Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
5.7
3.6
Journals
Biology
Special Issues
Inflammation in Cancer: A Target for Prevention and Therapy
share announcement

Inflammation in Cancer: A Target for Prevention and Therapy

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cell Biology".

Deadline for manuscript submissions: closed (15 August 2021) | Viewed by 32125

Special Issue Editors

Dr. Federica Finetti

E-Mail Website
Guest Editor
Department of Biotechnology, Chemistry and Pharmacy, University of Siena, 53100 Siena, SI, Italy
Interests: pharmacological characterization of new antitumoral drugs of chemical or natural origin; inflammation and cancer; role of prostaglandins in tumor progression and angiogenesis; tyrosine kinase receptor activity in tumor progression and angiogenesis; characterization of novel molecules with pro- and anti-angiogenic activity; molecular mechanisms underlying CCM pathogenesis; physio-pathological functions of KRIT1 protein and its signaling pathways
Special Issues, Collections and Topics in MDPI journals
Dr. Lorenza Trabalzini

E-Mail Website
Guest Editor
Department of Biotechnology, Chemistry and Pharmacy, University of Siena, 53100 Siena, SI, Italy
Interests: antioxidant; anti-inflammatory; antitumoral activity; natural compounds; nutraceutical applications; cerebral cavernous malformation; KRIT1
Special Issues, Collections and Topics in MDPI journals
Dr. Cristina Travelli

E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, University of Pavia, 27100 Pavia, PV, Italy
Interests: inflammatory disorders, breast cancer, and cancer-related-inflammation; preclinical and translational studies aimed at characterizing the role of NAD metabolism in the progression of cancer and inflammatory bowel disorders (IBD), in particular in studing the pathogenesis and progression of IBD and breast cancer at the molecular level; role of iNAMPT/eNAMPT in the progression and/or pathogenesis of breast cancer and IBD; pharmacological inhibition of the extracellular form of NAMPT (eNAMPT) using monoclonal antibodies in inflammatory disorders and cancer; pharmacological characterization of new antitumoral drugs (e.g., IDO inhibitors) of chemical origin and novel neutralizing antibodies; characterization of novel molecules as a drug with anti-inflammatory activity; study of novel biomarkers for clinical prediction of biological drug responses
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Chronic inflammation is a critical component of tumor progression and pathogenesis. Several inflammatory diseases increase risk of cancer, and moreover, the activation of a pathway promoting inflammatory cytokine production and inflammatory cell recruitment are observed in tumors that are not directly related to an inflammatory condition.

Several questions related to the role of inflammation in the molecular mechanisms and in tumor development are still unresolved.

In this Special issue, we aim to produce a collection of the latest progress associated with the role of inflammatory pathways in the development and progression of different tumors. Findings should provide insights into how inflammation can influence cell transformation, tumor formation, and metastasis and elucidate the therapeutic implications and effects given by modulating inflammatory signaling pathways.

Dear Colleagues,

The role of inflammation in cancer progression has been studied for many years. It has been widely reported that inflammatory processes modulate cancer course by stimulating or inhibiting its growth. The activity of inflammatory cells and the type and level of the inflammation-modulating factors affect the balance between their pro- and antitumor effects. Thorough knowledge and understanding of the mechanisms that correlate inflammation with neoplastic disease may provide tangible benefits both in the scientific and clinical aspects related to the introduction of new diagnostic and novel therapeutics.

Assessment of the involvement of inflammation in respective neoplastic lesions may affect the preventive and therapeutic measures in patients with chronic inflammations.

This Special Issue invites original research papers and reviews that cover all aspects of the role played by inflammation in cancer development and progression, comprising new implications and effects provided by modulating inflammatory signaling pathways.

Dr. Federica Finetti
Dr. Lorenza Trabalzini
Dr. Cristina Travelli
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. Biology is an international peer-reviewed open access monthly 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 2700 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
  • Cyclooxygenase 2
  • Microsomal Prostaglandin E synthase 1
  • Cancer
  • Epithelial mesenchymal transition
  • Biomarkers
  • Immunotherapy
  • Metabolism
  • Myeloid and lymphoid cells

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Related Special Issue

Published Papers (6 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

10 pages, 3876 KiB  
Communication
Senescent Thyrocytes, Similarly to Thyroid Tumor Cells, Elicit M2-like Macrophage Polarization In Vivo
by Mara Mazzoni, Giuseppe Mauro, Lucia Minoli, Loredana Cleris, Maria Chiara Anania, Tiziana Di Marco, Emanuela Minna, Sonia Pagliardini, Maria Grazia Rizzetti, Giacomo Manenti, Maria Grazia Borrello, Eugenio Scanziani and Angela Greco
Biology 2021, 10(10), 985; https://doi.org/10.3390/biology10100985 - 30 Sep 2021
Cited by 5 | Viewed by 2567
Abstract
Inflammation plays a critical role in thyroid cancer onset and progression. We previously characterized the in vitro interplay between macrophages and senescent human thyrocytes and thyroid tumor-derived cell lines, modeling the early and the late thyroid tumor phases, respectively. We reported that both [...] Read more.
Inflammation plays a critical role in thyroid cancer onset and progression. We previously characterized the in vitro interplay between macrophages and senescent human thyrocytes and thyroid tumor-derived cell lines, modeling the early and the late thyroid tumor phases, respectively. We reported that both models are able to induce pro-tumoral M2-like macrophage polarization, through the activation of the COX2-PGE2 axis. Here, we investigated the presence of macrophage infiltrating cells in mouse xenografts derived from the above described cells models. We showed that subcutaneous injection in immunodeficient mice of both senescent human thyrocytes and thyroid tumor-derived cell lines elicits macrophage recruitment. Furthermore, considering the type of macrophage infiltrate, we observed a stronger infiltration of Arginase I positive cells (M2-like). Overall, these results demonstrate the in vivo capability of senescent and tumor thyroid cells to recruit and polarize macrophages, suggesting that the promotion of a pro-tumoral microenvironment through tumor associated macrophages may occurs in late as well as in early thyroid tumor stages, favoring tumor onset and progression. Full article
(This article belongs to the Special Issue Inflammation in Cancer: A Target for Prevention and Therapy)
►▼ Show Figures

Figure 1

16 pages, 918 KiB  
Article
Equine Genital Squamous Cell Carcinoma Associated with EcPV2 Infection: RANKL Pathway Correlated to Inflammation and Wnt Signaling Activation
by Samanta Mecocci, Ilaria Porcellato, Federico Armando, Luca Mechelli, Chiara Brachelente, Marco Pepe, Rodolfo Gialletti, Benedetta Passeri, Paola Modesto, Alessandro Ghelardi, Katia Cappelli and Elisabetta Razzuoli
Biology 2021, 10(3), 244; https://doi.org/10.3390/biology10030244 - 21 Mar 2021
Cited by 12 | Viewed by 3717
Abstract
Equine genital squamous cell carcinomas (egSCCs) are among the most common equine tumors after sarcoids, severely impairing animal health and welfare. Equus caballus papillomavirus type 2 (EcPV2) infection is often related to these tumors. The aim of this study was to clarify the [...] Read more.
Equine genital squamous cell carcinomas (egSCCs) are among the most common equine tumors after sarcoids, severely impairing animal health and welfare. Equus caballus papillomavirus type 2 (EcPV2) infection is often related to these tumors. The aim of this study was to clarify the molecular mechanisms behind egSCCs associated with EcPV2 infection, investigating receptor activator of nuclear factor-kappa B ligand (RANKL) signaling in NF-kB pathway, together with the Wnt and IL17 signaling pathways. We analyzed the innate immune response through gene expression evaluation of key cytokines and transcription factors. Moreover, Ki67 index was assessed with immunohistochemistry. EcPV2-E6 DNA was checked, and viral presence was confirmed in 21 positive out to 23 cases (91%). Oncogene expression was confirmed in 14 cases (60.8%) for E6 and in 8 (34.7%) for E2. RANKL, nuclear factor kappa-light-chain-enhancer of activated B cells (NFKB)-p50, NFKBp65, interleukin (IL)-6, IL17, IL23p19, IL8, IL12p35, IL12p40, β-catenin (BCATN1), FOS like 1 (FOSL1), and lymphoid enhancer binding factor 1 (LEF1) showed a significant upregulation in tumor samples compared to healthy tissues. Our results describe an inflammatory environment characterized by the activation of RANKL/RANK and IL17 with the relative downstream pathways, and a positive modulation of inflammatory cytokines genes such as IL6 and IL8. Moreover, the increase of BCATN1, FOSL1, and LEF1 gene expression suggests an activation of both canonical and non-canonical Wnt signaling pathway that could be critical for carcinogenesis and tumor progression. Full article
(This article belongs to the Special Issue Inflammation in Cancer: A Target for Prevention and Therapy)
►▼ Show Figures

Figure 1

16 pages, 2658 KiB  
Article
IL-6, NLR, and SII Markers and Their Relation with Alterations in CD8+ T-Lymphocyte Subpopulations in Patients Treated for Lung Adenocarcinoma
by Lorenzo Islas-Vazquez, Dolores Aguilar-Cazares, Miriam Galicia-Velasco, Uriel Rumbo-Nava, Manuel Meneses-Flores, Cesar Luna-Rivero and Jose Sullivan Lopez-Gonzalez
Biology 2020, 9(11), 376; https://doi.org/10.3390/biology9110376 - 5 Nov 2020
Cited by 16 | Viewed by 2760
Abstract
Cytokines, key contributors to tumorigenesis, are mediators between inflammatory immune or nonimmune and cancer cells. Here, IL-6 production by tumor cells was assessed in a cohort of patients with lung adenocarcinoma treated with conventional therapy. IL-6 levels and neutrophil–lymphocyte ratio (NLR) or systemic [...] Read more.
Cytokines, key contributors to tumorigenesis, are mediators between inflammatory immune or nonimmune and cancer cells. Here, IL-6 production by tumor cells was assessed in a cohort of patients with lung adenocarcinoma treated with conventional therapy. IL-6 levels and neutrophil–lymphocyte ratio (NLR) or systemic immune-inflammation index (SII) markers were evaluated. Changes in pro- and anti-inflammatory cytokines, HMGB1 concentration, and CD4+ and CD8+ T-lymphocyte populations and their subpopulations were investigated. IL-6 expression was detected immunohistochemically in lung adenocarcinoma biopsies. Cytokines were quantified using the cytometric bead array, and TGF-β and HMGB-1 through ELISA. Clinical parameters were collected to assess NLR and SII. CD4+ and CD8+ T-lymphocytes and naïve, memory, and effector subpopulations were quantified by flow cytometry. The data obtained were associated with patients’ median overall survival (OS). IL-6 showed the highest increase, probably because the lung adenocarcinoma cells produced IL-6. Patients with higher OS had lower NLR and SII from the third cycle of chemotherapy. Patients with lower OS had significantly lower percentages of CD8+ T-lymphocyte and its effector subpopulations, with a concomitant increase in the naïve subpopulation. This study suggests that in addition to the known inflammatory markers, IL-6, CD8+ T-lymphocytes and their effector and naïve subpopulations could be useful as predictive markers in lung adenocarcinoma. Full article
(This article belongs to the Special Issue Inflammation in Cancer: A Target for Prevention and Therapy)
►▼ Show Figures

Figure 1

Review

Jump to: Research

12 pages, 610 KiB  
Review
Inflammatory Markers in Cancer Immunotherapy
by Deepak Ravindranathan, Viraj A. Master and Mehmet Asim Bilen
Biology 2021, 10(4), 325; https://doi.org/10.3390/biology10040325 - 13 Apr 2021
Cited by 39 | Viewed by 5545
Abstract
Chronic inflammation is considered a major risk factor for cancer formation. Inflammation within the tumor environment plays a role in its response to therapy, growth, and prognosis. Cancer associated inflammation is known to occur in the tumor microenvironment and in the systemic circulation, [...] Read more.
Chronic inflammation is considered a major risk factor for cancer formation. Inflammation within the tumor environment plays a role in its response to therapy, growth, and prognosis. Cancer associated inflammation is known to occur in the tumor microenvironment and in the systemic circulation, and is correlated with disease progression and prognosis in many cancers. Blood cells such as neutrophils, lymphocytes, platelets, and circulating proteins such as C-reactive protein, and interleukins, such as IL-6, have been associated with inflammatory responses, which contribute to tumorigenesis. Cancer has found ways to evade the immune response; a pathway that can attenuate the innate immune response is via blocking immune checkpoints. Development of monoclonal antibodies against inhibitory immune checkpoints such as cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) have given rise to immunotherapy, which has shown remarkable responses in anti-tumor activity resulting in several U.S. Federal and Drug Administration (FDA)-approved checkpoint inhibitors. Various inflammatory markers and their prognostic and predictive implications in malignancies treated with immunotherapy will be discussed in this review. Full article
(This article belongs to the Special Issue Inflammation in Cancer: A Target for Prevention and Therapy)
►▼ Show Figures

Figure 1

26 pages, 1951 KiB  
Review
Prostaglandin E2 and Cancer: Insight into Tumor Progression and Immunity
by Federica Finetti, Cristina Travelli, Jasmine Ercoli, Giorgia Colombo, Erica Buoso and Lorenza Trabalzini
Biology 2020, 9(12), 434; https://doi.org/10.3390/biology9120434 - 1 Dec 2020
Cited by 168 | Viewed by 13296
Abstract
The involvement of inflammation in cancer progression has been the subject of research for many years. Inflammatory milieu and immune response are associated with cancer progression and recurrence. In different types of tumors, growth and metastatic phenotype characterized by the epithelial mesenchymal transition [...] Read more.
The involvement of inflammation in cancer progression has been the subject of research for many years. Inflammatory milieu and immune response are associated with cancer progression and recurrence. In different types of tumors, growth and metastatic phenotype characterized by the epithelial mesenchymal transition (EMT) process, stemness, and angiogenesis, are increasingly associated with intrinsic or extrinsic inflammation. Among the inflammatory mediators, prostaglandin E2 (PGE2) supports epithelial tumor aggressiveness by several mechanisms, including growth promotion, escape from apoptosis, transactivation of tyrosine kinase growth factor receptors, and induction of angiogenesis. Moreover, PGE2 is an important player in the tumor microenvironment, where it suppresses antitumor immunity and regulates tumor immune evasion, leading to increased tumoral progression. In this review, we describe the current knowledge on the pro-tumoral activity of PGE2 focusing on its role in cancer progression and in the regulation of the tumor microenvironment. Full article
(This article belongs to the Special Issue Inflammation in Cancer: A Target for Prevention and Therapy)
►▼ Show Figures

Figure 1

15 pages, 735 KiB  
Review
Lymphotropic Viruses: Chronic Inflammation and Induction of Cancers
by Edward W. Harhaj and Noula Shembade
Biology 2020, 9(11), 390; https://doi.org/10.3390/biology9110390 - 10 Nov 2020
Cited by 9 | Viewed by 3208
Abstract
Inflammation induced by transcription factors, including Signal Transducers and Activators of Transcription (STATs) and NF-κB, in response to microbial pathogenic infections and ligand dependent receptors stimulation are critical for controlling infections. However, uncontrolled inflammation induced by these transcription factors could lead to immune [...] Read more.
Inflammation induced by transcription factors, including Signal Transducers and Activators of Transcription (STATs) and NF-κB, in response to microbial pathogenic infections and ligand dependent receptors stimulation are critical for controlling infections. However, uncontrolled inflammation induced by these transcription factors could lead to immune dysfunction, persistent infection, inflammatory related diseases and the development of cancers. Although the induction of innate immunity and inflammation in response to viral infection is important to control virus replication, its effects can be modulated by lymphotropic viruses including human T-cell leukemia virus type 1 (HTLV-1), Κaposi’s sarcoma herpesvirus (KSHV), and Epstein Barr virus (EBV) during de novo infection as well as latent infection. These lymphotropic viruses persistently activate JAK-STAT and NF-κB pathways. Long-term STAT and NF-κB activation by these viruses leads to the induction of chronic inflammation, which can support the persistence of these viruses and promote virus-mediated cancers. Here, we review how HTLV-1, KSHV and EBV hijack the function of host cell surface molecules (CSMs), which are involved in the regulation of chronic inflammation, innate and adaptive immune responses, cell death and the restoration of tissue homeostasis. Thus, better understanding of CSMs-mediated chronic activation of STATs and NF-κB pathways in lymphotropic virus-infected cells may pave the way for therapeutic intervention in malignancies caused by lymphotropic viruses. Full article
(This article belongs to the Special Issue Inflammation in Cancer: A Target for Prevention and Therapy)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-6
Back to TopTop