This review examines trends in the ESRD program, assessing progress in preventive care, hospitalizations, and mortality since 1989, the year of the Dallas Morbidity and Mortality Conference. The number of prevalent dialysis patients nearly tripled, to 366,000 in 2007 from 123,000 in 1989. Prevalent population mortality rates declined in the mid-1980s but did not change overall through the 1990s; rates declined for patients on dialysis for less than 5 yr but increased for patients on dialysis for longer than 5 yr. Death rates throughout the prevalent population have subsequently declined since 2000. In the incident dialysis population, death rates after the first year have declined, but first-year rates have remained flat since 1996; rates peak in months 2 and 3, then decline to the level of the first month by 12 mo. Infectious hospitalization rates in the prevalent population increased 40% in the last 10 yr. For incident patients, infectious hospitalizations increased almost 100% over 10 yr, vascular access hospitalizations by 200%, and cardiovascular hospitalizations by 30%. Use of dialysis catheters is high; 82% of patients start dialysis with a catheter. Poor planning for dialysis initiation may contribute to catheter use and the associated high infectious hospitalization rate, limiting potential for improved patient survival during the first year. Public health programs, including the new Medicare chronic kidney disease education benefit, are needed to promote better care of patients who may need dialysis to reduce the high morbidity and mortality in the first year.

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Our results indicate that aberrant SOX11 gene promoter methylation may underlie its down-regulation in GC. SOX11 gene promoter hyper-methylation may serve as a biomarker to predict the clinical outcome of GC.

Single nucleotide polymorphisms (SNPs) in energy metabolism related gene may be key agents in the development of human malignancies. In this study, we aimed to examine the association of transcription factor 7-like 2, Leptin (LEP) and LEP receptor (LEPR) polymorphisms with esophageal squamous cell carcinoma (ESCC). A total of 507 ESCC cases and 1,496 controls were enrolled. We found that LEPR rs6588147 AA genotype was associated with ESCC risk (AA vs. GG/GA: adjusted OR=1.90, 95%CI=1.00–3.61, P=0.049). In the stratified analyses, LEPR rs6588147 G>A polymorphism increased the risk of ESCC (<63 years subgroup: AA vs. GG: adjusted OR=2.58, 95%CI=1.00–6.62, P=0.049 and AA vs. GA/GG: adjusted OR=2.71, 95%CI=1.06–6.91, P=0.038; male subgroup: AA vs. GG: adjusted OR=2.19, 95%CI=1.02–4.67, P=0.044 and AA vs. GA/GG: adjusted OR=2.26, 95%CI=1.06–4.80, P=0.035). However, LEP rs7799039 A>G decreased the risk of ESCC (≥63 years subgroup: GG vs. AA: adjusted OR=0.47, 95%CI=0.23–0.95, P=0.035 and GG vs. AA/AG: adjusted OR=0.48, 95%CI=0.24–0.96, P=0.038; BMI≥24 kg/m2 subgroup: AG vs. AA: adjusted OR=0.66, 95%CI=0.45–0.99, P=0.044). In addition, LEPR rs1137101 G>A polymorphism decreased ESCC risk in some subgroups (ever smoking subgroup: GA vs. GG: adjusted OR=0.66, 95%CI=0.44–1.00, P=0.049; ever drinking subgroup: GA vs. GG: adjusted OR=0.54, 95%CI=0.31–0.95, P=0.031 and GA/AA vs. GG: adjusted OR=0.54, 95%CI=0.31–0.93, P=0.027). Our findings suggest that LEPR rs6588147 G>A polymorphism is associated with the increased risk of ESCC; however, LEP rs7799039 A>G and LEPR rs1137101 G>A polymorphisms may be protective factors for ESCC.

Single nucleotide polymorphisms (SNPs) in Programmed cell death 1 (PD-1) gene may contribute to the development of cancer. In this study, we selected PD-1 rs10204525 T>C, rs2227982 A>G, rs36084323 T>C and rs7421861 A>G polymorphisms and designed a hospital-based case-control study to determine the potential relationship between these functional SNPs in PD-1 gene and esophagogastric junction adenocarcinoma (EGJA) risk. A total of 1,063 EGJA patients and 1,677 controls were enrolled from Eastern Chinese Han population. SNPscanTMgenotyping assay was used to analyze the genotyping of PD-1 polymorphisms. We found that PD-1 rs7421861 A>G polymorphism was associated with the development of EGJA. However, PD-1 rs2227982 A>G polymorphism was a protective factor for EGJA. In addition, PD-1 rs36084323 CC homozygote genotype might be associated with a borderline decreased risk of EGJA. In a subgroup analysis, a decreased risk of EGJA in never drinking and never smoking groups was identified. Haplotype comparison analysis suggested that PD-1 Trs10204525Grs2227982C36084323Ars7421861 haplotype significantly decreased the risk of EGJA. However, Trs10204525Grs2227982C36084323Grs7421861 haplotype in PD-1 gene may confer risk to EGJA. In conclusion, our study highlights rs2227982 A>G, rs36084323 T>C and rs7421861 A>G polymorphisms and haplotypes in PD-1 gene, especially within the intron region, are significantly associated with the risk of EGJA. Further case-control studies with larger sample size and detailed gene-environmental data to replicate these findings in different populations are needed to validate our conclusion.

To assess the potential effects of Cytotoxic T-lymphocyte antigen 4 (CTLA4) gene polymorphisms on susceptibility to gastric cardia adenocarcinoma (GCA), we genotyped four polymorphisms (rs733618 A>G, rs16840252 C>T, rs231775 G>A and rs3087243 G>A) in CTLA4 and calculated odds ratios (ORs) with the corresponding 95% confidence intervals (95% CIs) for the genotype and allele distributions between GCA cases and controls. The CTLA4 genotypes were determined by the polymerase chain reaction-ligase detection reaction (PCR-LDR) analysis in 330 GCA patients and 608 unrelated cancerfree controls. In this case-control study, there was no significant difference in the genotype and allele distributions of four CTLA4 polymorphisms between GCA patients and controls. However, haplotype association analysis indicated that compared with CTLA4 G rs733618 C rs16840252 G rs231775 C rs3087243 , CTLA4 G rs733618 C rs16840252 A rs231775 G rs3087243 and A rs733618 C rs16840252 G rs231775 A rs3087243 haplotypes conferred increased risks of GCA (OR = 6.46, 95% CI = 1.33-31.28; P = 0.012; both); however, CTLA4 A rs733618 C rs16840252Ars231775 G rs3087243 and A rs733618 T rs16840252 G rs231775 G rs3087243 haplotypes conferred decreased risks of GCA (P = 0.001 and P = 0.011, respectively). These results highlight that the rare CTLA4 haplotypes may affect the development of GCA in the Chinese population.

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