ArticleOncology letters2015
Endostatin improves cancer-associated systemic syndrome in a lung cancer model.
Article in Oncology letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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8 authors at 2 institutions in 1 country.
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Abstract
Cancer-associated systemic syndrome (CASS) is characterized by a constellation of symptoms, including progressive weight loss, anemia, endocrine disorders, gastrointestinal dysfunction, muscle and adipose atrophy, hepatic peliosis and kidney failure. The present study assesses the effects of endostatin on CASS and any possible underlying mechanism in tumor-bearing mice. The results showed that the inoculation of Lewis lung carcinoma cells into mice led to CASS that was characterized by a notable decrease in body weight, severe anemia phenotype, disordered biochemistry, hepatosplenomegaly, and a marked increase in serum vascular endothelial growth factor (VEGF), tumor necrosis factor α and interleukin-6 (IL-6). The continuous injection of 10 mg/kg/day endostatin suppressed tumor growth and alleviated CASS in the tumor-bearing mice, as shown by weight gain, improvement in biochemistry and anemia, and the preservation of organ function. The effects of endostatin on CASS in the tumor-bearing mice were accompanied by the downregulation of serum VEGF and IL-6. Collectively, these findings indicate that endostatin improves CASS in tumor-bearing mice by decreasing the serum levels of VEGF and IL-6.
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