Cell Death in Cancer and Inflammation: From Pathogenesis to Treatment 2.0

Dear Colleagues,

Cell death plays a crucial role in maintaining homeostasis through the elimination of excessive, infected, malignant, and damaged cells. Over the past decade, the field of cell death has rapidly evolved and now encompasses over 12 distinct forms of programmed cell death (PCD). In addition to the classically studied mechanisms of intrinsic and extrinsic apoptosis, PCD also includes necroptosis, pyroptosis, NETosis, and ferroptosis, all which have distinct molecular characteristics and consequences in homeostasis and disease.

The tight molecular regulation of how and when cells die allows for the maintenance of cellular homeostasis. Not surprisingly, the dysregulation of PCD pathways has been linked to a variety of diseases. For example, the numbers of proliferating blood cells need to be carefully controlled, and mutations in proteins responsible for the precise regulation of apoptosis (e.g., BCL2) result in the development of cancers such as lymphoma. In contrast, excessive death can lead to significant tissue damage and degeneration, like that observed in various neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease and motor neurone disease. Finally, the precise execution of cell death pathways as well as the efficient removal of dying cells are extremely important as the incomplete induction of cell death and uncleared dying cells result in inflammation and can contribute to the development of autoimmune disorders.

Due to its vital role in homeostasis and disease, the development of novel therapeutics that target various cell-death regulators are of significant interest. Whether the goal is to prolong the life of neurons in neurodegenerative disease, or to induce death in malignant cancer, understanding the details of how cell death pathways are controlled will allow the development of these sought-after therapeutic interventions. This Special issue of Biomolecules will showcase the latest studies aiming to understand how well-timed and programmed cell death can control inflammation and cancer.

For this Special Issue of Biomolecules, “Cell Death in Cancer and Inflammation: From Pathogenesis to Treatment 2.0”, we encourage the submission of review and primary research articles that showcase both the role of cell death and therapeutic approaches targeting cell death pathways in cancer and inflammation.

Dr. Georgia Atkin-Smith
Dr. Chien-Hsiung Alan Yu
Dr. Tahnee Saunders
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. Biomolecules 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.

• cell death
• apoptosis
• necroptosis
• pyroptosis
• ferroptosis
• netosis
• inflammation
• complement-mediated death
• neurodegeneration
• mitochondria
• engulfment
• cancer