St. Jude Children's Research Hospital

About: St. Jude Children's Research Hospital is a healthcare organization based out in Memphis, Tennessee, United States. It is known for research contribution in the topics: Population & Virus. The organization has 9344 authors who have published 19233 publications receiving 1233399 citations. The organization is also known as: St. Jude Children's Hospital & St. Jude Hospital.

The origins of medulloblastoma subtypes.

Abstract: Childhood tumors containing cells that are morphologically and functionally similar to normal progenitor cells provide fertile ground for investigating the links between development and cancer. In this respect, integrated studies of normal cerebellar development and the medulloblastoma, a malignant embryonal tumor of the cerebellum, have proven especially fruitful. Emerging evidence indicates that the different precursor cell populations that form the cerebellum and the cell signaling pathways that regulate its development likely represent distinct compartments from which the various subtypes of medulloblastoma arise. Definitive characterization of each medulloblastoma subtype will undoubtedly improve treatment of this disease and provide important insights to the origins of cancer.

Cutting Edge: Molecular Analysis of the Negative Regulatory Function of Lymphocyte Activation Gene-3

Abstract: Lymphocyte activation gene (LAG)-3 (CD223) is a CD4-related activation-induced cell surface molecule that binds to MHC class II molecules with high affinity and negatively regulates T cell expansion and homeostasis. In this study, we show that LAG-3 inhibits CD4-dependent, but not CD4-independent, T cell function via its cytoplasmic domain. Although high affinity interaction with MHC class II molecules is essential for LAG-3 function, tailless LAG-3 does not compete with CD4 for ligand binding. A single lysine residue (K468) within a conserved "KIEELE" motif is essential for interaction with downstream signaling molecules. These data provide insight into the mechanism of action of this important T cell regulatory molecule.

Aspirin and reduced risk of esophageal carcinoma

Abstract: Background. Aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs) have been shown experimentally to inhibit chemically induced esophageal cancers. An epidemiologic study of more than 600,000 adults in the United States followed for 6 years found that aspirin use was associated with a reduced risk of death from esophageal cancer. Methods. The relation of aspirin use and esophageal cancer was examined using data from the National Health and Nutrition Examination Survey (NHANES I) and the National Epidemiologic Follow-up Studies (NEFS). Of the 14,407 United States residents followed for 12–16 years, esophageal cancer developed in 15. Persons were classified as nonusers, occasional users, or regular users of aspirin based on their response to two questions at the baseline examination: whether they had taken aspirin in the past 30 days and whether they had used pain medications regularly during the prior 6 months. Results. Occasional use was associated with a 90% decreased risk (95% confidence interval, 0.01–0.76) of developing esophageal cancer, and no person classified as a regular user developed the disease. Adjusting for cigarette smoking (ever vs. never) and alcohol intake (at least monthly vs. not) did not explain the finding. Conclusion. Aspirin use was associated with a 90% decreased risk of developing esophageal carcinoma. Further studies to determine whether aspirin is protective against both squamous cell esophageal carcinoma and adenocarcinoma of the esophagus are indicated.

Measuring the diaspora for virus-specific CD8+ T cells.

Abstract: The CD8+ T cell diaspora has been analyzed after secondary challenge with an influenza A virus that replicates only in the respiratory tract. Numbers of DbNP366- and DbPA224-specific CD8+ T cells were measured by tetramer staining at the end of the recall response, then followed sequentially in the lung, lymph nodes, spleen, blood, and other organs. The extent of clonal expansion did not reflect the sizes of the preexisting memory T cell pools. Although the high-frequency CD8+ tetramer+ populations in the pneumonic lung and mediastinal lymph nodes fell rapidly from peak values, the “whole mouse” virus-specific CD8+ T cell counts decreased only 2-fold over the 4 weeks after infection, then subsided at a fairly steady rate to reach a plateau at about 2 months. The largest numbers were found throughout in the spleen, then the bone marrow. The CD8+DbNP366+ and CD8+DbPA224+ sets remained significantly enlarged for at least 4 months, declining at equivalent rates while retaining the nucleoprotein > acid polymerase immunodominance hierarchy characteristic of the earlier antigen-driven phase. Lowest levels of the CD69 “activation marker” were detected consistently on virus-specific CD8+ T cells in the blood, then the spleen. Those in the bone marrow and liver were intermediate, and CD69hi T cells were very prominent in the regional lymph nodes and the nasal-associated lymphoid tissue. Any population of “resting” CD8+ memory T cells is thus phenotypically heterogeneous, widely dispersed, and subject to broad homeostatic and local environmental effects irrespective of epitope specificity or magnitude.