Pre-B cell proliferation and lymphoblastic leukemia/high-grade lymphoma in E(mu)-miR155 transgenic mice.

By S. Costinean, N. Zanesi, Y. Pekarsky, E. Tili, Stefano Volinia, Nyla Heerema, Carlo Maria Croce. Proceedings of the National Academy of Sciences of the United States of America, 2006

862 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/0d4e7ba53fdb275dce7abb4a32f3310905e198c3

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Citations in the corpus

microRNA-155 Regulates the Generation of Immunoglobulin Class-Switched Plasma Cells (2007, background): “When over-expressed as a transgene in B cells miR-155 gives rise to pre-B cell lymphomas (Costinean et al., 2006).”
microRNAs in cancer (2013, background): “Several strains of mice lacking or overexpressing cancer-associated miRNAs have been developed and characterized, including the germ-line transgenic or knockout mice of miR155 (39), miR-17/92 and its paralogs (60–62), miR-21 (40), miR-221 (63), the miR-15/16-1 cluster (64), miR-122 (65, 66), and miR”
MicroRNAs in stress signaling and human disease (2012, background): “For example, transgenic expression of miR-155 (Costinean et al., 2006) or miR-21 (Medina et al.”
MicroRNA-155 Is Regulated by the Transforming Growth Factor β/Smad Pathway and Contributes to Epithelial Cell Plasticity by Targeting RhoA (2008, background): “B-cell malignancies (4), whereas miR-155 knockout mice ex-”
MicroRNA expression patterns to differentiate pancreatic adenocarcinoma from normal pancreas and chronic pancreatitis. (2007, background): “It has also been shown to be involved in leukemogenesis in transgenic mice.(17) The most consistently highly expressed miRNA in the pancreatic cancers in our study was miR-221 when compared with normal pancreas and chronic pancreatitis.”
MicroRNA-10a binds the 5'UTR of ribosomal protein mRNAs and enhances their translation. (2008, background): “In addition, a number of studies have demonstrated causal links between miRNA deregulation and cancer-related processes (Costinean et al., 2006; He et al., 2005; Voorhoeve et al., 2006).”
OncomiRs: the discovery and progress of microRNAs in cancers (2007, background): “Their findings indicated that miR-155 could induce polyclonal expansion, favoring the capture of secondary genetic changes for full transformation [23].”
Inositol phosphatase SHIP1 is a primary target of miR-155 (2009, background): “found that transgenic expression of miR-155 from a B-cell specific promoter can trigger a B-cell malignancy (4).”
MicroRNA control in the immune system: basic principles. (2009, background): “In the case of miR-155, transgenic mice overexpressing this miRNA in B cells developed polyclonal pre-B cell proliferation followed by B cell malignancy (Costinean et al., 2006).”
MicroRNAs: key players in the immune system, differentiation, tumorigenesis and cell death (2008, background): “…immunoglobulin transcriptional enhancer element (Em-mmu-miR-155) exhibit preleukemic pre-B-cell proliferation that result in B-cell malignancy (Costinean et al., 2006). miRNAs have also been directly linked to metastasis formation. miR-10b was one of a few miRNAs whose expression was found to…”
Modulation of miR-155 and miR-125b Levels following Lipopolysaccharide/TNF-α Stimulation and Their Possible Roles in Regulating the Response to Endotoxin Shock1 (2007, methodology): “In addition, the splenocytes of E miR-155 transgenic mice displayed lower levels of transcripts coding for IKK (another kinase involved in NF- B activation) than their wild-type counterparts, as shown by Affymetrix microarray analysis (28).”