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Leslie E. Rogler

Researcher at Albert Einstein College of Medicine

Publications -  20
Citations -  1281

Leslie E. Rogler is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Cellular differentiation & Stem cell. The author has an hindex of 14, co-authored 20 publications receiving 1225 citations. Previous affiliations of Leslie E. Rogler include Yeshiva University.

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Elevated expression of the miR-17-92 polycistron and miR-21 in hepadnavirus-associated hepatocellular carcinoma contributes to the malignant phenotype.

TL;DR: A role for these miRNAs in the maintenance of the malignant transformation of hepatocytes is supported, and separate treatments with antisense oligonucleotides specific for either the miR-17-92 polycistron (all six members) or mi-21 caused a 50% reduction in both hepatocyte proliferation and anchorage-independent growth.
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MicroRNA‐23b cluster microRNAs regulate transforming growth factor‐beta/bone morphogenetic protein signaling and liver stem cell differentiation by targeting Smads

TL;DR: The data provide a model in which miR‐23b miRNAs repress bile duct gene expression in fetal hepatocytes while promoting their growth by down‐regulating Smads and consequently TGFβ signaling.
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Identification of hepatocytic and bile ductular cell lineages and candidate stem cells in bipolar ductular reactions in cirrhotic human liver

TL;DR: Staining with NCAM, CK19, and HepPar1 has revealed a distinctly bipolar structure to DRs that are embedded in cirrhotic tissue, and the locations of other intermediate hepatobiliary cells, which have combinations of markers, suggest that CK19+/NCAM+ cells are transitional cells in the biliary lineage and that rare cells that are negative for all three markers are transitions in the hepatocytic lineage.
Journal Article

Selective bipotential differentiation of mouse embryonic hepatoblasts in vitro.

TL;DR: A line of hepatic endoderm cells, hepatoblast cell line 3 (HBC-3), was derived from the liver diverticulum of the mouse on day 9.5 of gestation by culture on a mitomycin C treated STON+ feeder layer in a liver culture medium consisting of Dulbecco's modified Eagle's medium, nonessential amino acids, fetal calf serum, and beta-mercaptoethanol.
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Overexpression of miR-21 promotes an in vitro metastatic phenotype by targeting the tumor suppressor RHOB.

TL;DR: It is shown that oncogenic microRNA, miR-21, represses RHOB expression by directly targeting the 3′ untranslated region and promotes multiple components of the metastatic phenotype in vitro by regulating several important tumor suppressors, including RHOB.