ABSTRACT
Hairy polyps, considered a highly unusual congenital anomaly of the pharynx, are believed by many scholars to arise from the ectoderm and mesoderm during the embryonic stage. These growths often have a pear or sausage shape, are pedunculated, and their size ranges between 0.5 and 6 cm. They are typically grayish white or pink in color. This article discusses a 12-year-old female who had a growth at the Eustachian tube's entrance on the left side of the nasopharyngeal wall, as identified by a computed tomography scan of the neck soft tissue; it was suspected to be a hairy polyp originating from the left Eustachian tube. The diagnosis of a hairy polyp was confirmed through pathology. The hairy polyp at the Eustachian tube, in this case, showed an irregular form with a wide base, making it look similar to an adenoid; thus, increasing the risk of it being misdiagnosed as residual adenoid tissue.
ABSTRACT
Gastric cancer (GC) is a common malignancy worldwide and its pathogenesis remains unclear. Long non-coding RNAs (lncRNAs) serve an important function in cancer development, therefore identification of functional lncRNAs in GC is required. The results of the present study demonstrate that an lncRNA, LINC00857, was increased in GC tissues compared with adjacent non-tumor tissues. Overexpression of LINC00857 was positively associated with poor survival rate, as well as with the tumor size of patients with GC. LINC00857 knockdown induced by specific small interfering RNAs significantly inhibited GC cell proliferation in vitro. Genome-wide analysis revealed that LINC00857 knockdown deregulated the cell cycle. Western blot analysis confirmed that LINC00857 knockdown decreased protein expression of cyclin D1 and cyclin E1 in GC cells. Taken together, the results indicated that LINC00857 knockdown suppressed GC cell proliferation through deregulating the cell cycle, resulting in the downregulation of cyclin D1 and cyclin E1. Therefore, LINC00857 expression may be an independent biomarker for the diagnosis and prognosis of GC.
ABSTRACT
AIM: To comparatively investigate the cellular and molecular characteristics of low-grade slightly elevated adenomas and polypoid adenomas. METHODS: Colorectal tumors were collected from 24 patients with slightly elevated adenomas and 23 patients with polypoid adenomas. Five commonly mutated genes (APC, BRAF, KRAS, NRAS, and PIK3CA) were selected for mutational analysis. Paraffin-embedded tumor sections were used to calculate the apoptotic index (AI) and Ki-67 labeling index (KLI). Two pure colorectal epithelial cell lines were created by pooling the slightly elevated and polypoid tumors. Western blots, luciferase assays for ß-catenin-T-cell factor protein/ß-catenin-lymphoid enhancer factor (ß-catenin-TCF/LEF)-driven transcriptional activity, and caspase activity assays were conducted on the two cell lines. RESULTS: Slightly elevated lesions showed a significantly lower APC mutational frequency and a significantly higher KRAS mutational frequency (both P < 0.05). Slightly elevated lesions showed a significantly lower AI (P < 0.05). ß-catenin and ß-catenin-TCF/LEF-driven transcriptional activity was significantly upregulated in slightly elevated lesions (both P < 0.05). In slightly elevated lesions, c-Myc was significantly downregulated, while cyclin D1 was significantly upregulated (both P < 0.05). ß-catenin-TCF/LEF-driven transcriptional activity was negatively correlated with c-Myc (ρ = -0.78). Slightly elevated lesions displayed significant Bcl-2 and Bcl-xL upregulation (both P < 0.05) along with significant decreases in caspase-9 and caspase-3 activity (both P < 0.05). c-Myc was negatively correlated with Bcl-2 and Bcl-xL (ρ = -0.74 and -0.78, respectively). CONCLUSION: The lower apoptotic activity of low-grade slightly elevated adenomas can be partly attributed to upregulated ß-catenin pathway activity and downregulated c-Myc expression.
