Philadelphia-chromosome negative myeloproliferative neoplasms (MPN) are a heterogeneous group of clonal hematopoietic stem cell disorders characterized by an increased risk of thrombosis and progression to acute myeloid leukemia. MPN are associated with driver mutations in JAK2, CALR and MPL which are crucial for the diagnosis and lead to a constitutive activation of the JAK-STAT signaling, independent of cytokine regulation. Moreover, most patients have concomitant mutations in genes involved in DNA methylation, chromatin modification, messenger RNA splicing, transcription regulation and signal transduction. These additional mutations may arise before, in the context of clonal hematopoiesis of indeterminate potential (CHIP), or after the acquisition of the driver mutation. The clinical phenotype of MPN results from complex interactions between mutations and host factors. The increased application of next-generation sequencing (NGS) techniques to a large series of patients with MPN has expanded the knowledge of mutational landscape and contributed to define the clinical significance of mutations. This molecular information is being increasingly used to refine diagnosis, risk stratification, monitoring of residual disease and response to treatment. ASXL1, SRSF2, EZH2, IDH1/IDH2 and U2AF1 mutations are associated with a more advanced disease and reduced overall survival in primary myelofibrosis (PMF), whereas spliceosome mutations in Polycythemia vera (PV) and essential thrombocythemia (ET) adversely affect both overall (SF3B1, SRSF2 in ET and SRSF2 in PV) and myelofibrosis-free (U2AF1, SF3B1 in ET) survival. This review discusses current knowledge of the molecular landscape of MPN, and how the availability of those molecular information may impact patient management.[This corrects the article DOI 10.2147/OTT.S229614.].Langerhans cell histiocytosis (LCH) is a rare myeloid neoplasia in children. BRAF mutations are associated with permanent diabetes insipidus (DI). The onset of clinical DI is always latent with imaging evidence of pituitary involvement. In this study, we reported three children with BRAF-mutated LCH with pituitary involvement who improved after targeted therapy (dabrafenib and trametinib). The results may indicate that pituitary involvement may be reversible in some patients with LCH if it is observed and treated before clinical DI. Targeted therapy may be an effective choice for LCH patients with early pituitary involvement who were irresponsive to first-line or second-line chemotherapy. However, a relapse after targeted therapy is completed in patients with persistently positive cfBRAFV600E mutations is still a challenge that needs to be resolved. The timing of introducing targeted therapy, its appropriate duration and effective combinations with chemotherapy or other targeted drugs should be explored further. To establish a novel circRNA-miRNA-mRNA network associated with the poor prognosis of hepatocellular carcinoma (HCC). Quantitative real-time PCR was used to verify the differentially expressed circRNA. Moreover, the competing endogenous RNA networks were established using bioinformatics methods. Meanwhile, the prognostic value and potential mechanism of ceRNA network in hepatocellular carcinoma (HCC) were analyzed. This work found that was highly expressed in HCC tissues and early recurring HCC. Further, we effectively constructed a ceRNA network. The ceRNA network regulated by might influence the prognosis of HCC by regulating cell cycle-related pathways. The ceRNA network proposed here can be used as a novel biomarker for the prognosis of HCC, thereby providing new insights for the targeted therapy of HCC.The ceRNA network proposed here can be used as a novel biomarker for the prognosis of HCC, thereby providing new insights for the targeted therapy of HCC. Apatinib has been proved effective in the treatment of advanced gastric cancer and a variety of solid tumors. Raltitrexed is emerging as a promising alternative for treating advanced colorectal cancer in China. This work aims to study the combinatory antitumor effect of apatinib and raltitrexed on human esophageal squamous carcinoma cells (ESCC). Two VEGFR-2-positive human ESCC lines, KYSE-30 and TE-1, were treated with apatinib or raltitrexed, or both, then the cell proliferation rate was measured by MTS assay; cell migration and invasion were studied by transwell assays; cell apoptosis rate was determined by flow cytometry; cellular autophagy level affected was analyzed by Western blot analysis; finally, quantitative polymerase chain reaction (qPCR) was used to monitor transcription and Western blot was performed to check phosphorylation of apoptotic proteins after treatment. Both apatinib and raltitrexed significantly inhibited KYSE-30 and TE-1 cell proliferation in a dose-dependent manner. Treatmentnib on human ESCC cells by down-regulating phosphorylation of Akt and Erk, implying a combination of raltitrexed and apatinib might be an effective option for treating esophageal squamous cell carcinoma patients. Human telomerase reverse transcriptase (hTERT), a crucial enzyme for telomere maintenance, has been associated with the development of ovarian cancer (OC). The purpose of this study was to investigate the difference of methylation rates of hTERT promoter in tumour tissues and plasma samples of patients with ovarian magnificent tumour and those with ovarian benign tumour, as well as in plasma samples of healthy women. This study further aimed to establish a possible association between increased methylation rate of hTERT promoter and circulating tumour DNAs (ctDNA) amongst patients with ovarian magnificent tumour. Tumour tissue samples and plasma samples were separately obtained from 17 patients with ovarian magnificent tumour (experiment group, group A) and from 15 patients with ovarian benign tumour (control group, group B). DOX inhibitor clinical trial Another 15 plasma samples were acquired from healthy women (control group, group C). Promoter methylation was assessed by methylation-specific PCR (MSP). Statistical analysis was conducted using SPSS 22.0. Methylation of hTERT was observed in 76.5% of tumour tissue samples and in 70.6% of plasma samples from patients with ovarian magnificent tumour. It was also observed in 26.7% of tumour tissue samples and 20% of plasma samples from patients with ovarian benign tumour, and in 13.3% of plasma samples from healthy women. Comparing between plasmas and tissues, the respective rates of consistency, sensitivity and specificity were 70.59%, 76.9% and 50% in group A, and 80%, 50% and 90.9% in group B. Hence, the associations of hTERT methylation with ctDNAs (p=0.001) and tumour tissue samples (p=0.012) amongst patients with ovarian magnificent tumour were established. An increased methylation of hTERT promoter is related to ctDNAs and tumour tissues of patients with ovarian magnificent tumour.An increased methylation of hTERT promoter is related to ctDNAs and tumour tissues of patients with ovarian magnificent tumour.