Anti-CDKN1B (aa 55-198) polyclonal antibody

Extra-nodal natural killer/T-cell lymphoma (ENKTL) is an aggressive lymphoid malignancy and advanced ENKTL is characterized by a dismal survival outcome. Distant metastasis is frequently common in advanced ENKTLs, while the glans is rarely involved. Here we report a 67-year-old Chinese male with glans metastasis ENKTL, nasal type secondary from the nasal cavity, treated with modified SMILE regimen plus glans radiotherapy and achieved a complete remission (CR). Since the poor prognosis of metastatic ENKTL and unfitness for hematological stem cell transplant (HSCT) we administered histone deacetylase MAC) inhibitor Chidamide as maintenance therapy, which was resulted in a progression-free survival (ITS) of 12 months. To investigate the gene alternations, the whole exon sequencing and the 446-gene panel sequencing were performed and we found the BCOR, KRAS, CDKN1B, XPO1, DOT1L, genes mutations. Best to our knowledge, this is a glans metastasis ENKTL with the longest PFS and die most successful treatment.

Subarachnoid hemorrhage is a common disease in the neural system, which causes high fatality rate. Therefore, it is necessary to figure out inner mechanisms of factors related to this disease. RT-qPCR was applied for measuring expressions of CDKN1B and miR-502-5p and other factors of apoptosis and inflammation. Cell viabilities were detected through CCK-8. Binding conditions between miR-502-5p and CDKN1B were detected through luciferase report assay. Western blot was used for measuring levels of proteins in PPAR gamma/NF-kappa B signaling pathway. Apoptosis and inflammation of HT22 cell line, a kind of nerve cell line, were enhanced and viabilities were suppressed by oxyhemoglobin. CDKN1B expressed lower in induced HT22 cell line and overexpressed CDKN1B could promote viabilities and suppress apoptosis as well as inflammation. MiR-502-5p was the target gene of CDKN1B and enhanced apoptosis and inflammation of cells in HT22 cell line. Furthermore, miR-502-5p reversed functions of CKDN1B in induced cells through regulating proteins in PPAR gamma/NF-kappa B signaling pathway. CDKN1B was the gene that could inhibit SAH caused by apoptosis in nerve cells and inflammation by sponging miR-502-5p and regulating factors in PPAR gamma/NF-kappa B signaling pathway, suggesting it could be a factor for protecting functions of nerve cells after SAH.