Tumor Necrosis Factor: Molecular Insights and Clinical Implications (Volume II)

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

Deadline for manuscript submissions: closed (30 September 2024) | Viewed by 1444

Special Issue Editor


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Guest Editor
The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3052, Australia
Interests: inflammation-associated cancers; relationship between cytokines, the JAK/STAT and NF-kB signaling pathways in upper gastrointestinal cancers
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Special Issue Information

Dear Colleagues,

This Special Issue is the second edition of the Special Issue "Tumor Necrosis Factor: Molecular Insights and Clinical Implications", with 6 papers published online. Feel free to read via the following link: https://www.mdpi.com/journal/cancers/special_issues/TNFa.

Tumour necrosis factor-alpha (TNF/TNFa), as the foremost pro-inflammatory cytokine, is a pivotal regulator of conventional innate and adaptive immune responses, with diverse functions in cellular processes such as differentiation, proliferation, inflammation, apoptosis, and necroptosis. Since its discovery nearly 40 years ago, the TNF superfamily has grown to 19 members, with 29 interacting receptors and multiple scaffolding proteins. Binding of TNF to either TNFR1 or TNFR2 mediates the activation of tightly regulated and complex downstream signalling cascades, resulting in cell death or activation of the transcription factors NF-kB (nuclear factor-kappaB) and AP-1 (activation protein-1). Dysregulation of these signalling pathways is associated with a multitude of inflammatory conditions and an increased risk for several cancers, although the exact role TNF plays in cancer is contradictory and much debated. TNF biologics, while established therapeutically for inflammatory/autoimmune diseases, have been disappointing for cancer therapy.

In this Special Issue, we would like to comprehensively address the role of the molecular complexities of TNF signalling, particularly in relation to inflammation as a cancer driver. To additionally address these concepts, we welcome original publications or reviews on recent insights into the control of TNF superfamily activity and its manipulation to curtail cancer development. Finally, we would like to highlight and discuss the success and challenges of newer therapeutic approaches aimed at manipulating TNF signalling for cancer therapy. Such therapies are not limited to IAP inhibitors, antagonistic TNFR2 antibodies and various new combinative approaches with other agents, including immunotherapies or therapy related to TNF or other members of the TNF superfamily to expand TNF-mediated improvements for clinical outcomes.

We therefore invite colleagues to submit their contributions on the topic to this Special Issue.

I look forward to receiving your contributions.

Dr. Lorraine A. O'Reilly
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as 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

  • TNF
  • cancer
  • cell death
  • inflammation
  • clinical
  • therapy
  • immunotherapy
  • biosimilars

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Published Papers (1 paper)

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Review

19 pages, 1422 KiB  
Review
The Exacerbating Effects of the Tumor Necrosis Factor in Cardiovascular Stenosis: Intimal Hyperplasia
by Chandra Shekhar Boosani and Laxminarayana Burela
Cancers 2024, 16(7), 1435; https://doi.org/10.3390/cancers16071435 - 8 Apr 2024
Viewed by 1082
Abstract
TNF-α functions as a master regulator of inflammation, and it plays a prominent role in several immunological diseases. By promoting important cellular mechanisms, such as cell proliferation, migration, and phenotype switch, TNF-α induces its exacerbating effects, which are the underlying cause of many [...] Read more.
TNF-α functions as a master regulator of inflammation, and it plays a prominent role in several immunological diseases. By promoting important cellular mechanisms, such as cell proliferation, migration, and phenotype switch, TNF-α induces its exacerbating effects, which are the underlying cause of many proliferative diseases such as cancer and cardiovascular disease. TNF-α primarily alters the immune component of the disease, which subsequently affects normal functioning of the cells. Monoclonal antibodies and synthetic drugs that can target TNF-α and impair its effects have been developed and are currently used in the treatment of a few select human diseases. Vascular restenosis is a proliferative disorder that is initiated by immunological mechanisms. In this review, the role of TNF-α in exacerbating restenosis resulting from neointimal hyperplasia, as well as molecular mechanisms and cellular processes affected or induced by TNF-α, are discussed. As TNF-α-targeting drugs are currently not approved for the treatment of restenosis, the summation of the topics discussed here is anticipated to provide information that can emphasize on the use of TNF-α-targeting drug candidates to prevent vascular restenosis. Full article
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