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Background: Body mass index (BMI) has been associated with a risk of esophageal cancer. However, the influence of BMI and BMI loss on people with esophageal cancer that were treated with different therapies has not been described in China. Methods: In total, 615 consecutive patients that underwent esophagectomy and/or chemotherapy/radiotherapy were classified according to the Asian-specific BMI (kg/m 2 ) cutoff values. The impact of BMI and BMI loss on long-term overall survival (OS) was estimated using the Kaplan–Meier method and Cox proportional hazard models. Results: Multivariate analysis showed that overweight and obese patients had a more favorable survival than normal weight and underweight patients ( p =0.017). Patients with a low BMI and high BMI loss before therapy had worse OS than others ( p =0.001). Subgroup analysis showed that patients with a high BMI were more likely to suffer hypertension ( p <0.001) and receive only surgery ( p <0.001), and they were less likely to be smokers ( p =0.007) and anemic ( p <0.001). Conversely, patients with high BMI loss were more likely to be anemic ( p =0.001), to have advanced pathological stage ( p =0.012), and to receive chemotherapy and radiotherapy ( p =0.001). Moreover, the mortality rate was higher when patients had a high BMI loss. There is no survival benefit of higher BMI in the non-esophageal squamous cell carcinoma (ESCC) group. Conclusion: Pretreatment BMI was an independent prognostic factor for long-term survival in esophageal cancer patients treated with different treatments. The overall survival was increased in esophageal cancer patients with a high pretreatment BMI and no BMI loss. There is no survival benefit of higher BMI in the non-ESCC group.

Interleukin-21 (IL-21) is a pleiotropic cytokine linking innate and adaptive immune responses, which has been reported to play a key role in multiple autoimmune diseases. The aim of the present case-control study was to investigate the genetic association between single nucleotide polymorphisms (SNPs) of rs907715 within the IL-21 gene and Graves’ disease (GD) in a Southern Chinese population. A total of 211 patients with GD and 212 control subjects were recruited for the study. IL-21 gene rs907715 polymorphisms were detected by direct DNA sequencing. The results indicated that the frequencies of the GG genotype and the G allele in GD patients were significantly increased when compared with the frequencies in the controls (P=6.7×10−3 and P=2.0×10−5, respectively). In addition, the frequency of the AA genotype was much lower in the patient group when compared with the control group (16.6 vs. 34.0%; P=4.0×10−5). Furthermore, the G allele of rs907715 was associated with relapse in GD patients. These observations indicated that polymorphisms of IL-21/rs907715 may affect the susceptibility to GD in a Southern Chinese population. The G allele was significantly associated with an increased risk of GD development, whereas the A allele may lower the susceptibility to GD.

Abstract. It has been widely reported that the CT60 single-nucleotide polymorphism (SNP), which is in the 3'-untranslated region of the cytotoxic T lymphocyte associated 4 (CTLA4) gene, is strongly correlated with certain immune-mediated diseases. The present case-control study aimed to investigate the genetic association between the CT60 SNP within the CTLA4 gene and Graves' disease (GD). A total of 288 patients with GD and 290 control subjects were recruited for the study. The CT60 SNP of the CTLA4 gene was detected by direct DNA sequencing. The results indicated that the frequencies of the GG genotype and G allele in the case group were evidently higher than that in the control group (P=4x10 , respectively). Furthermore, the G/G genotype of the CT60 SNP was associated with an increased risk for GD (odds ratio=2.223). In conclusion, these results suggested that the CT60 SNP is associated with susceptibility to GD. The frequency of the disease-susceptible G allele of CT60 was significantly associated with an increased risk of GD development. IntroductionGraves' Disease (GD), also known as toxic diffuse goiter, can increase the level of thyroid hormone, is one of the organ-specific autoimmune diseases and it accounts for 85% of all clinical hyperthyroidism (1,2). The disease often presents in patients aged from 20-40 years old, with a male to female ratio of ~1:8 and a significant familial tendency (3). The clinical performance of GD is not limited to the thyroid, but is a multi-system syndrome, including the high metabolic syndrome group, diffuse goiter, eye symptoms, lesions and thyroid extremity diseases (4-6). Immunologically, GD is characterized by increased circulating antibodies against thyroid-stimulating hormone receptor (TSHR), thyroglobulin (TG) and thyroid peroxidase (TPO). Although the precise pathogenesis involved in the process of GD is not completely understood, certain findings indicate that complex interactions between environmental, genetic, endogenous and local factors are involved in its pathogenesis (7-9). A study on the genetic susceptibility genes of GD has become of interest (10-13).Previous studies have demonstrated that a number of susceptibility genes are associated with the autoimmune thyroid diseases, including interleukin-21, TSHR, human leukocyte antigen class I and II, cluster of differentiation 40 (CD40) and cytotoxic T lymphocyte associated 4 (CTLA4) (10-15). Among them, CTLA4 as a key negative regulator of the T lymphocyte immune response has attracted an increasing focus on the susceptibility to autoimmune disease. CTLA4, which is expressed by activate T cells, is a type of transmembrane protein. The CTLA4 gene is located on human chromosome 2q33 (16). The most significant function of the CTLA4 gene is negative regulation of the human immune response. Several polymorphic sites in the CTLA4 gene are associated with thyroid diseases, such as -318C/T promoter and 49A/G exon 1, -224(AT)n dinucleotide repeat sequence single-nucleotide polymorphism (SNP), -1722C/T, -1661A/G, CT60 (...

Background: In this study, we aimed to establish and validate a mathematical diagnosis model to distinguish benign pulmonary nodules (BPNs) from early non-small cell lung cancer (eNSCLC) based on clinical characteristics, radiomics features, and hematological biomarkers.Methods: Medical records from 81 patients (27 BPNs, 54 eNSCLC) were used to establish a novel mathematical diagnosis model and an additional 61 patients (21 BPNs, 40 eNSCLC) were used to validate this new model. To establish a clinical diagnosis model, a least absolute shrinkage and selection operator (LASSO) regression was applied to select predictors for eNSCLC, then multivariate logistic regression analysis was performed to determine independent predictors of the probability of eNSCLC, and to establish a clinical diagnosis model. The diagnostic accuracy and discriminative ability of our model were compared with the PKUPH and Mayo models using the following 4 indices: area under the receiver-operating characteristics curve (ROC), net reclassification improvement index (NRI), integrated discrimination improvement index (IDI), and decision curve analysis (DCA).Results: Multivariate logistic regression analysis identified age, border, and albumin (ALB) as independent diagnostic markers of eNSCLC. In the training cohort, the AUC of our model was 0.740, which was larger than the AUCs for the PKUPH model (0.717, P=0.755) and the Mayo model (0.652, P=0.275). Compared with the PKUPH and Mayo models, the NRI of our model increased by 3.7% (P=0.731) and 27.78% (P=0.008), respectively, while the IDI changed −4.77% (P=0.437) and 11.67% (P=0.015), respectively. Moreover, the DCA demonstrated that our model had a higher overall net benefit compared to previously published models. Importantly, similar findings were confirmed in the validation cohort.Conclusions: Age, border, and serum ALB levels were independent diagnostic markers of eNSCLC. Thus, our model could more accurately distinguish BPNs from eNSCLC and outperformed previously published models.