Pancreatic cancer (PC) is one of the deadliest cancers worldwide. Surgical resection remains the only curative therapeutic treatment for this disease, although only the minority of patients can be resected due to late diagnosis. Systemic gemcitabine-based chemotherapy plus nab-paclitaxel are used as the gold-standard therapy for patients with advanced PC; although this treatment is associated with a better overall survival compared to the old treatment, many side effects and poor results are still present. Therefore, new alternative therapies have been considered for treatment of advanced PC. Several preclinical studies have demonstrated that curcumin, a naturally occurring polyphenolic compound, has anticancer effects against different types of cancer, including PC, by modulating many molecular targets. Regarding PC, in vitro studies have shown potent cytotoxic effects of curcumin on different PC cell lines including MiaPaCa-2, Panc-1, AsPC-1, and BxPC-3. In addition, in vivo studies on PC models have shown that the anti-proliferative effects of curcumin are caused by the inhibition of oxidative stress and angiogenesis and are due to the induction of apoptosis. On the basis of these results, several researchers tested the anticancer effects of curcumin in clinical trials, trying to overcome the poor bioavailability of this agent by developing new bioavailable forms of curcumin. In this article, we review the results of pre-clinical and clinical studies on the effects of curcumin in the treatment of PC.

MicroRNAs are short (21–23 nucleotides), noncoding RNAs that typically silence posttranscriptional gene expression through interaction with target messenger RNAs. Currently, miRNAs have been identified in almost all studied multicellular eukaryotes in the plant and animal kingdoms. Additionally, recent studies reported that miRNAs can also be encoded by certain single‐cell eukaryotes and by viruses. The vast majority of viral miRNAs are encoded by the herpesviruses family. These DNA viruses including Epstein‐Barr virus encode their own miRNAs and/or manipulate the expression of cellular miRNAs to facilitate respective infection cycles. Modulation of the control pathways of miRNAs expression is often involved in the promotion of tumorigenesis through a specific cascade of transduction signals. Notably, latent infection with Epstein‐Barr virus is considered liable of causing several types of malignancies, including the majority of gastric carcinoma cases detected worldwide. In this review, we describe the role of the Epstein‐Barr virus in gastric carcinogenesis, summarizing the functions of the Epstein‐Barr virus‐encoded viral proteins and related epigenetic alterations as well as the roles of Epstein‐Barr virus‐encoded and virally modulated cellular miRNAs.

Corticosteroids induce apoptosis in both normal and neoplastic lymphocytes. For this reason they are commonly used to treat autoimmune disorders and lymphoid malignancies also. The exact mechanism of corticosteroid-induced apoptosis is not fully understood despite the fact that much has been found in respect to several supposed involved mechanisms. This process is arbitrarily divided in several phases. Firstly, glucocorticoid enters the cell and binds to the glucocorticoid receptor (GR) in the cytoplasm. The GR changes conformation and the heat shock proteins, normally bound to the receptor in the steady state, fall off. The activated GR-hormone complex enters the nucleus and binds to its specific DNA binding site, the glucocorticoid responsive element (GRE), thus resulting in activating or repressing transcription of genes. The activation of caspases or other proteases and endonucleases finally results in the commitment to cell death.