Ramiro Garzon

Bio: Ramiro Garzon is an academic researcher from Thomas Jefferson University. The author has contributed to research in topics: microRNA & Gene expression profiling. The author has an hindex of 2, co-authored 6 publications receiving 2485 citations.

A MicroRNA Signature Associated with Prognosis and Progression in Chronic Lymphocytic Leukemia

Abstract: Background MicroRNA expression profiles can be used to distinguish normal B cells from malignant B cells in patients with chronic lymphocytic leukemia (CLL). We investigated whether microRNA profiles are associated with known prognostic factors in CLL. Methods We evaluated the microRNA expression profiles of 94 samples of CLL cells for which the level of expression of 70-kD zeta-associated protein (ZAP-70), the mutational status of the rearranged immunoglobulin heavy-chain variable-region (IgVH ) gene, and the time from diagnosis to initial treatment were known. We also investigated the genomic sequence of 42 microRNA genes to identify abnormalities. Results A unique microRNA expression signature composed of 13 genes (of 190 analyzed) differentiated cases of CLL with low levels of ZAP-70 expression from those with high levels and cases with unmutated IgVH from those with mutated IgVH . The same microRNA signature was also associated with the presence or absence of disease progression. We also identified a...

Supplemental Data Article NF-κB-YY1-miR-29 Regulatory Circuitry in Skeletal Myogenesis and Rhabdomyosarcoma

Abstract: To construct the miR-29b/c-enhancer-Luc-wt reporter plasmid, a ~ 4.5 kb fragment containing the YY1 D site along with the other myogenic regulator factor binding sites was amplified from a BAC clone (PR24-332J17) (Children’s Hospital Oakland Research Institute) and cloned into the Xho I and Hind III sites of the pGL3-basic vector (Promega). For the construction of miR-29b/c-enhancer-Luc-mutant plasmid, the YY1 binding site D was deleted from the miR-29b/c-enhancer-Luc-wt construct using QuikChange XL-mutagenesis (Stratagene). To construct the YY1-3’UTR-luc reporter plasmid, a 500 base pair fragment or the full length (~800bp) of the YY1 3’UTR was PCR amplified from mouse genomic cDNA and cloned in a Xba I site of the pGL3-control vector (Promega), downstream of the luciferase gene, thus generating the Luc-YY1-3’UTR-wild type (WT) plasmid. The Luc-YY1-3’UTR-Mutant plasmid was generated by deleting the seed region of the predicted miR-29 binding site using QuikChange XL-mutagenesis (Stratagene). Replication-deficient lentivirus-based expression plasmids pMIF-cGFP-Zeo-vector and pMIF-cGFP-Zeo-miR-29b, along with the packaging plasmid mix (pPACK), were obtained from System Biosciences (SBI). An YY1 expression plasmid was a gift from Y. Shi (Harvard University) and used as described (Wang et al., 2007). MyHC and troponin reporters were used as described (Wang et al., 2007).

Empreintes digitales micro-ARN pendant une mégacaryocytopoïese

Abstract: L'invention concerne de nouveaux procedes et de nouvelles compositions pour le diagnostic, le pronostic et le traitement du cancer et des troubles myeloproliferatifs. L'invention concerne egalement des procedes d'identification d'agents anticancereux.

Oncomirs : microRNAs with a role in cancer

Abstract: I MicroRNAs (miRNAs) are an abundant class of small non-protein-coding RNAs that function as negative gene regulators. They regulate diverse biological processes, and bioinformatic data indicates that each miRNA can control hundreds of gene targets, underscoring the potential influence of miRNAs on almost every genetic pathway. Recent evidence has shown that miRNA mutations or mis-expression correlate with various human cancers and indicates that miRNAs can function as tumour suppressors and oncogenes. miRNAs have been shown to repress the expression of important cancer-related genes and might prove useful in the diagnosis and treatment of cancer.

A microRNA expression signature of human solid tumors defines cancer gene targets

Abstract: Small noncoding microRNAs (miRNAs) can contribute to cancer development and progression and are differentially expressed in normal tissues and cancers From a large-scale miRnome analysis on 540 samples including lung, breast, stomach, prostate, colon, and pancreatic tumors, we identified a solid cancer miRNA signature composed by a large portion of overexpressed miRNAs Among these miRNAs are some with well characterized cancer association, such as miR-17-5p, miR-20a, miR-21, miR-92, miR-106a, and miR-155 The predicted targets for the differentially expressed miRNAs are significantly enriched for protein-coding tumor suppressors and oncogenes (P < 00001) A number of the predicted targets, including the tumor suppressors RB1 (Retinoblastoma 1) and TGFBR2 (transforming growth factor, beta receptor II) genes were confirmed experimentally Our results indicate that miRNAs are extensively involved in cancer pathogenesis of solid tumors and support their function as either dominant or recessive cancer genes

Oncomirs — microRNAs with a role in cancer

Abstract: MicroRNAs (miRNAs) are an abundant class of small non-protein-coding RNAs that function as negative gene regulators They regulate diverse biological processes, and bioinformatic data indicates that each miRNA can control hundreds of gene targets, underscoring the potential influence of miRNAs on almost every genetic pathway Recent evidence has shown that miRNA mutations or mis-expression correlate with various human cancers and indicates that miRNAs can function as tumour suppressors and oncogenes miRNAs have been shown to repress the expression of important cancer-related genes and might prove useful in the diagnosis and treatment of cancer

Regulation of microRNA biogenesis

Abstract: MicroRNAs (miRNAs) are small non-coding RNAs that function as guide molecules in RNA silencing. Targeting most protein-coding transcripts, miRNAs are involved in nearly all developmental and pathological processes in animals. The biogenesis of miRNAs is under tight temporal and spatial control, and their dysregulation is associated with many human diseases, particularly cancer. In animals, miRNAs are ∼22 nucleotides in length, and they are produced by two RNase III proteins--Drosha and Dicer. miRNA biogenesis is regulated at multiple levels, including at the level of miRNA transcription; its processing by Drosha and Dicer in the nucleus and cytoplasm, respectively; its modification by RNA editing, RNA methylation, uridylation and adenylation; Argonaute loading; and RNA decay. Non-canonical pathways for miRNA biogenesis, including those that are independent of Drosha or Dicer, are also emerging.

NF-κB-dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses

Abstract: Activation of mammalian innate and acquired immune responses must be tightly regulated by elaborate mechanisms to control their onset and termination. MicroRNAs have been implicated as negative regulators controlling diverse biological processes at the level of posttranscriptional repression. Expression profiling of 200 microRNAs in human monocytes revealed that several of them (miR-146a/b, miR-132, and miR-155) are endotoxin-responsive genes. Analysis of miR-146a and miR-146b gene expression unveiled a pattern of induction in response to a variety of microbial components and proinflammatory cytokines. By means of promoter analysis, miR-146a was found to be a NF-κB-dependent gene. Importantly, miR-146a/b were predicted to base-pair with sequences in the 3′ UTRs of the TNF receptor-associated factor 6 and IL-1 receptor-associated kinase 1 genes, and we found that these UTRs inhibit expression of a linked reporter gene. These genes encode two key adapter molecules downstream of Toll-like and cytokine receptors. Thus, we propose a role for miR-146 in control of Toll-like receptor and cytokine signaling through a negative feedback regulation loop involving down-regulation of IL-1 receptor-associated kinase 1 and TNF receptor-associated factor 6 protein levels.