Background PD-L1 immunohistochemistry (IHC) data in China was less reported. We systematically investigated PD-L1 IHC data of Chinese patients generated by Origimed. Methods PD-L1 was stained using IHC on cancer samples from 2060 Chinese patients in Origimed since 2017. Written informed consent was obtained from each patient. IHC staining was performed on FFPE tissue sections using anti-PD-L1 antibody 28-8. Tumor Proportion Score (TPS) was applied on all the samples. We investigated PD-L1 TPS in lung adenocarcinoma (n = 893), lung squamous carcinoma (n = 172), liver cancer (n = 404), esophageal cancer (n = 186), colorectal cancer (n = 166), pancreatic cancer (n = 136) and gastric cancer (n = 103). We then further applied PD-L1 combined positive score (CPS) on the 103 gastric cancer samples. All the slides were reviewed by the same senior pathologist. 95% confidence interval (CI) was obtained by bootstrap. Information entropy (Shannon’s formula) was measured in natural units. Results The highest proportion of PD-L1 TPS > = 1% was observed in lung squamous carcinoma (49%; 95% CI: [43%, 59%]), followed by lung adenocarcinoma (25%; 95% CI: [22%, 28%]), liver cancer (14%; 95% CI: [11%, 18%]), esophageal cancer (12%; 95% CI: [8.1%, 17%]), pancreatic cancer (11%; 95% CI: [5.9%, 16%]), gastric cancer (7%; 95% CI: [1.9%, 12%]) and colorectal cancer (4%; 95% CI: [1.2%, 6.6%]). The proportion of PD-L1 CPS > = 1 for gastric cancer was 17% (95% CI: [9.7%, 24%]). In gastric cancer, information entropy of TPS and CPS was 0.40 and 0.78, respectively. Conclusions The proportion of PD-L1 TPS > = 1% in Chinese lung squamous cell carcinoma (49%) was much higher than that in lung adenocarcinoma (25%). PD-L1 CPS contained more information than TPS in gastric cancer. Thus, we recommend applying CPS to gastric cancer in China. Legal entity responsible for the study The authors. Funding Has not received any funding. Disclosure X. Pan: Full / Part-time employment: Origimed. Y. Dai: Full / Part-time employment: Origimed. D. Chen: Full / Part-time employment: Origimed. K. Wang: Full / Part-time employment: Origimed. X. Dong: Full / Part-time employment: Origimed. All other authors have declared no conflicts of interest.

The microsomal epoxide hydrolase 1 (EPHX1) Tyr113His and His139Arg polymorphisms have been reported to be associated with esophageal cancer (EC) risk, yet the results of these previous results have been inconsistent or controversial. The objective of this study was to explore whether the EPHX1 Tyr113His and His139Arg polymorphisms confer risk to EC. The relevant studies were identified through a search of PubMed, Excerpta Medica Database (Embase), Elsevier Science Direct, and Chinese Biomedical Literature Database until May 2013. The association between the EPHX1 Tyr113His and His139Arg polymorphisms and EC risk was pooled by odds ratios (ORs) together with their 95% confidence intervals (95%CIs). A total of eight case-control studies with 1163 EC patients and 1868 controls (seven studies for both Tyr113His and His139Arg polymorphisms, one study only for Tyr113His polymorphism) were eventually identified. We found no association between EPHX1 Tyr113His and His139Arg polymorphisms and EC risk in overall population (For Tyr113His: His vs. Tyr: OR = 1.05, 95%CI = 0.95-1.15, P = 0.379; His/His vs. Tyr/Tyr: OR = 1.04, 95%CI = 0.88-1.22, P = 0.208; His/Tyr vs. Tyr/Tyr: OR = 0.96, 95%CI = 0.80-1.15, P = 0.577; His/His vs. His/Tyr + Tyr/Tyr: OR = 1.10, 95%CI = 0.96-1.26, P = 0.164; His/His + His/Tyr vs. Tyr/Tyr: OR = 1.01, 95%CI = 0.90-1.12, P = 0.543. For His139Arg: Arg vs. His: OR = 1.04, 95%CI = 0.94-1.14, P = 0.465; Arg/Arg vs. His/His: OR = 1.06, 95%CI = 0.91-1.24, P = 0.470; Arg/His vs. His/His: OR = 1.03, 95%CI = 0.91-1.16, P = 0.673; Arg/Arg vs. Arg/His + His/His: OR = 1.04, 95%CI = 0.85-1.27, P = 0.708; Arg/Arg + Arg/His vs. His/His: OR = 1.02, 95%CI = 0.93-1.13, P = 0.617). In subgroup analysis based on ethnicity, significant association has been found in neither EPHX1 Tyr113His nor His139Arg polymorphism. The current meta-analysis suggests no evidence of association between the EPHX1 polymorphism and EC risk.

The WW domain-containing oxidoreductase (WWOX) gene is a candidate tumor suppressor gene. However, its exact mechanism is unclear. This study aimed to investigate the role of the WWOX gene in the development of nasopharyngeal carcinoma (NPC). Tissues were collected from 65 NPC patients. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis and immunohistochemistry were performed on NPC tissues to determine the expression of WWOX in NPC. The status of WWOX promoter methylation was analyzed by methylation-specific PCR. Moreover, a PCR-based loss of heterozygosity (LOH) assay was conducted to detect the presence of WWOX deletion in NPC. The expression of WWOX in NPC tissues was significantly downregulated compared with that in non-tumorous tissues (P<0.05). The low expression of WWOX was significantly correlated with clinical TNM stage (P<0.05). In addition, methylation of WWOX was detected in 27 (87%) of 31 WWOX protein negative tissues, suggesting that methylation of the WWOX promoter may regulate its expression. We found that a relatively high percentage of LOH was observed in NPC tissues. A significant inverse correlation between WWOX expression and methylation of its promoter was found in NPC tissue (rs=-0.582, P=0.001). However, LOH was not correlated with WWOX expression and methylation of its promoter. Our results show that WWOX gene alteration is an early genetic alteration and may contribute to tumorigenesis of NPC. WWOX may be an important prognostic marker in NPC.