Low-dose apatinib and tegafur-gimeracil-oteracil as palliative treatment in recurrent cervical cancer patients with poor performance status: A case series.

WHAT IS KNOWN AND OBJECTIVE: A large proportion of recurrent cervical cancer (RCC) patients present with poor performance status (PS) after comprehensive treatments, which usually prevents them from opting for clinical trials. We retrospectively analysed the effect and safety of low-dose apatinib and tegafur-gimeracil-oteracil (TGO) in the treatment of these patients. CASE SUMMARY: Six patients treated with low-dose apatinib and TGO showed a disease control rate of 83.3% and grade 1-2 adverse events (AEs). WHAT IS NEW AND CONCLUSION: This case series indicates that low-dose apatinib and TGO could be considered as palliative therapy for RCC patients with poor PS.

Relevance function of microRNA-708 in the pathogenesis of cancer.

MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression post-transcriptionally responsible for regulating >70% of human genes. MicroRNA-708 (miR-708) is encoded in the intron 1 of the Odd Oz/ten-m homolog 4 (ODZ4) gene. Numerous researches have confirmed that the abnormal expressed miR-708 is involved in the regulation of multiple types of cancer. Notably, the expression level of miR-708 was higher in lung cancer, bladder cancer (BC) and colorectal cancer (CRC) cell lines while lower in hepatocellular carcinoma (HCC), prostate cancer (PC), gastric cancer (GC) and so on. This review provides a current view on the association between miR-708 and several cancers and focuses on the recent studies of miR-708 regulation, discussing its potential as an epigenetic biomarker and therapeutic target for these cancers. In particular, the regulated mechanisms and clinical application of miR-708 in these cancers are also discussed.

Histone deacetylases function as novel potential therapeutic targets for cancer.

Diverse cellular functions, including tumor suppressor gene expression, DNA repair, cell proliferation and apoptosis, are regulated by histone acetylation and deacetylation. Histone deacetylases (HDACs) are enzymes involved in remodeling of chromatin by deacetylating the lysine residues. They play a pivotal role in epigenetic regulation of gene expression. Dysregulation of HDACs and aberrant chromatin acetylation and deacetylation have been implicated in the pathogenesis of various diseases, including cancer. Histone deacetylases have become a target for the development of drugs for treating cancer because of their major contribution to oncogenic cell transformation. Overexpression of HDACs correlates with tumorigenesis. Previous work showed that inhibition of HDACs results in apoptosis and the inhibition of cell proliferation in multiple cells. A significant number of HDAC inhibitors have been developed in the past decade. These inhibitors have strong anticancer effects in vitro and in vivo, inducing growth arrest, differentiation, and programmed cell death, inhibiting cell migration, invasion, and metastasis, and suppressing angiogenesis. In addition, HDAC-mediated deacetylation alters the transcriptional activity of nuclear transcription factors, including p53, E2F, c-Myc, and nuclear factor-κB, as well as the extracellular signal-regulated kinase1/2, phosphatidylinositol 3-kinase, Notch, and Wnt signaling pathways. This review highlights the role of HDACs in cancer pathogenesis and, more importantly, that HDACs are potential novel therapeutic targets.