Heterogeneity of IKZF1 genomic alterations and risk of relapse in childhood B-cell precursor acute lymphoblastic leukemia.

Genomic alterations of IKZF1 are common and associated with adverse clinical features in B-progenitor acute lymphoblastic leukemia (B-ALL). The relationship between the type of IKZF1 alteration, B-ALL genomic subtype and outcome are incompletely understood. B-ALL subtype and genomic alterations were determined using transcriptome and genomic sequencing, and SNP microarray analysis in 688 pediatric patients with B-ALL in the St.

An Atypical Case of Hemoptysis.

Hemoptysis, a common sign of diffuse alveolar hemorrhage, can be caused by multiple factors, both infectious and noninfectious. A 45-year-old male with hypertension, obstructive sleep apnea, and stage IV pulmonary sarcoidosis with cardiac involvement, presented with a two-month history of cough and acute nonmassive hemoptysis with hypoxia. A chest CT showed ground glass consolidation and interlobular septal thickening, concerning for diffuse alveolar hemorrhage.

Relapse of polymicrobial endocarditis in an intravenous drug user.

A 26-year-old male intravenous drug user (IDU) presented twice within 6 months with relapsed polymicrobial infective endocarditis (IE) due to Eikenella corrodens and Streptococcus constellatus after completing two courses of appropriate antimicrobial therapy. This report points to relapsing endocarditis as a clinical entity that warrants attention in IDUs when E. corrodens or S.

TORC1 kinase and the S-phase cyclin Clb5 collaborate to promote mitotic spindle assembly and DNA replication in S. cerevisiae.

The Target of Rapamycin complex 1 (TORC1) is a central regulator of eukaryotic cell growth that is inhibited by the drug rapamycin. In the budding yeast Saccharomyces cerevisiae, translational defects associated with TORC1 inactivation inhibit cell cycle progression at an early stage in G1, but little is known about the possible roles for TORC1 later in the cell cycle. We investigated the rapamycin-hypersensitivity phenotype of cells lacking the S phase cyclin Clb5 (clb5Δ) as a basis for uncovering novel connections between TORC1 and the cell cycle regulatory machinery.