Publications

2026

Gilligan, Molly M, and Dipak Panigrahy. (2026) 2026. “Resolving Cancer: Specialized Pro-Resolving Mediators As Host-Directed Regulators of Tumor Progression and Therapy Response.”. Current Topics in Microbiology and Immunology. https://doi.org/10.1007/82_2026_356.

Publisher's Version

Cancer is sustained not only by pro-inflammatory signaling but also by inadequate restoration of tissue homeostasis, e.g., failed or dysregulated resolution. Specialized pro-resolving mediators (SPMs) are enzymatically generated lipid autacoids that actively coordinate termination of inflammation, including limiting neutrophil influx, stimulating macrophage efferocytosis, counter-regulating inflammatory mediator production, and supporting tissue repair and regeneration. In oncology, these processes intersect with tumor progression, perioperative biology, treatment-induced cell death, immunotherapy responsiveness, and late metastatic recurrence. Since 2021, major advances have reframed how we view SPMs in the context of cancer: (i) efferocytosis has emerged as a central but paradoxical mechanism that can both suppress debris-driven inflammation and enable tumor immune escape; (ii) resolution-phase macrophage mediators have been reported to target dormant disseminated tumor cells and their fibrotic niche; (iii) resolution defects linked to impaired SPM biosynthesis (including ALOX15 loss) may explain inconsistent omega-3 prevention trials; (iv) neutrophil extracellular traps (NETs) have become a rapidly expanding interface between inflammation, therapy stress, and metastatic risk; and (v) mechanistic updates, including SPM receptor signaling models, have sharpened the need for rigorous, context-aware interpretation. This chapter focuses specifically on cancer biology and translation, positioning SPMs as unique host-directed modulators with attractive potential for therapeutic intervention in cancer treatment and cancer prevention. Rather than blocking inflammation, SPMs actively reprogram inflammatory responses to maintain tumor dormancy and precancer conditions. This distinction is particularly relevant in cancer, where chronic non-resolving inflammation arises not only from tumor biology itself but also from therapeutic interventions such as surgery, chemotherapy, cytotoxic and immune-targeting therapy, and radiation.

Hernandez-Garcia, Eva, Andrew Edkins, Evangelia Chrysikou, José M Ordóñez-Mena, Larissa Nekhlyudov, Juyong Brian Kim, Gary R McLean, Hannah Frost, and Dipak Panigrahy. (2026) 2026. “In-Bedroom Renewed Air As Anti-Inflammatory Adjuvant Therapy in Cancer Survivors: Protocol for the Randomised, Placebo-Controlled BREATHS N-of-1 Trial Series.”. BMJ Open 16 (6): e111748. https://doi.org/10.1136/bmjopen-2025-111748.

Publisher's Version

INTRODUCTION: Inflammation is causally related to cancer progression and cardiovascular toxicities of anticancer treatments. Fine particulate matter (PM2.5) air filtration lowers interleukin-6 and C reactive protein (CRP) levels in high-risk cardiopulmonary groups, though potential synergistic or confounding effects with routine medications-statins, cyclo-oxygenase-2 inhibitors, beta-blockers-remain poorly understood. Whether overnight in-bedroom PM2.5 air filtration effectively reduces inflammation and prothrombotic biomarkers in survivors of adult-onset cancer at high cardiovascular toxicity risk is unknown.

METHODS AND ANALYSIS: BREATHS is a series of randomised, adaptive, blinded, placebo-controlled N-of-1 trials conducted in densely populated urban areas of Valencia, Spain, during winter when PM2.5 concentrations historically exceed WHO guidelines. Eligible participants are aged ≥18 years with a history of breast, colorectal, prostate, lung or haematological cancer, prior cardiotoxic cancer therapy and CRP ≥3 mg/L. Each participant will undergo up to three cycles, each comprising two 14-day periods of advanced submicron air filtration (clean air delivery rate: 275 m3/hour nightly) or placebo (sham filtration), in random order. Sequence duration ranges from 4 weeks to 12 weeks, depending on whether a clinically meaningful CRP reduction (<2 mg/L or ≥35% relative to placebo) is achieved during active treatment of each cycle. Non-responders will enter an open-label phase (OLP) of two 14-day periods: no treatment followed by continuous filtration. The primary endpoint is change in CRP between active and placebo phases. Secondary endpoints include changes in serum amyloid A, haemoglobin A1c and blood pressure. Indoor and outdoor particulate exposure will be quantified using paired real-time monitors at each home.

ETHICS AND DISSEMINATION: The trial protocol was approved by the research ethics committees of University College London (REC UCL: 22105/001), Doctor Peset University Hospital (CEIm: 044/25) and General University Hospital of Valencia (CEIm: 1/2026 EO-PS), Spain. Results will be presented at relevant conferences and published in peer-reviewed journals.

TRIAL REGISTRATION NUMBER: NCT06778122.

2024

Fames, Pulvinar, Hasellus Dignissim, Imperdiet Sociosqu, and Dictum Gravida. 2024. “[Sample 3] Mauris Felis ante Montes Rhoncus Semper, Iaculis Nisl Facilisis Malesuada Maecenas”. Journal of Iaculis Nisl Facilisis Malesuada Maecenas.

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