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Adipocytokines and squamous cell carcinoma of the esophagus

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Abstract

Purpose

Adipocytokines are adipocyte-secreted hormones associated with some malignancies. It has been reported that the impaired response of adipocytokines to body weight loss may play a role in the pathogenesis of cancer-induced cachexia. We investigated the association between adipocytokines with squamous cell carcinoma of the esophagus (SCCE).

Methods

The levels of body mass index (BMI) and adiponectin, leptin, resistin, visfatin and C-peptide in the blood at diagnosis were measured in 117 SCCE patients and 117 age- and sex-matched controls. Logistic regression models were employed to estimate odds ratio. One-way analysis was performed to examine the prevalence of variables between two or more groups. A non-parametric Spearman correlation test was conducted to examine the associations between BMI and other variables.

Results

Adiponectin and BMI levels were significantly lower, and resistin level was significantly higher in the patients on multivariate analysis (P = 0.01, <0.01 and <0.01 respectively). BMI gradually decreased with stage progression, and resistin level gradually increased with stage progression (P < 0.01 for both). The inverse correlation between BMI and adiponectin was comparatively strong in the controls, but was weak in the patients. Leptin showed comparatively strong correlation with BMI in the controls, but was weakly correlated in the patients. The correlation between BMI and resistin or C-peptide was demonstrated weakly only in the controls, and visfatin did not correlate with BMI.

Conclusions

Resistin may be a biomarker for the progression of SCCE. In addition, the impaired responses to body weight loss of adiponectin and leptin in the patients with SCCE were suggested.

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Acknowledgment

This work was supported by the Ministry of Health, Labor and Welfare of Japan.

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Correspondence to Yasuhide Yamada.

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Nakajima, T.E., Yamada, Y., Hamano, T. et al. Adipocytokines and squamous cell carcinoma of the esophagus. J Cancer Res Clin Oncol 136, 261–266 (2010). https://doi.org/10.1007/s00432-009-0657-6

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  • DOI: https://doi.org/10.1007/s00432-009-0657-6

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