A5015206951- Neuroblastoma Research and Treatments
- Cancer, Hypoxia, and Metabolism
- Virus-based gene therapy research
- Chronic Lymphocytic Leukemia Research
- Cancer-related molecular mechanisms research
- RNA modifications and cancer
- RNA Research and Splicing
- Galectins and Cancer Biology
- MicroRNA in disease regulation
- Peroxisome Proliferator-Activated Receptors
- Ubiquitin and proteasome pathways
- Phagocytosis and Immune Regulation
- Cancer Genomics and Diagnostics
- Health, psychology, and well-being
- Circular RNAs in diseases
- Therapeutic Uses of Natural Elements
- Microtubule and mitosis dynamics
- Genetic factors in colorectal cancer
- RNA regulation and disease
- Immune Cell Function and Interaction
- Plant Disease Resistance and Genetics
- Calcium signaling and nucleotide metabolism
- Cancer Cells and Metastasis
- CAR-T cell therapy research
University of Gothenburg
2020-2023
University of Chieti-Pescara
2013-2021
Aim: To investigate the genome-wide methylation of genetically characterized colorectal cancer stem cell (CR-CSC) lines. Materials & methods: Eight CR-CSC lines were isolated from primary (CRC) tissues, cultured and for aneuploidy, mutational status CRC-related genes microsatellite instability (MSI). Genome-wide DNA was assessed by MethylationEPIC microarray. Results: We describe a distinctive pattern that is maintained following in vivo passages immune-compromised mice. identified an...
Abstract Neuroblastoma has a low mutation rate for the p53 gene. Alternative ways of inactivation have been proposed in neuroblastoma, such as abnormal cytoplasmic accumulation wild-type p53. However, mechanisms leading to via are not well investigated. Here we show that neuroblastoma risk-associated locus 6p22.3-derived tumor suppressor NBAT1 is p53-responsive lncRNA regulates subcellular levels. Low expression provided resistance genotoxic drugs by promoting cytoplasm and loss from...
Abstract Although antisense transcription is a widespread event in the mammalian genome, double-stranded RNA (dsRNA) formation between sense and transcripts very rare mechanisms that control dsRNA remain unknown. By characterizing FGF-2 regulated transcriptome normal cancer cells, we identified IER3 IER3-AS1 play critical role controlled oncogenic pathways. We show regulate each other’s through HnRNPK-mediated post-transcriptional regulation. HnRNPK controls mRNA stability colocalization of...
The clinical progression of B cell chronic lymphocytic leukemia (CLL) is associated with immune dysfunction and a strong decrease miR-181b-5p (miR-181b), promoting the death CLL cells. Here we investigated whether reduction miR-181b impairs response in CLL. We demonstrate that activated CD4+ T cells increase expression through CD40–CD40L signaling, which enhances maturation activity cytotoxic and, consequently, apoptotic facilitated by depletion anti-inflammatory cytokine interleukin 10,...
Deregulation of the miR-15a/16-1 cluster has a key role in pathogenesis chronic lymphocytic leukemia (CLL), clinically heterogeneous disease with indolent and aggressive forms. The locus is located at 13q14, most frequently deleted region CLL. Starting from functional investigations rare SNP upstream miR cluster, we identified novel allele-specific mechanism that exploits cryptic activator to recruit RNA polymerase III for transcription. This regulation miR-15a/16- independent DLEU2 host...
// Sara Pagotto 1, 2, * , Angelo Veronese Alessandra Soranno 2 Paola Lanuti 3 Mirco Di Marco Vincenzo Russo 1 Alice Ramassone Marchisio Pasquale Simeone Paolo E. Guanciali Franchi Giandomenico Palka Renato Mariani Costantini Carlo M. Croce 4, 5 and Rosa Visone Aging Research Center Translational Medicine-CeSI-MeT, Chieti, 66100, Italy Department of Medical, Oral Biotechnological Sciences, "G. d'Annunzio" University Chieti-Pescara, Medicine 4 Molecular Virology, Immunology, Medical Genetics,...
MYCN has been an attractive therapeutic target in neuroblastoma considering the widespread amplification of locus neuroblastoma, and its established role development progression. Thus, understanding neuroblastoma-specific control expression at transcriptional post-transcriptional level would lead to identification novel MYCN-dependent oncogenic pathways potential strategies.By performing loss- gain-of-function experiments hotspot 6p22.3 derived lncRNAs CASC15-003 NBAT1, together with...
<p>Differentially expressed genes in SH-SY5Y neuroblastoma cells after treatment with nutlin-3a, as detected by RNA-seq.</p>
<div>Abstract<p>Neuroblastoma has a low mutation rate for the <i>p53</i> gene. Alternative ways of p53 inactivation have been proposed in neuroblastoma, such as abnormal cytoplasmic accumulation wild-type p53. However, mechanisms leading to via are not well investigated. Here we show that neuroblastoma risk-associated locus 6p22.3-derived tumor suppressor <i>NBAT1</i> is p53-responsive lncRNA regulates subcellular levels. Low expression provided resistance...
<p>Supplementary Text, Supplementary Table Legends</p>
<p>Supplementary Figures S1-S6</p>
<p>Supplementary Text, Supplementary Table Legends</p>
<p>Primers used in the current investigation.</p>
<p>GSEA enriched pathways and list of p53 pathway genes in nutlin-3a treated control NBAT1 depleted SH-SY5Y cells detected by RNA-seq.</p>
<div>Abstract<p>Neuroblastoma has a low mutation rate for the <i>p53</i> gene. Alternative ways of p53 inactivation have been proposed in neuroblastoma, such as abnormal cytoplasmic accumulation wild-type p53. However, mechanisms leading to via are not well investigated. Here we show that neuroblastoma risk-associated locus 6p22.3-derived tumor suppressor <i>NBAT1</i> is p53-responsive lncRNA regulates subcellular levels. Low expression provided resistance...
<p>Differentially expressed genes in SH-SY5Y neuroblastoma cells after treatment with nutlin-3a, as detected by RNA-seq.</p>
<p>Details of NB tumors with NBAT1 expression, p53 localization.</p>
<p>Primers used in the current investigation.</p>
<p>GSEA enriched pathways and list of p53 pathway genes in nutlin-3a treated control NBAT1 depleted SH-SY5Y cells detected by RNA-seq.</p>
<p>Details of NB tumors with NBAT1 expression, p53 localization.</p>