Circular RNA (circRNA) is a key regulator of cancer, and it has been proved to be involved in the regulation of cancer progression including non-small cell lung cancer (NSCLC). Circ-PITX1 was found to be a significantly upregulated circRNA in NSCLC, and its role and potential mechanism in NSCLC progression deserve further investigation.
 
  The expression levels of circ-PITX1, microRNA (miR)-1248 and cyclin D2 (CCND2) were examined by quantitative real-time PCR (qRT-PCR). Cell proliferation, apoptosis, cell cycle process, migration and invasion were determined using cell counting kit 8 (CCK8) assay, colony formation assay, flow cytometry, wound healing assay and transwell assay. Xenograft models were built to explore the role of circ-PITX1 in NSCLC tumor growth in vivo. The glycolysis and glutamine metabolism of cells were assessed by detecting the consumptions of glucose and glutamine, cell extracellular acidification rate (ECAR), and the productions of lactate, α-ketoglutaric acid (α-KG) and ATP. The proteionge of miR-1248 to promote NSCLC progression by upregulating CCND2.Hairy cell leukemia variant (HCL-v) is a rare B-cell lymphoproliferative disorder with distinct immunophenotypic and molecular characteristics when compared to classical hairy cell leukemia (HCL-c). In contrast to the enormous progress in therapeutic options for HCL-c, HCL-v remains a therapeutic challenge due to inferior outcomes with standard chemoimmunotherapy and BCR signaling pathway inhibitors, and due to the fact that HCL-v has limited molecular therapeutic targets. In addition, because of the rarity of the disease, there is a paucity of later phase studies or multicenter trials to guide treatment decisions. In this article, we briefly review the diagnostic criteria and clinical characteristics of HCL-v and present a comprehensive overview of current therapeutic options in HCL-v.
  Polymerase epsilon (POLE) mutations are considered as one of the most potential and promising biomarkers for immune checkpoint inhibitors (ICIs) in patients with colorectal cancer. However, the treatment of ICIs sometimes also resulted in unsatisfactory results in patients with POLE mutations, which revealed that not all mutations on POLE contribute to tumor regression in colorectal cancer.
 
  We herein reported a case in which the patient with advanced colon cancer harboring somatic POLE F367S mutation, along with microsatellite stability status, has achieved efficacy of complete response to the programmed cell death 1 (PD-1) receptor inhibitor pembrolizumab, as well as a progression-free survival more than 49 months, and still in extension.
 
  Somatic POLE F367S mutation might be presented as a sensitive predictor to pembrolizumab in patients with colon cancer.
 Somatic POLE F367S mutation might be presented as a sensitive predictor to pembrolizumab in patients with colon cancer.
  Perivascular epithelioid cell neoplasms (PEComas) are rare mesenchymal tumors that originate from perivascular epithelioid cells. The uterus is the second most common organ to be affected by PEComa. Most PEComas are benign and the prognosis is usually good. Surgery is the main treatment at present, and adjuvant therapy is mainly used for malignant cases. However, because of the lack of described cases, the best diagnosis and treatment of these tumors cannot be determined.
 
  From 2009 to 2020, 13 patients from Shengjing Hospital (China Medical University), with uterine PEComa, who met the inclusion criteria and appropriate pathological diagnosis were enrolled in this study. Clinical, pathological, and therapeutic features were retrospectively analyzed to determine the best approach towards diagnosis and treatment.
 
  All the enrolled patients underwent surgical treatment; four of them had a malignant PEComa. Three of the malignant patients received chemotherapy after surgery; among them, one died, another shoill the main treatment, high-risk patients can be given adjuvant treatment to strengthen disease control.
  Polarization of microglia cells in the glioma microenvironment is closely related to the malignant progression and invasion of gliomas. Prolyl 4-hydroxylase subunit α1 (P4HA1) is the rate-limiting subunit of prolyl 4-hydroxylase (P4H). In previous studies, we showed that P4HA1 could promote the proliferation, migration, and invasion of glioma cells, but the specific mechanisms through which this occurs have not been fully elucidated.
 
  Interactions between glioma and microglia cells were analyzed using bioinformatics. Then, co-culture models were used to obtain conditioned media. To characterize microglial cell polarization, we used PCR and immunofluorescence. Proliferation and invasion assays were used to explore the biological behavior of glioma cells affected by microglia. Finally, marker expression was detected using immunohistochemistry in glioblastoma multiform (GBM) specimens.
 
  Knockdown of P4HA1 resulted in reduced chemotaxis of microglia toward GBM cells and increased polarization of microglia toward the M1 phenotype. The changed microglial polarization state, in turn, inhibited the proliferation and invasion of GBM cells. Moreover, in GBM tissue specimens, the P4HA1 expression level is negatively correlated with that of the CD86 microglia M1-specific marker.
 
  Our results show that P4HA1 promotes immunosuppressive microenvironment formation by cross-talk between GBM and microglia cells and indirectly increases the aggressiveness of GBM.
 Our results show that P4HA1 promotes immunosuppressive microenvironment formation by cross-talk between GBM and microglia cells and indirectly increases the aggressiveness of GBM.
  As one of the most common neoplastic diseases, hepatocellular carcinoma (HCC) has a high morbidity and mortality, which seriously threatens human health and places a heavy burden on society and medical care.  https://www.selleckchem.com/products/almorexant-hcl.html  At present, effective early diagnosis, prognosis and treatment of HCC are limited. Altered gene expression patterns of lncRNA are associated with the occurrence, development and prognosis of various malignancies, including HCC. The aim of this study was to investigate the correlation between the expression of LINC01268 and HCC, and to elucidate the potential underlying molecular mechanism.
 
  Expression level and localization of LINC01268 in human liver cancer cells and HCC tissues were investigated using RT-qPCR and fluorescent in situ hybridization (FISH), respectively. Correlation of expression levels of LINC01268 and MAP3K7 with differentiation and poor overall patient survival of HCC were analyzed using in house collected and publicly available HCC tissue data. RT-qPCR and Western blot were applied to inspect the effects of depletion and overexpression of LINC01268 on MAP3K7 expression.