Valentina Agnusdei

ORCID: 0000-0002-2617-360X
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About
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Research Areas
  • Acute Lymphoblastic Leukemia research
  • Acute Myeloid Leukemia Research
  • Histone Deacetylase Inhibitors Research
  • Epigenetics and DNA Methylation
  • Chronic Myeloid Leukemia Treatments
  • Cancer, Hypoxia, and Metabolism
  • Genetic factors in colorectal cancer
  • Heme Oxygenase-1 and Carbon Monoxide
  • Cytokine Signaling Pathways and Interactions
  • Chronic Lymphocytic Leukemia Research
  • Adenosine and Purinergic Signaling
  • Nitric Oxide and Endothelin Effects
  • RNA and protein synthesis mechanisms
  • Aldose Reductase and Taurine
  • NF-κB Signaling Pathways
  • RNA Research and Splicing
  • Cannabis and Cannabinoid Research
  • Genetics and Neurodevelopmental Disorders
  • Immune cells in cancer
  • Glutathione Transferases and Polymorphisms
  • Neonatal Respiratory Health Research
  • Signaling Pathways in Disease
  • Genomics, phytochemicals, and oxidative stress
  • RNA Interference and Gene Delivery
  • Infectious Diseases and Mycology

Istituto Oncologico Veneto
2013-2023

Istituti di Ricovero e Cura a Carattere Scientifico
2015-2023

University of Padua
2011-2014

Despite chemotherapy intensification, a subgroup of high-risk paediatric T-cell acute lymphoblastic leukemia (T-ALL) patients still experience treatment failure. In this context, we hypothesised that therapy resistance in T-ALL might involve aldo-keto reductase 1C (AKR1C) enzymes as previously reported for solid tumors.Expression NRF2-AKR1C signaling components has been analysed samples endowed with different outcomes well patient-derived xenografts T-ALL. The effects AKR1C enzyme modulation...

10.1038/s41416-018-0014-0 article EN cc-by British Journal of Cancer 2018-03-06

Activation of the NOTCH pathway occurs commonly in T acute lymphoblastic leukemia (T-ALL) mainly due to mutations NOTCH1 or alterations FBW7 and is involved regulation cell proliferation survival. Since hit different domains receptor, they are predicted heterogeneously perturb ligand-induced activity. Moreover, T-ALL cells also co-express NOTCH3 receptors which could be triggered by ligands. In this study, we aimed investigate role DLL4 signaling context types mutation wild-type as well...

10.1093/carcin/bgu223 article EN Carcinogenesis 2014-10-29

Several studies have revealed that endosomal sorting controls the steady-state levels of Notch at cell surface in normal cells and prevents its inappropriate activation absence ligands. However, whether this highly dynamic physiologic process can be exploited to counteract dysregulated signaling cancer remains unknown. T-ALL is a malignancy characterized by aberrant signaling, sustained activating mutations Notch1 as well overexpression Notch3, paralog physiologically subjected...

10.1038/s41388-018-0234-z article EN cc-by Oncogene 2018-04-10

Abstract Despite some success with certain hematological malignancies and in contrast the strong pro-apoptotic effects measured vitro , overall response rate of acute lymphoblastic leukemia (ALL) to histone deacetylase inhibitors (HDACis) is low. With aim improve understanding how HDACis work vivo we investigated therapeutic efficacy clinically approved HDACi Givinostat a collection nine pediatric human T-ALL engrafted systemically NOD/SCID mice. We observed highly heterogeneous antileukemia...

10.1038/cddis.2015.394 article EN cc-by Cell Death and Disease 2016-01-14

Despite substantial progress in treatment of T-cell acute lymphoblastic leukemia (T-ALL), mortality remains relatively high, mainly due to primary or acquired resistance chemotherapy. Further improvements survival demand better understanding T-ALL biology and development new therapeutic strategies. The Notch pathway has been involved the pathogenesis this disease various strategies are currently under development, including selective targeting NOTCH receptors by inhibitory antibodies. We...

10.3324/haematol.2019.217687 article EN cc-by-nc Haematologica 2019-08-29

The liver kinase B1 (LKB1) gene is a tumor suppressor with an established role in the control of cell metabolism and oxidative stress. However, whether dis-regulated stress promotes growth LKB1-deficient tumors remains substantially unknown. Through vitro studies, we observed that loss LKB1 perturbed expression several genes involved ROS homeostasis. In particular, this analysis evidenced strongly up-modulated NADPH oxidase 1 (NOX1) transcript levels cells lacking LKB1. NOX1 accounted part...

10.3389/fonc.2018.00195 article EN cc-by Frontiers in Oncology 2018-06-04

Inference of gene regulation from expression data may help to unravel regulatory mechanisms involved in complex diseases or the action specific drugs. A challenging task for many researchers working field systems biology is build up an experiment with a limited budget and produce dataset suitable reconstruct putative modules worth biological validation. Here, we focus on small-scale screens introduce novel experimental set-up customized method analysis make inference starting genetic...

10.1186/s12864-016-2525-5 article EN cc-by BMC Genomics 2016-03-12

approach to discover the upstream modulators of IRF4 expression in melanoma cells.In parallel, we have performed localization (ChIP-seq) and transcriptomic (RNA-seq) assays order identify genome-wide targets cell lines.Results discussions As regulators expression, identified a known master transcription factor major signalling pathway with therapeutic targeting options.For downstream IRF4, together The Cancer Genome Atlas (TCGA) data analyses, our point role epigenetic regulation cells,...

10.1136/esmoopen-2018-eacr25.155 article EN cc-by-nc ESMO Open 2018-06-01
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