Because reduced DNA repair capacity (phenotype) has been suggested as a risk factor for squamous cell carcinoma of the head and neck (SCCHN), newly-identified DNA repair gene polymorphisms (genotype) may also be implicated in risk. To test this hypothesis, we conducted a case-control study of 203 SCCHN patients and 424 control subjects (matched for age, sex and ethnicity) to investigate the role of two XRCC1 polymorphisms (XRCC1 26304 T and XRCC1 28152 A, respectively) in SCCHN. Multivariate logistic regression analysis was performed to calculate the adjusted odds ratio (OR) and 95% confidence interval (CI). A total of 180 cases (88.7%) and 363 controls (85.6%) lacked the XRCC1 26304 T allele [adjusted OR = 1.34 (CI, 0.80-2.25)]. Lack of this polymorphism was a significant risk factor specifically for cancers of the oral cavity and pharynx [adjusted OR = 2.46 (CI, 1.22-4.97)]. Thirty-two cases (15.8%) and 46 controls (10.8%) were homozygous for the XRCC1 28152 A allele [adjusted OR = 1.59 (CI, 0.97-2.61) for all cases, and 1.41 (CI, 0. 80-2.48) for oral and pharyngeal cancer only]. Furthermore, when the two genotypes were combined into a three-level model of risk, a polymorphism-polymorphism interaction of increasing risk (trend test, P = 0.049) was evident: OR = 1.0 for those with neither risk genotype (referent group), adjusted OR = 1.51 (CI, 0.87-2.61) for those with either risk genotype, and 2.02 (CI, 1.00-4.05) for those with both risk genotypes. For oral and pharyngeal cancer, this trend was even more pronounced with the adjusted OR = 2.68 (CI, 1.28-5.61) for those with either risk genotype, and 3.22 (CI, 1.33-7.81) for those with both risk genotypes. The findings support the hypothesis that a polymorphic XRCC1 DNA repair gene contributes to risk of developing SCCHN.

In this case-control analysis, the XRCC3 18067T polymorphism is associated with DTC risk. However, such work needs confirmation in larger studies.

SLFN11 is frequently methylated in human CRC, and the expression of SLFN11 is regulated by promoter region methylation. Methylation of SLFN11 reduced the sensitivity of CRC cells to cisplatin.

Background:The purpose of this meta-analysis from randomized controlled trials (RCTs) was to determine the efficacy and safety of the preoperative use of gabapentin for the treatment of acute and chronic postoperative pain following breast cancer surgery.Methods:In November 2017, a systematic computer-based search was conducted in PubMed, Embase, Web of Science, Cochrane Library, and Google databases. RCTs comparing gabapentin with placebo in patients undergoing breast cancer surgery were retrieved. The primary endpoint was the visual analog scale (VAS) after surgery and 24 hours after surgery and total morphine consumption. The secondary outcomes were incidence of chronic pain and complications (the incidence of nausea). Software Stata 12.0 was used for meta-analysis.Results:Finally, 9 RCTs were included in the meta-analysis. Results indicated that gabapentin was associated with reduced pain scores after surgery and 24 hours after surgery. Meanwhile, oral gabapentin was associated with a reduction of the total morphine consumption after breast cancer surgery. Similarly, gabapentin was associated with a reduction in the incidence of chronic pain and the incidence of nausea.Conclusions:Preoperative use of gabapentin was able to reduce acute and chronic postoperative pain, total morphine consumption and the occurrence of nausea following breast cancer surgery. Further studies should determine the optimal dose of gabapentin for pain control after breast cancer surgery.

Background DIRAS1 is a new member of the Ras gene family. It was described as a potential tumor suppressor in human glioblastomas and esophageal cancer. The role of DIRAS1 in colorectal cancer remains unclear.MethodsTo explore the epigenetic changes and function of DIRAS1 in human colorectal cancer, we studied ten colorectal cancer cell lines and 146 primary colorectal cancer samples and 50 matched adjacent samples using semi-quantitative reverse transcription PCR, immunohistochemistry, methylation-specific PCR and bisulfite sequencing, western blot, flow cytometry, and transwell assays.Results DIRAS1 expression was found in DKO and HCT116 cells, while reduced expression was detected in LoVo, SW48, LS180, and SW620 cells, and there was no expression detected in DLD1, HT29, RKO, and SW480 cells. Complete methylation was found in the promoter region of DLD1, HT29, RKO, and SW480 cells. Partial methylation was detected in LoVo, LS180, SW48, and SW620 cells, and unmethylation was found in DKO and HCT116 cells. These results indicate that promoter region methylation correlated with loss of/reduced expression of DIRAS1. Re-expression of DIRAS1 was induced by 5-aza-2′-deoxycytidine, suggesting that the expression of DIRAS1 is regulated by promoter region methylation. DIRAS1 was methylated in 47.3% (69/146) of primary colorectal cancer samples, no methylation was found in non-cancerous colonic tissue samples. Methylation of DIRAS1 was significantly associated with TNM stage (P < 0.05) and short survival time (P = 0.0121). DIRAS1 induced apoptosis and inhibited cell proliferation, migration, and invasion in colorectal cancer. Finally, DIRAS1 suppressed colorectal cancer cell xenograft growth in nude mice.Conclusions DIRAS1 is frequently methylated in human colorectal cancer and the expression of DIRAS1 is regulated by promoter region methylation. Methylation of DIRAS1 is a marker of poor prognosis in human colorectal cancer.Electronic supplementary materialThe online version of this article (doi:10.1186/s13148-017-0348-0) contains supplementary material, which is available to authorized users.

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Preliminary results indicated that pretreatment WTLG measured by F-FDG-PET/CT could independently predict survival in patients with locally advanced SCCC.

Objective: To determine the association between glutathione S-transferase (GST) polymorphisms and the risk of differentiated thyroid carcinoma (DTC) and benign thyroid tumors.Design: Case-control study.Setting: Tertiary care cancer center. Patients:Two hundred one patients with DTC, 103 patients with benign thyroid tumors, and 680 cancer-free control subjects. Main Outcome Measures:Results of a polymerase chain reaction-based assay for genotyping. A multivariate logistic regression analysis was performed with adjustment for age, sex, ethnicity, tobacco use, and alcohol use. Results:The patients with DTC were younger, more likely to be female and nonwhite, and less likely to smoke or consume alcohol than the controls. Overall, 55.2% of the DTC cases and 52.6% of the controls were null for the gene for GST-µ1 (GSTM1) (P=.52), and 25.4% of the DTC subjects and 20.6% of the controls were null for the GST-1 gene (GSTT1) (P=.15). However, 15.9% of the DTC cases but only 9.4% of the controls were null for both genes (P =.009). In addition, the results of the adjusted multivariate regression analysis suggested that having both null genotypes was associated with an increased risk for DTC (odds ratio [OR], 2.1 [95% confidence interval, 1.3-3.5; P=.003]). This was particularly true for women (OR, 2.5), current smokers (OR, 3.6), and nonwhites (OR, 5.6). A similar analysis demonstrated a nonsignificant association between these genotypes and benign thyroid tumors (OR, 1.5 [95% confidence interval, 0.7-3.0; P=.30). Conclusions:Our results suggest that the simultaneous presence of the GSTM1-and GSTT1-null genotypes is a susceptibility factor for DTC. Such knowledge may ultimately help refine cancer prevention efforts; however, larger studies are needed to verify these findings.