A Pan-Cancer Analysis Reveals CLEC5A as a Biomarker for Cancer Immunity and Prognosis.

Background: CLEC5A is a member of the C-type lectin superfamily. It can activate macrophages and lead to a series of immune-inflammation reactions. Previous studies reveal the role of CLEC5A in infection and inflammation diseases. Method: We acquire and analyze data from The Cancer Genome Atlas (TCGA) database, Genotype-Tissue Expression (GTEx) database, and other comprehensive databases via GSCALite, cBioPortal, and TIMER 2.0 platforms or software. Single-cell sequencing analysis was performed for quantifying the tumor microenvironment of several types of cancers. Results: CLEC5A is differentially expressed in a few cancer types, of which overexpression accompanies low overall survival of patients. DNA methylation mainly negatively correlates with CLEC5A expression. Moreover, CLEC5A is positively related to immune infiltration, including macrophages, cancer-associated fibroblasts (CAFs), and regulatory T cells (Tregs). Immune checkpoint genes are significantly associated with CLEC5A expression in diverse cancers. In addition, CLEC5A expression correlates with mismatch repair (MMR) in several cancers. Tumor mutation burden (TMB), microsatellite instability (MSI), and neoantigens show a positive association with CLEC5A expression in several cancers. Furthermore, CLEC5A in cancer correlates with signal transduction, the immune system, EMT, and apoptosis process. The drug sensitivity analysis screens out potential therapeutic agents associated with CLEC5A expression, including FR-180204, Tivozanib, OSI-930, Linifanib, AC220, VNLG/124, Bexarotene, omacetaxine mepesuccinate, narciclasine, leptomycin B, PHA-793887, LRRK2-IN-1, and CR-1-31B. Conclusion: CLEC5A overexpresses in multiple cancers in contrast to normal tissues, and high CLEC5A expression predicts poor prognosis of patients and immune infiltration. CLEC5A is a potential prognostic biomarker of diverse cancers and a target for anti-tumor therapy.

Application of 3-Dimensional Computerized Tomography Angiography for Defining Cavernous Sinus Aneurysms and Intradural Aneurysms Involving the Internal Carotid Artery Around the Anterior Clinoid Process.

OBJECTIVE: This study aimed to investigate the application of 3-dimensional computed tomography angiography (3D-CTA) for defining cavernous sinus aneurysms and intradural aneurysms involving the internal carotid artery around the anterior clinoid process. METHODS: Results from 42 patients with an aneurysm of the internal carotid artery around the anterior clinoid process who underwent 3D-CTA were reviewed and compared with those of observed clinical operations. RESULTS: Among the 42 patients, there was a total of 45 aneurysms of the internal carotid artery around the anterior clinoid process. After surgery, 33 of the 45 aneurysms were confirmed as intradural aneurysms, and the other 12 were confirmed as aneurysms in the cavernous sinus. 3D-CTA imaging of the medial sagittal plane showed that 31 out of 31 (100%) intradural aneurysms of the internal carotid artery were above the virtual line between the inferior border of the anterior clinoid process and the tuberculum sellae, and 12 out of 14 (86%) cavernous sinus aneurysms were below the virtual line (P < 0.0001). CONCLUSIONS: The virtual line between the inferior border of the anterior clinoid process and the tuberculum sellae on 3D-CTA indicates the proximal dural ring of the internal carotid artery. This line helps differentiate cavernous sinus aneurysms from intradural aneurysms involving the internal carotid artery around the anterior clinoid process.

The antitumor activity of recombinant antitumor antiviral protein and the associated molecular mechanism in pancreatic tumor cells.

BACKGROUND: Pancreatic cancer has poor prognosis and high mortality. Currently, the therapy of pancreatic cancer remains a challenge. In this study, we compared the antitumor activity of the recombinant antitumor antiviral protein (RAAP), an improved interferon, with gemcitabine, a classic chemotherapy agent used for pancreatic cancer treatment. METHODS: The proliferation of Bx-PC3 pancreatic cancer cells was evaluated by an MTT assay. Cell cycle arrest and apoptosis were evaluated by flow cytometry and annexin V-FITC/propidium iodide double staining, respectively. The expressions of matrix metalloproteinase (MMP)-2, MMP-9, caspase-3, caspase-8, and caspase-9 genes were evaluated by reverse transcription-polymerase chain reaction and the Western blot analysis. A xenograft pancreatic cancer model was established by inoculating Bx-PC3 cells into athymic nude mice. The antitumor activity of RAAP and gemcitabine was tested in the xenograft tumor model. RESULTS: RAAP significantly inhibited proliferation, induced cell cycle arrest, and induced apoptosis in Bx-PC3 cells in vitro and delayed tumor growth in vivo. The antitumor activity of 20 ng/mL of RAAP was a little more effective than 10 µM of gemcitabine. The antitumor activity of RAAP was associated with its role in inducing caspase-3 and caspase-8 expression as well as downregulating MMP-2 expression. CONCLUSIONS: RAAP can effectively suppress human pancreatic cancer cell growth in vitro and in vivo. The antitumor efficacy of RAAP is similar to gemcitabine.