<p>XLSX - 1231K, Supplementary Table 1: List of genes deleted in 75 to 100% of the end-stage *PTEN tumors Supplementary Table 2: List of genes showing copy number gains in *PTEN end-stage and *PTEN/p53 mouse tumors. Supplementary Table 3: Genes that were deleted in 75-100% of *PTEN end-stage mouse tumors and at least 10% of human tumors within one of the four GBM subtypes mapped to their chromosomal location in the human genome. Supplementary Table 4: List of gene deletions that were specific for one of the four GBM subtypes. Supplementary Table 5: Correlation of proneural-specific genetic alterations and deletions identified by cross-species comparison. Supplementary Table 6: Spearman correlation for Verhaak gene sets show highest correlation for human proneural GBM subtype for 21 dpi *PTEN tumors, end-stage *PTEN tumors and *p53 end-stage tumors. Supplementary Table 7: MR identified from NB versus *PTEN 21 dpi and NB versus *PTEN end-stage mouse MARINas, and human NB versus proneural GBM (TCGA) MARINa.</p>
Lymphadenoma of the salivary gland is a rare benign tumor with only 11 reported cases in the English language literature, most of which have occurred in adults. We report a case of a lymphadenoma occurring in the parotid gland of a 15-year-old girl. The tumor was composed of variably sized cystic cavities within abundant reactive lymphoid tissue. The cystic spaces were filled with eosinophilic secretions with occasional histiocytes. Many of these features were also apparent on cytologic preparations. The cysts were lined by epithelium lacking atypia and showed luminal and abluminal differentiation both by immunohistochemistry and by electron microscopy. Tumor cells were not cycling as determined by MIB1 immunostaining, and the tumor karyotype was normal. This is only the second case to be reported in the pediatric age group. Ultrastructural features and karyotype analysis are reported for the first time. Although this tumor is rarely encountered by pediatric pathologists, awareness of its existence is important to distinguish it from possible malignant mimics, such as lymphoepithelial carcinoma and metastatic mucoepidermoid carcinoma in a lymph node.
"An Association between Positive Airway Pressure Device Manufacturer and Incident Cancer? A Secondary Data Analysis." American Journal of Respiratory and Critical Care Medicine, 204(12), pp. 1484–1488
Objective— Human and mouse megakaryocytes lacking NBEAL2 (neurobeachin-like 2) produce platelets where α-granules lack protein cargo. This cargo is mostly megakaryocyte-synthesized, but some proteins, including FGN (fibrinogen), are endocytosed. In this study, we examined the trafficking of both types of cargo within primary megakaryocytes cultured from normal and NBEAL2-null mice, to determine the role of NBEAL2 in α-granule maturation. We also examined the interaction of NBEAL2 with the granule-associated protein P-selectin in human megakaryocytes and platelets. Approach and Results— Fluorescence microscopy was used to compare uptake of labeled FGN by normal and NBEAL2-null mouse megakaryocytes, which was similar in both. NBEAL2-null cells, however, showed decreased FGN retention, and studies with biotinylated protein showed rapid loss rather than increased degradation. Intracellular tracking via fluorescence microscopy revealed that in normal megakaryocytes, endocytosed FGN sequentially associated with compartments expressing RAB5 (Ras-related protein in brain 5), RAB7 (Ras-related protein in brain 7), and P-selectin, where it was retained. A similar initial pattern was observed in NBEAL2-null megakaryocytes, but then FGN passed from the P-selectin compartment to RAB11 (Ras-related protein in brain 11)-associated endosomes before release. Megakaryocyte-synthesized VWF (Von Willebrand factor) was observed to follow the same route out of NBEAL2-null cells. Immunofluorescence microscopy revealed intracellular colocalization of NBEAL2 with P-selectin in human megakaryocytes, proplatelets, and platelets. Native NBEAL2 and P-selectin were coimmunoprecipitated from platelets and megakaryocytes. Conclusions— NBEAL2 is not required for FGN uptake by megakaryocytes. NBEAL2 is required for the retention of both endocytosed and megakaryocyte-synthesized proteins by maturing α-granules, and possibly by platelet-borne granules. This function may involve interaction of NBEAL2 with P-selectin.
