BackgroundRecently, serum 25-hydroxyvitamin D (25OHD) levels were shown to be associated with the survival of patients with colorectal cancer. However, 25OHD levels were measured a median of 6 years before diagnosis or were predicted levels. In this study, we directly measured serum 25OHD levels at surgery and examined the association with survival among patients with colorectal cancer.MethodsWe started a prospective cohort study to find prognostic factors in patients with colorectal cancer from 2003 to 2008 and stored serum samples and clinical data. As part of a post-hoc analysis, serum 25OHD levels were measured by radioimmunoassay. Association between overall survival and serum 25OHD levels were computed using the Cox proportional hazard model adjusted for month of serum sampling as well as age at diagnosis, gender, cancer stage, residual tumor after surgery, time period of surgery, location of tumor, adjuvant chemotherapy and number of lymph nodes with metastasis at surgery. Unadjusted and adjusted hazard ratios (HR) and 95% confidence intervals (95% CI) were determined.ResultsSerum 25OHD levels were measured in 257 patients. Only 3% had sufficient levels (30 ng/ml and greater). Based on month of blood sampling, an annual oscillation of 25OHD levels was seen, with levels being lower in spring and higher in late summer. Higher 25OHD levels were associated with better overall survival under multi-variate analysis (HR, 0.91: 95% CI, 0.84 to 0.99, P = 0.027).ConclusionsThese results suggest that higher 25OHD levels at surgery may be associated with a better survival rate of patients with colorectal cancer.

Background: To elucidate whether maternal vitamin D supplementation during lactation improves infantile eczema and other subsequent allergic disorders, a randomized, double-blind, placebo-controlled trial was performed. Methods: Mothers (n = 164) of infants with facial eczema at 1 month check-up were randomly assigned to receive vitamin D3 supplements (n = 82; 800 IU/day) or placebo (n = 82) for 6 weeks from May 2009 to January 2011. The primary outcome was infantile eczema quantified on Scoring Atopic Dermatitis (SCORAD) index at 3 month check-up, and the secondary outcomes were atopic dermatitis, food allergy, and wheeze diagnosed by doctors up to 2 years of age.Results: There was no significant difference in SCORAD at 3 month check-up between the two groups. Doctordiagnosed food allergy was significantly more common up to age 2 years in the vitamin D group (10/39, 25.7%) than in the placebo group (3/40, 7.5%; risk ratio (RR), 3.42; 95% confidence interval [CI]: 1.02-11.77; P = 0.030). Moreover, at least one secondary outcome was also significantly more common in the vitamin D group (17/39, 43.6%) than in the placebo group (7/40, 17.5%; RR, 2.49; 95%CI: 1.16-5.34; P = 0.012).Conclusions: Vitamin D supplementation may not decrease the severity of infantile eczema at 3 months of age, but may rather increase the risk of later food allergy up to 2 years of age. Because a large number of subjects was lost to follow up, further study is needed to confirm the findings.Key words food allergy, infantile eczema, prevention, randomized controlled trial, vitamin D.The discovery that immune cells possess both the enzyme to activate 25-hydroxyvitamin D (25OHD), the major circulating form of vitamin D in serum, and its receptor within the cells 1,2 has provided new insights into the immune function of this vitamin. Following extensive research in the field of immunology, active vitamin D was found to suppress dendritic cell maturation and consequent T-helper (Th) 1 cell development.3 It has been implied that delayed maturation of Th1-associated functions during early postnatal life increases the risk for sensitization to allergens, resulting in atopic disorders. 4 Of interest, the time course of the vitamin D intervention policy for early infants to prevent rickets during the last 30 years runs in parallel with the increased prevalence of allergic diseases.5 Therefore, Wjst and Dold hypothesized that vitamin D supplementation either through cod oil or formula milk during early infancy may be a risk factor for atopic disorders later in life. 6,7 Indeed, the UK long-term cohort study showed that children whose mothers had 25OHD concentration in pregnancy >30 ng/mL, which is considered within the normal range for adults, had an increased risk of eczema on examination at 9 months and of asthma at age 9 years compared with children whose mothers had a concentration <12 ng/mL. 8 Moreover, a Finnish 30 year long-term cohort study demonstrated an association between vitamin D supplementation in infancy and an increased risk ...

BACKGROUND: Recently, the vitamin D receptor (VDR) polymorphism FokI was shown to be associated with susceptibility to ovarian cancer. We aimed to examine whether VDR FokI polymorphisms influence the survivals of patients with epithelial ovarian cancer (EOC). METHODS: VDR polymorphisms from FokI in 101 patients with EOC were genotyped by sequencing. Overall survival was compared between FokI single nucleotide polymorphism using Kaplan -Meier survival curves with log-rank tests and the Cox proportional hazard model adjusted for ages, stages, histology, and existence of residual tumour. RESULTS: The FokI C/C genotypes were associated with better prognosis compared with the C/T and T/T genotypes (log-rank test: P ¼ 0.008; adjusted hazard ratio, 0.18; 95%CI 0.05 -0.61; P ¼ 0.006). CONCLUSIONS: These results suggest that the VDR polymorphisms from the FokI genotype may be associated with improved prognosis of patients with EOC.

BackgroundIn patients with advanced non-small-cell lung cancer, vitamin D receptor (VDR) polymorphisms and haplotypes are reported to be associated with survival. We hypothesized that a similar association would be observed in patients with head and neck squamous-cell carcinoma (HNSCC).MethodsIn a post-hoc analysis of our previous prospective cohort study, VDR polymorphisms including Cdx2 G/A (rs11568820), FokI C/T (rs10735810), BsmI A/G (rs1544410), ApaI G/T (rs7976091), and TaqI T/C (rs731236) were genotyped by sequencing in 204 consecutive patients with HNSCC who underwent tumor resection. Progression-free survival was compared between VDR polymorphisms using Kaplan-Meier survival curves with log-rank tests and Cox proportional hazard models adjusting for age, gender, smoking status, primary tumor sites, postoperative stages, existence of residual tumor, and postoperative treatment with chemotherapy or radiotherapy.ResultsDuring a median follow-up of 1,047 days, tumor progression and death occurred in 76 (37.3%) and 27 (13.2%) patients, respectively. The FokI T/T genotype was associated with poor progression-free survival: median survival for T/T was 265 days compared with 1,127 days for C/C or C/T (log-rank test: P = 0.0004; adjusted hazard ratio, 3.03; 95% confidence interval, 1.62 to 5.67; P = 0.001). In contrast, the other polymorphisms (Cdx2, BsmI, ApaI, TaqI) showed no significant association with progression-free survival. The A-T-G (Cdx2-FokI-ApaI) haplotype demonstrated a significant association with a higher progression rate (P = 0.02).ConclusionThese results suggest that VDR polymorphisms and haplotypes may be associated with prognosis in patients with HNSCC, although the sample size is not large enough to draw definitive conclusions.

Tumors with certain mutations in the epidermal growth factor receptor (EGFR) family genes dramatically respond to EGFR inhibitors. Therefore, these mutations are important factors that influence disease progression and patient survival. We previously studied the mutation status of EGFR in patients with head and neck squamous cell carcinoma (HNSCC). However, the mutation status of lymph node metastases and the frequency of mutations in EGFR family genes have not been extensively studied. In this study, we sequenced the catalytic domains of the three other members of the EGFR family, HER2, HER3, and HER4 in 92 clinical samples of HNSCC. We identified a HER2 mutation (K716E) in one sample but no mutations were found in HER3 or HER4. Next to investigate the relationship between EGFR mutations and tumor metastasis, we compared the DNA sequences of the EGFR gene between the primary tumor and the lymph node metastasis in 31 clinical samples. Only one of the patients with an EGFR mutation in the primary HNSCC carried the same mutation (L858R) in the lymph node metastasis. Finally, we explored the tumorigenic potential of the EGFR mutations that we had previously identified and their sensitivity to two different EGFR tyrosine kinase inhibitors (CL-387785, OSI-420). Ba/F3 cells transformed with mutant EGFR genes were sensitive to treatment with lower concentrations of CL-387785 than of OSI-420. These results contribute to our understanding of the genetic basis of drug sensitivity and will help design drugs that specifically target different subtypes of HNSCC.