MicroRNAs (miRNAs) are often deregulated in cancer and are thought to play an important role in cancer development. Large amount of differentially expressed miRNAs have been identified in various cancers by using high-throughput methods. It is therefore quite important to make a comprehensive collection of these miRNAs and to decipher their roles in oncogenesis and tumor progression. In 2010, we presented the first release of dbDEMC, representing a database for collection of differentially expressed miRNAs in human cancers obtained from microarray data. Here we describe an update of the database. dbDEMC 2.0 documents 209 expression profiling data sets across 36 cancer types and 73 subtypes, and a total of 2224 differentially expressed miRNAs were identified. An easy-to-use web interface was constructed that allows users to make a quick search of the differentially expressed miRNAs in certain cancer types. In addition, a new function of ‘meta-profiling’ was added to view differential expression events according to user-defined miRNAs and cancer types. We expect this database to continue to serve as a valuable source for cancer investigation and potential clinical application related to miRNAs. dbDEMC 2.0 is freely available at http://www.picb.ac.cn/dbDEMC.

Hepatocellular-cholangiocarcinoma (H-ChC) is a rare subtype of liver cancer with clinicopathological features of both hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA). To date, molecular mechanisms underlying the co-existence of HCC and iCCA components in a single tumor remain elusive. Here, we show that H-ChC samples contain substantial private mutations from WES analyses, ranging from 33.1 to 86.4%, indicative of substantive intratumor heterogeneity (ITH). However, on the other hand, numerous ubiquitous mutations shared by HCC and iCCA suggest the monoclonal origin of H-ChC. Mutated genes identified herein, e.g., VCAN, ACVR2A, and FCGBP, are speculated to contribute to distinct differentiation of HCC and iCCA within H-ChC. Moreover, immunohistochemistry demonstrates that EpCAM is highly expressed in 80% of H-ChC, implying the stemness of such liver cancer. In summary, our data highlight the monoclonal origin and stemness of H-ChC, as well as substantial intratumoral heterogeneity.

Meta-analyses on coffee and cancer incidence mainly restricted to limited cancers. We carried out a more comprehensive meta-analysis of cohort studies to explore association between coffee and most cancer types. We conducted comprehensive search and summarized relative risk (RR) and 95% confidence intervals for the highest versus lowest coffee intake and cancer using STATA12. We conducted dose-analysis if result suggested significant association. The publication bias was evaluated with begg’s and egger’s test. Finally, 105 individual prospective studies were included. Inverse associations were observed on oral, pharyngeal, colon, liver, prostate, endometrial cancer and melanoma, with RR 0.69 (95% CI = 0.48–0.99, I2 = 73.4%, P = 0.044), 0.87 (95% CI = 0.78–0.96, I2 = 28.4%, P = 0.007), 0.46 (95% CI = 0.37–0.57, I2 = 0%, P = 0), 0.89 (95% CI = 0.84–0.93, I2 = 30.3%, P = 0.003), 0.73 (95% CI = 0.67–0.80, I2  = 0%, P = 0) and 0.89 (95% CI = 0.80–0.99, I2  = 0%, P = 0.031) respectively. However, the relative risk for lung cancer is 2.18 (95% CI = 1.26–3.75, I2  = 63.3%, P = 0.005). The summary relative risk for increment of 2 cups of coffee were RR = 0.73, 95% CI = 0.67–0.79 for liver cancer, RR = 0.97, 95% CI = 0.96–0.98 for prostate cancer and RR = 0.88, 95% CI = 0.85–0.92 for endometrial cancer. Accordingly, coffee intake was associated with reduced risk of oral, pharynx, liver, colon, prostate, endometrial cancer and melanoma and increased lung cancer risk.