.org/10.3390/ijms231810389 - 8 Sep 2022

Cited by 6 | Viewed by 2070

Abstract

The Janus kinase (JAK) signal transducer and activator of transcription (STAT) pathway has been shown to govern various physiological processes, including immune responses, hematopoiesis, cell growth, and differentiation. Recent studies show that suppressors of cytokine signaling (SOCS) proteins attenuate JAK-STAT signaling in mammals; [...] Read more.

The Janus kinase (JAK) signal transducer and activator of transcription (STAT) pathway has been shown to govern various physiological processes, including immune responses, hematopoiesis, cell growth, and differentiation. Recent studies show that suppressors of cytokine signaling (SOCS) proteins attenuate JAK-STAT signaling in mammals; however, their functions are less clear in lepidopteran insects. Here, we report a full-length sequence of SOCS-2 from the Chinese oak silkworm Antheraea pernyi (designated as ApSOCS-2) and study its biological role in immune responses via the JAK-STAT pathway. ApSOCS-2 expression was high in the fat bodies and hemocytes of A. pernyi fifth instar larvae. After pathogen infection with nucleopolyhedrovirus, Beauveria bassiana, Escherichia coli, and Microccus luteus, ApSOCS-2 mRNA was strongly increased compared to the control group. To elucidate the possible involvement in innate immunity, we measured antimicrobial peptide genes expression profiles in the fat body of A. pernyi. In contrast, recombinant ApSOCS-2 protein administration significantly reduced the AMPs transcription, while the depletion of ApSOCS-2 by RNAi increased their expression. Furthermore, we observed higher antibacterial activity and lower bacterial replication in dsApSOCS-2-treated larvae. The ApSOCS-2 transcription level was reduced in STAT depleted A. pernyi larvae challenged by M. luteus. The ApSOCS-2 RNAi data sets were also subjected to transcriptomic analysis, which suggests that ApSOCS-2 is a key regulator of immune function. Taken together, our data suggest that ApSOCS-2 is required for the negative regulation of AMPs transcripts via the JAK-STAT pathway in the insect. Full article

(This article belongs to the Special Issue Cytokines: From Cancer to Autoimmunity)

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14 pages, 3050 KiB

Open AccessArticle

Heparan Sulfate Facilitates Binding of hIFNγ to Its Cell-Surface Receptor hIFNGR1

by Elisaveta Miladinova, Elena Lilkova, Elena Krachmarova, Kristina Malinova, Peicho Petkov, Nevena Ilieva, Genoveva Nacheva and Leandar Litov

Int. J. Mol. Sci. 2022, 23(16), 9415; https://doi.org/10.3390/ijms23169415 - 20 Aug 2022

Viewed by 1833

Abstract

Human interferon-gamma (hIFN

γ

) is a crucial signaling molecule with an important role in the initialization and development of the immune response of the host. However, its aberrant activity is also associated with the progression of a multitude of autoimmune and other [...] Read more.

Human interferon-gamma (hIFN

γ

) is a crucial signaling molecule with an important role in the initialization and development of the immune response of the host. However, its aberrant activity is also associated with the progression of a multitude of autoimmune and other diseases, which determines the need for effective inhibitors of its activity. The development of such treatments requires proper understanding of the interaction of hIFN

γ

to its cell-surface receptor hIFNGR1. Currently, there is no comprehensive model of the mechanism of this binding process. Here, we employ molecular dynamics simulations to study on a microscopic level the process of hIFN

γ

–hIFNGR1 complex formation in different scenarios. We find that the two molecules alone fail to form a stable complex, but the presence of heparan-sulfate-like oligosaccharides largely facilitates the process by both demobilizing the highly flexible C-termini of the cytokine and assisting in the proper positioning of its globule between the receptor subunits. An antiproliferative-activity assay on cells depleted from cell-surface heparan sulfate (HS) sulfation together with the phosphorylation levels of the signal transducer and activator of transcription STAT1 confirms qualitatively the simulation-based multistage complex-formation model. Our results reveal the key role of HS and its proteoglycans in all processes involving hIFN

γ

signalling. Full article

(This article belongs to the Special Issue Cytokines: From Cancer to Autoimmunity)

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11 pages, 2878 KiB

Open AccessArticle

TNF-α Induces Mitophagy in Rheumatoid Arthritis Synovial Fibroblasts, and Mitophagy Inhibition Alleviates Synovitis in Collagen Antibody-Induced Arthritis

by Ji-Hee Nam, Jun-Ho Lee, Hyun-Ji Choi, So-Yeon Choi, Kyung-Eun Noh, Nam-Chul Jung, Jie-Young Song, Jinjung Choi, Han Geuk Seo, Sang Youn Jung and Dae-Seog Lim

Int. J. Mol. Sci. 2022, 23(10), 5650; https://doi.org/10.3390/ijms23105650 - 18 May 2022

Cited by 15 | Viewed by 2857

Abstract

Mitophagy is a selective form of autophagy that removes damaged mitochondria. Increasing evidence indicates that dysregulated mitophagy is implicated in numerous autoimmune diseases, but the role of mitophagy in rheumatoid arthritis (RA) has not yet been reported. The aim of the present study [...] Read more.

Mitophagy is a selective form of autophagy that removes damaged mitochondria. Increasing evidence indicates that dysregulated mitophagy is implicated in numerous autoimmune diseases, but the role of mitophagy in rheumatoid arthritis (RA) has not yet been reported. The aim of the present study was to determine the roles of mitophagy in patient-derived RA synovial fibroblasts (RASFs) and in the collagen antibody-induced arthritis mouse model. We measured the mitophagy marker PTEN-induced putative kinase 1 (PINK1) in RASFs treated with tumor necrosis factor-α (TNF-α) using Western blotting and immunofluorescence. Arthritis was induced in PINK1^−/− mice by intraperitoneal injection of an anti-type II collagen antibody cocktail and lipopolysaccharide. RA severity was assessed by histopathology. PINK1 expression and damaged mitochondria increased in TNF-α treated RASFs via increased intracellular levels of reactive oxygen species. PINK1 knockdown RASFs decreased cellular migration and invasion functions. In addition, PINK1^−/− mice with arthritis exhibited markedly reduced swelling and inflammation relative to wild-type mice with arthritis. Taken together, these findings suggest that regulation of PINK1 expression in RA could represent a potential therapeutic and diagnostic target for RA. Full article

(This article belongs to the Special Issue Cytokines: From Cancer to Autoimmunity)

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Review

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14 pages, 2978 KiB

Open AccessReview

IL-18 in Autoinflammatory Diseases: Focus on Adult Onset Still Disease and Macrophages Activation Syndrome

by Chiara Baggio, Sara Bindoli, Irina Guidea, Andrea Doria, Francesca Oliviero and Paolo Sfriso

Int. J. Mol. Sci. 2023, 24(13), 11125; https://doi.org/10.3390/ijms241311125 - 5 Jul 2023

Cited by 4 | Viewed by 3906

Abstract

Interleukin-18 (IL-18) is a potent pro-inflammatory cytokine that is involved in various innate and adaptive immune processes related to infection, inflammation, and autoimmunity. Therefore, it is described as a key mediator of autoinflammatory diseases associated with the development of macrophage activation syndrome (MAS), [...] Read more.

Interleukin-18 (IL-18) is a potent pro-inflammatory cytokine that is involved in various innate and adaptive immune processes related to infection, inflammation, and autoimmunity. Therefore, it is described as a key mediator of autoinflammatory diseases associated with the development of macrophage activation syndrome (MAS), including systemic juvenile idiopathic arthritis and adult-onset Still’s disease. This review focuses on the role of IL-18 in inflammatory responses, placing emphasis on autoinflammatory diseases associated with chronic excess of serum IL-18, which correlate with clinical and biological signs of the disease. Therefore, it is useful for the diagnosis and monitoring of disease activity. Researchers are currently investigating IL-18’s role as a therapeutic target for the treatment of inflammatory diseases. The inhibition of IL-18 signaling through recombinant human IL-18BP (IL-18 binding protein) seems to be an effective therapeutic strategy, though further studies are necessary to clarify its importance as a therapeutic target. Full article

(This article belongs to the Special Issue Cytokines: From Cancer to Autoimmunity)

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13 pages, 1039 KiB

Open AccessReview

Pro- and Anti-Inflammatory Prostaglandins and Cytokines in Humans: A Mini Review

by Jean-Luc Wautier and Marie-Paule Wautier

Int. J. Mol. Sci. 2023, 24(11), 9647; https://doi.org/10.3390/ijms24119647 - 1 Jun 2023

Cited by 33 | Viewed by 8745

Abstract

Inflammation has been described for two millennia, but cellular aspects and the paradigm involving different mediators have been identified in the recent century. Two main groups of molecules, the prostaglandins (PG) and the cytokines, have been discovered and play a major role in [...] Read more.

Inflammation has been described for two millennia, but cellular aspects and the paradigm involving different mediators have been identified in the recent century. Two main groups of molecules, the prostaglandins (PG) and the cytokines, have been discovered and play a major role in inflammatory processes. The activation of prostaglandins PGE2, PGD2 and PGI2 results in prominent symptoms during cardiovascular and rheumatoid diseases. The balance between pro- and anti-inflammatory compounds is nowadays a challenge for more targeted therapeutic approaches. The first cytokine was described more than a century ago and is now a part of different families of cytokines (38 interleukins), including the IL-1 and IL-6 families and TNF and TGFβ families. Cytokines can perform a dual role, being growth promotors or inhibitors and having pro- and anti-inflammatory properties. The complex interactions between cytokines, vascular cells and immune cells are responsible for dramatic conditions and lead to the concept of cytokine storm observed during sepsis, multi-organ failure and, recently, in some cases of COVID-19 infection. Cytokines such as interferon and hematopoietic growth factor have been used as therapy. Alternatively, the inhibition of cytokine functions has been largely developed using anti-interleukin or anti-TNF monoclonal antibodies in the treatment of sepsis or chronic inflammation. Full article

(This article belongs to the Special Issue Cytokines: From Cancer to Autoimmunity)

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17 pages, 1994 KiB

Open AccessReview

Activation of Mast Cells by Neuropeptides: The Role of Pro-Inflammatory and Anti-Inflammatory Cytokines

by Dorina Lauritano, Filiberto Mastrangelo, Cristian D’Ovidio, Gianpaolo Ronconi, Alessandro Caraffa, Carla E. Gallenga, Ilias Frydas, Spyros K. Kritas, Matteo Trimarchi, Francesco Carinci and Pio Conti

Int. J. Mol. Sci. 2023, 24(5), 4811; https://doi.org/10.3390/ijms24054811 - 2 Mar 2023

Cited by 23 | Viewed by 4409

Abstract

Mast cells (MCs) are tissue cells that are derived from bone marrow stem cells that contribute to allergic reactions, inflammatory diseases, innate and adaptive immunity, autoimmunity, and mental disorders. MCs located near the meninges communicate with microglia through the production of mediators such [...] Read more.

Mast cells (MCs) are tissue cells that are derived from bone marrow stem cells that contribute to allergic reactions, inflammatory diseases, innate and adaptive immunity, autoimmunity, and mental disorders. MCs located near the meninges communicate with microglia through the production of mediators such as histamine and tryptase, but also through the secretion of IL-1, IL-6 and TNF, which can create pathological effects in the brain. Preformed chemical mediators of inflammation and tumor necrosis factor (TNF) are rapidly released from the granules of MCs, the only immune cells capable of storing the cytokine TNF, although it can also be produced later through mRNA. The role of MCs in nervous system diseases has been extensively studied and reported in the scientific literature; it is of great clinical interest. However, many of the published articles concern studies on animals (mainly rats or mice) and not on humans. MCs are known to interact with neuropeptides that mediate endothelial cell activation, resulting in central nervous system (CNS) inflammatory disorders. In the brain, MCs interact with neurons causing neuronal excitation with the production of neuropeptides and the release of inflammatory mediators such as cytokines and chemokines. This article explores the current understanding of MC activation by neuropeptide substance P (SP), corticotropin-releasing hormone (CRH), and neurotensin, and the role of pro-inflammatory cytokines, suggesting a therapeutic effect of the anti-inflammatory cytokines IL-37 and IL-38. Full article

(This article belongs to the Special Issue Cytokines: From Cancer to Autoimmunity)

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16 pages, 1153 KiB

Open AccessReview

Insights behind the Relationship between Colorectal Cancer and Obesity: Is Visceral Adipose Tissue the Missing Link?

by Alice Chaplin, Ramon Maria Rodriguez, Juan José Segura-Sampedro, Aina Ochogavía-Seguí, Dora Romaguera and Gwendolyn Barceló-Coblijn

Int. J. Mol. Sci. 2022, 23(21), 13128; https://doi.org/10.3390/ijms232113128 - 28 Oct 2022

Cited by 17 | Viewed by 4444

Abstract

Colorectal cancer (CRC) is a major health problem worldwide, with an estimated 1.9 million new cases and 915,880 deaths in 2020 alone. The etiology of CRC is complex and involves both genetic and lifestyle factors. Obesity is a major risk factor for CRC, [...] Read more.

Colorectal cancer (CRC) is a major health problem worldwide, with an estimated 1.9 million new cases and 915,880 deaths in 2020 alone. The etiology of CRC is complex and involves both genetic and lifestyle factors. Obesity is a major risk factor for CRC, and the mechanisms underlying this link are still unclear. However, the generalized inflammatory state of adipose tissue in obesity is thought to play a role in the association between CRC risk and development. Visceral adipose tissue (VAT) is a major source of proinflammatory cytokines and other factors that contribute to the characteristic systemic low-grade inflammation associated with obesity. VAT is also closely associated with the tumor microenvironment (TME), and recent evidence suggests that adipocytes within the TME undergo phenotypic changes that contribute to tumor progression. In this review, we aim to summarize the current evidence linking obesity and CRC, with a focus on the role of VAT in tumor etiology and progression. Full article

(This article belongs to the Special Issue Cytokines: From Cancer to Autoimmunity)

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13 pages, 1586 KiB

Open AccessReview

Old and New Blood Markers in Human Colorectal Cancer

by Jean-Luc Wautier and Marie-Paule Wautier

Int. J. Mol. Sci. 2022, 23(21), 12968; https://doi.org/10.3390/ijms232112968 - 26 Oct 2022

Cited by 11 | Viewed by 4468

Abstract

Cancer is a predominant cause of mortality all over the world. Lung, prostate, and colorectal cancer are the more frequent in men while breast and colorectal have a high incidence in women. Major progress aside, some cancers are still frequent and one major [...] Read more.

Cancer is a predominant cause of mortality all over the world. Lung, prostate, and colorectal cancer are the more frequent in men while breast and colorectal have a high incidence in women. Major progress aside, some cancers are still frequent and one major issue is improvements in detection methods. Imaging techniques have a major role, but inflammatory, tumoral markers and calculated scores may contribute to the assessment of prognosis. The erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and carcinoembryonic antigen cell adhesion molecule (CEACAM) have been used for decades and do not have a clear use for diagnosis or prognosis yet. The CEACAM family includes 12 human members, and some of them have a cluster differentiation (CD). CD66 may be an interesting indicator of disease severity. Beside interleukin-6 (IL-6), the high level of which is observed in patients with a high mortality rate, other cytokines IL-17A, IL-22, and transforming growth factor -β (TGF-β) are expressed at the tumor level. The detection of circulating tumor cells has been improved but is still of undetermined value. Circulating tumor DNA (ctDNA) was recently studied in CRC stage II patients and may be helpful for chemotherapy management. Full article

(This article belongs to the Special Issue Cytokines: From Cancer to Autoimmunity)

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