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Mir-135 suppresses glycolysis and promotes pancreatic cancer cell adaptation to metabolic stress by targeting phosphofructokinase-1

Possibilities include microbial signatures in stool (e.g., a high abundance of pro-inflammatory bacteria could flag patients who might benefit from microbiome therapy or might flare on IL-17 blockers), biomarkers of gut permeability or inflammation (such as fecal calprotectin, whichif elevatedmight prompt concurrent treatment of gut inflammation even if the patient is asymptomatic), or blood T cell profiles (for example, a patient with high circulating Th17/Th22 cells might have a different optimal therapy than one with primarily TNF-driven inflammation)[25, 71, 72]

Solution: Liposomes offer a modular platform for customizable encapsulation, surface labeling, and targeted payload release