This large population-based analysis of second cancers among thyroid cancer patients suggests that there was an increase of second cancers in all sites, and the most commonly elevated second cancers were the salivary gland and kidney. Additionally, the increase in second cancers in patients with recently diagnosed thyroid microcarcinomas (<10 mm) suggests that aggressive radiation treatment of the first primary thyroid cancer, the environment, and genetic susceptibility, may increase the risk of a second cancer.

Despite an increase in the number of molecular epidemiological studies conducted in recent years to evaluate the association between HPV infection and risk of breast carcinoma, the studies remain inconclusive. Here, a meta-analysis was conducted to estimate the prevalence of HPV in breast carcinoma and test the association. Studies on HPV DNA detection in sporadic breast carcinoma in female using polymerase chain reaction were included. Information on overall and type-specific (HPV 6, 11, 16, 18, 31, 33, 35, 45 and 51) HPV prevalence were required, plus detailed descriptions of study populations, HPV DNA source, publication calendar period and PCR primers used for HPV DNA detection and typing. We revealed that 24.49% of the breast carcinoma cases were associated with HPV, 32.42% occurred in Asia and 12.91% in Europe. The four most commonly identified HPV types, in the order of decreased prevalence, were HPV33, 18, 16, and 35. The detection of HPV was mostly influenced by publication calendar period and PCR primers used. In addition, the analysis of ten case–control studies containing 447 breast carcinoma cases and 275 controls showed a significant increase in breast carcinoma risk with HPV positivity (OR = 3.63, 95% CI = 1.42–9.27). These results suggest that it’s difficult to rule out the possibility of the association of HPV and breast carcinoma at present according to available publication proofs.

Background: Recent genome-wide association studies have identified 10 single nucleotide polymorphisms (SNP) associated with colorectal cancer (CRC) in Caucasians. This study evaluated the effects of these newly identified SNPs in a Chinese population.Methods: We assessed the associations of these 10 SNPs with CRC in a case-control study that consisted of 2,124 cases and 2,124 controls. Odds ratios (OR) and 95% confidence intervals were computed by logistic regression, and cumulative effect of risk genotypes were also calculated.Results: We found that only five SNPs (rs6983267, rs4939827, rs10795668, rs3802842, and rs961253) were significantly associated with risk of CRC in our study population in the same direction as reported by previous genome-wide association studies, with the ORs ranging from 1.11 to 2.96. A cumulative effect was observed with the ORs being gradually elevated with increasing number of risk genotypes (P trend = 1.32 × 10 −21 ), and patients carrying ≥4 risk genotypes had 3.25-fold increased CRC risk (95% confidence interval,

Metabonomics is an important platform for investigating the metabolites of integrated living systems and their dynamic responses to changes caused by both endogenous and exogenous factors. A metabonomics strategy based on liquid chromatography-mass spectrometry/mass spectrometry in both positive and negative ion modes was applied to investigate the short-term and long-term stability of metabolites in plasma. Principal components analysis and ten types of identified metabolites were used to summarize the time-dependent change rules in metabolites systematically at different temperatures. The long-term stability of metabolites in plasma specimens stored at -80 °C for five years was also studied. Analysis of these subjects identified 36 metabolites with statistically significant changes in expression (p < 0.05) and found a kind of metabolite with a hundred-fold change. The stability of metabolites in blood at 4 °C for 24 h was also investigated. These studies show that a thorough understanding of the effects of metabolite stability are necessary for improving the reliability of potential biomarkers.

The introduction of new treatments for esophageal cancer including surgery, chemotherapy, radiotherapy, or a combination of these modalities has not only improved patient survival, but may also increase the risk of the second primary cancers. The available evidence is conflicting with most risk estimates based on sparse numbers. Here we estimated standardized incidence ratios (SIRs) of second cancer among 24,557 esophageal cancer survivors (at least 2 months) in the Surveillance, Epidemiology, and End Results (SEER) Program between 1973 and 2007, who had been followed up for median 6.5 years (range 2 months-29.3 years). Second cancer risk was statistically significantly elevated (SIR = 1.34, 95% confidence interval [CI]= 1.25-1.42) among the survivors compared with the general population; the SIRs for cancers of oral and pharynx, stomach, small intestine, larynx, lung and bronchus, thyroid and prostate cancer were 8.64 (95% CI = 7.36-10.07), 2.87 (95% CI = 2.10-3.82), 3.80 (95% CI = 1.82-7.00), 3.19 (95% CI = 2.12-4.61), 1.68 (95% CI = 1.46-1.93), 2.50 (95% CI = 1.25-4.47), and 0.77 (95% CI = 0.65-0.90), respectively. Radiotherapy raised cancer risk of larynx (SIR = 3.98, 95% CI = 2.43-6.14) and thyroid (SIR = 3.57, 95% CI = 1.54-7.03) among all esophageal cancer survivors. For patients who had 5-9 years of follow up after radiotherapy, the SIR for lung cancer was 3.46 (95% CI = 2.41-4.82). Patients with esophageal cancer are at increased risks of second cancers of oral and pharynx, larynx, lung, and thyroid, while at a decreased risk for prostate cancer. These findings indicate that radiotherapy for esophageal cancer patients may increase risk of developing second cancers of larynx, lung, and thyroid. Thus, randomized clinical trials to address the association of radiotherapy and the risk of secondary cancer are warranted.

Background and Aims. The nucleotide-binding domain and leucine-rich repeat containing PYD-3 (NLRP3) inflammasome has been implicated in the pathogenesis of chronic kidney disease (CKD); however, its exact role in glomerular injury and tubulointerstitial fibrosis is still undefined. The present study was performed to identify the function of NLRP3 in modulating renal injury and fibrosis and the potential involvement of mitochondrial dysfunction in the murine unilateral ureteral obstruction (UUO) model of CKD. Methods. Employing wild-type (WT) and NLRP3−/− mice with or without UUO, we evaluated renal structure, tissue injury, and mitochondrial ultrastructure, as well as expression of some vital molecules involved in the progression of fibrosis, apoptosis, inflammation, and mitochondrial dysfunction. Results. The severe glomerular injury and tubulointerstitial fibrosis induced in WT mice by UUO was markedly attenuated in NLRP3−/− mice as evidenced by blockade of extracellular matrix deposition, decreased cell apoptosis, and phenotypic alterations. Moreover, NLRP3 deletion reversed UUO-induced impairment of mitochondrial morphology and function. Conclusions. NLRP3 deletion ameliorates mitochondrial dysfunction and alleviates renal fibrosis in a murine UUO model of CKD.

No abstract

Background/Aims: Growing evidence suggests mitochondrial dysfunction (MtD) and the Nlrp3 inflammasome play critical roles in chronic kidney disease (CKD) progression. We previously reported that Aldosterone (Aldo)-induced renal injury in vitro is directly caused by mitochondrial reactive oxygen species (mtROS)-mediated activation of the Nlrp3 inflammasome. Here we aimed to determine whether a mitochondria-targeted antioxidant (Mito-Tempo) could prevent Aldo-induced kidney damage in vivo. Methods: C57BL/6J mice were treated with Aldo and/or Mito-Tempo (or ethanol as a control) for 4 weeks. Renal injury was evaluated by Periodic Acid-Schiff reagent or Masson’s trichrome staining and electron microscopy. ROS were measured by DCFDA fluorescence and ELISA. MtD was determined by real-time PCR and electron microscopy. Activation of the Nlrp3 inflammasome and endoplasmic reticulum stress (ERS) was detected via western blot. Results: Compared with control mice, Aldo-infused mice showed impaired renal function, increased mtROS production and MtD, Nlrp3 inflammasome activation, and elevated ERS. We showed administration of Mito-Tempo significantly improved renal function and MtD, and reduced Nlrp3 inflammasome activation and ERS in vivo. Conclusion: Mitochondria-targeted antioxidants may attenuate Aldo-infused renal injury by inhibiting MtD, the Nlrp3 inflammasome, and ERS in vivo. Therefore, targeting mtROS might be an effective strategy for preventing CKD.