PP290 - ASSOCIATION BETWEEN INCREASED SERUM LIPOCALIN-2 LEVELS AND CANCER-RELATED ANOREXIA IN GASTROINTESTINAL CANCER PATIENTS

Linked sessions

PP290

ASSOCIATION BETWEEN INCREASED SERUM LIPOCALIN-2 LEVELS AND CANCER-RELATED ANOREXIA IN GASTROINTESTINAL CANCER PATIENTS

G. Imbimbo1,*, F. Tambaro1, S. Orlando1, C. Gallicchio1, M. Muscaritoli1, A. Molfino1,2

1Department of Translational and Precision Medicine, 2Department of Interdisciplinary Studies on WellBeing, Health and Environmental Sustainability (BeSSA), Sapienza University , Rome, Italy

 

Rationale: Cancer-associated anorexia is a frequent and debilitating condition that contributes to weight loss, sarcopenia, and poor prognosis. Lipocalin-2 (LCN2), a pleiotropic mediator of inflammation and metabolism, was identified as a key regulator of appetite. Experimental models demonstrated that LCN2 deletion protects against anorexia and cachexia, but translational evidence in humans remains limited.

In this study, we investigated the association between circulating levels of LCN2 and anorexia in a cohort of gastrointestinal cancer patients (GI-CP) and assessed their association with body weight loss.

Methods: We conducted an observational study including GI-CP at diagnosis, before anticancer treatment, and healthy controls (C). Clinical, nutritional and biochemical data were collected. Anorexia was assessed by the FAACT questionnaire (cutoff ≤30). Serum LCN2 was measured by ELISA.

Results: We enrolled a total of 28 GI-CP and 10 controls. LCN2 levels were significantly higher in GI-CP compared to C (p<0.01). Stratification by presence/absence of anorexia revealed that anorexic GI-CP (n=13) showed significantly higher LCN2 levels compared C (n=8) (p=0.008). LCN2 correlated inversely with BMI in GI-CP (p=0.028; r=-0.430). GI-CP with weight loss (n=16) showed significantly higher LCN2 levels than weight-stable GI-CP (n=12) (p=0.031) and vs C (p=0.003).

Conclusion: Our findings provide novel evidence linking circulating LCN2 with anorexia, weight loss and impaired nutritional status in gastrointestinal cancer, supporting the hypothesis of LCN2 as an appetite-suppressing mediator in this setting. Further studies are warranted to clarify its role in the pathophysiology of cancer-associated anorexia.

Disclosure of Interest: None declared