Abstract
The aim of the study was the investigation of relationship between cachexia syndrome and serum resistin, adiponectin, and apelin in patients with gastroesophageal cancer (GEC). Material and Methods. Adipocytokines concentrations were measured in sera of 85 GEC patients and 60 healthy controls. They were also evaluated in tumor tissue and appropriate normal mucosa of 38 operated cancer patients. Results. Resistin and apelin concentrations were significantly higher in GEC patients than in the controls. The highest resistin levels were found in cachectic patients and in patients with distant metastasis. Serum adiponectin significantly decreased in GEC patients with regional and distant metastasis. Serum apelin was significantly higher in cachectic patients than in the controls. Apelin was positively correlated with hsCRP level. Resistin and apelin levels increased significantly in tumor tissues. Weak positive correlations between adipocytokines levels in serum and in tumor tissue were observed. Conclusions. Resistin is associated with cachexia and metastasis processes of GEC. Reduction of serum adiponectin reflects adipose tissue wasting in relation to GEC progression. Correlation of apelin with hsCRP can reflect a presumable role of apelin in systemic inflammatory response in esophageal and gastric cancer.
Highlights
Advanced malignances of esophagus, esophageal-gastric junction, and stomach are associated with weight loss, muscle atrophy, anorexia, hypercatabolism, malabsorption, and production of acute phase proteins, which lead to cancer cachexia [1, 2]
In present study we demonstrated that the level of serum resistin was significantly higher in gastroesophageal cancer (GEC) patients than in the controls
This result is in agreement with previous studies, which reported that serum resistin is elevated in lung, colorectal, gastric, and esophageal cancers [8, 10, 15,16,17,18,19]
Summary
Esophageal-gastric junction, and stomach are associated with weight loss, muscle atrophy, anorexia, hypercatabolism, malabsorption, and production of acute phase proteins, which lead to cancer cachexia [1, 2]. Several studies show a model of development of cancer cachexia in relation to tumorinduced chronic inflammation [2,3,4]. In this model, the presence of low-grade tumor induces host immune reactions, which lead to the chronic inflammatory response. Systemic inflammatory response in advanced cancer is associated with long persisted macromolecules catabolism and in consequence with poor prognosis and shortened survival of patients [2, 3]
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