Showing posts from 2022

Lab Spotlight: Sturgeon Lab

Each month, Simply Blood spotlights a lab focused on the research of basic hematology, immunology, stem cell research, cell and gene therapy, and other related aspects. Get to know these different labs around the world! This month, we are featuring the Sturgeon Lab ( )  at the Icahn School of Medicine at Mount Sinai located in New York City, New York, USA. Sturgeon Lab at Icahn School of Medicine at Mount Sinai, Twitter: @Dr_Sturgeon How long have you had your lab? I first opened my lab at Washington University, in March of 2014.   We then moved to Mount Sinai in New York in August of 2020. What was your biggest transition from a post-doc to a group leader/lab PI? Or what do you miss most from your post-doc time? I remember being so overwhelmed and star-struck just seeing, for the first time, the space that was going to be my lab.   So much so, that I forgot to ask key questions about how things like renovations could be handled, HVAC and electrical limitat

Exploring Experimental Hematology: June 2021 (Volume 98)

DNA methylation therapy joins forces in IDH2 -mutant AML Isocitrate dehydrogenases 1 and 2 ( IDH1 /2) are frequently mutated in Acute Myeloid Leukemia (AML), with nearly 20% of patients carrying gain-of-function point mutations in these genes (Ley et al., 2013) . IDH2 is a metabolic enzyme that catalyzes the conversion of isocitrate to 2-oxoglutarate during the Krebs cycle. Patients carrying IDH2 gain-of-function mutations produce instead high levels of the oncometabolite 2-hydroxyglutarate (2-HG), which inhibits oxoglutarate-dependent enzymes such as the TET family of methylcytosine dioxygenases, responsible for active DNA demethylation (Xu et al., 2011) . As a consequence, IDH2 mutations in AML patients induce DNA hypermethylation and inhibit hematopoietic differentiation (Figueroa et al., 2010) . Azacytidine (AZA) and enasidenib (ENA) are commonly used AML therapies which induce DNA hypomethylation, albeit through different mechanisms. AZA is a nucleoside analog that inhibits