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Article: The Anti-Leukemia Effect of Ascorbic Acid: From the Pro-Oxidant Potential to the Epigenetic Role in Acute Myeloid Leukemia.

Travaglini, S / Gurnari, C / Antonelli, S / Silvestrini, G / Noguera, N I / Ottone, T / Voso, M T

Frontiers in cell and developmental biology

2022 Volume 10, Page(s) 930205

Abstract: Data derived from high-throughput sequencing technologies have allowed a deeper understanding of the molecular landscape of Acute Myeloid Leukemia (AML), paving the way for the development of novel therapeutic options, with a higher efficacy and a lower ... ...

Abstract	Data derived from high-throughput sequencing technologies have allowed a deeper understanding of the molecular landscape of Acute Myeloid Leukemia (AML), paving the way for the development of novel therapeutic options, with a higher efficacy and a lower toxicity than conventional chemotherapy. In the antileukemia drug development scenario, ascorbic acid, a natural compound also known as Vitamin C, has emerged for its potential anti-proliferative and pro-apoptotic activities on leukemic cells. However, the role of ascorbic acid (vitamin C) in the treatment of AML has been debated for decades. Mechanistic insight into its role in many biological processes and, especially, in epigenetic regulation has provided the rationale for the use of this agent as a novel anti-leukemia therapy in AML. Acting as a co-factor for 2-oxoglutarate-dependent dioxygenases (2-OGDDs), ascorbic acid is involved in the epigenetic regulations through the control of TET (ten-eleven translocation) enzymes, epigenetic master regulators with a critical role in aberrant hematopoiesis and leukemogenesis. In line with this discovery, great interest has been emerging for the clinical testing of this drug targeting leukemia epigenome. Besides its role in epigenetics, ascorbic acid is also a pivotal regulator of many physiological processes in human, particularly in the antioxidant cellular response, being able to scavenge reactive oxygen species (ROS) to prevent DNA damage and other effects involved in cancer transformation. Thus, for this wide spectrum of biological activities, ascorbic acid possesses some pharmacologic properties attractive for anti-leukemia therapy. The present review outlines the evidence and mechanism of ascorbic acid in leukemogenesis and its therapeutic potential in AML. With the growing evidence derived from the literature on situations in which the use of ascorbate may be beneficial
Language	English
Publishing date	2022-07-22
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2022.930205
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Article: Acute Promyelocytic Leukemia: Update on the Mechanisms of Leukemogenesis, Resistance and on Innovative Treatment Strategies.

Noguera, N I / Catalano, G / Banella, C / Divona, M / Faraoni, I / Ottone, T / Arcese, W / Voso, M T

Cancers

2019 Volume 11, Issue 10

Abstract: This review highlights new findings that have deepened our understanding of the mechanisms of leukemogenesis, therapy and resistance in acute promyelocytic leukemia (APL). Promyelocytic leukemia-retinoic acid receptor α (PML-RARa) sets the cellular ... ...

Abstract	This review highlights new findings that have deepened our understanding of the mechanisms of leukemogenesis, therapy and resistance in acute promyelocytic leukemia (APL). Promyelocytic leukemia-retinoic acid receptor α (PML-RARa) sets the cellular landscape of acute promyelocytic leukemia (APL) by repressing the transcription of RARa target genes and disrupting PML-NBs. The RAR receptors control the homeostasis of tissue growth, modeling and regeneration, and PML-NBs are involved in self-renewal of normal and cancer stem cells, DNA damage response, senescence and stress response. The additional somatic mutations in APL mainly involve FLT3, WT1, NRAS, KRAS, ARID1B and ARID1A genes. The treatment outcomes in patients with newly diagnosed APL improved dramatically since the advent of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). ATRA activates the transcription of blocked genes and degrades PML-RARα, while ATO degrades PML-RARa by promoting apoptosis and has a pro-oxidant effect. The resistance to ATRA and ATO may derive from the mutations in the RARa ligand binding domain (LBD) and in the PML-B2 domain of PML-RARa, but such mutations cannot explain the majority of resistances experienced in the clinic, globally accounting for 5-10% of cases. Several studies are ongoing to unravel clonal evolution and resistance, suggesting the therapeutic potential of new retinoid molecules and combinatorial treatments of ATRA or ATO with different drugs acting through alternative mechanisms of action, which may lead to synergistic effects on growth control or the induction of apoptosis in APL cells.
Language	English
Publishing date	2019-10-18
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers11101591
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Article: Absence of FGFR3-TACC3 rearrangement in hematological malignancies with numerical chromosomal alteration.

Banella, C / Ginevrino, M / Catalano, G / Fabiani, E / Falconi, G / Divona, M / Curzi, P / Panetta, P / Voso, M T / Noguera, N I

Hematology/oncology and stem cell therapy

2020 Volume 14, Issue 2, Page(s) 163–168

Abstract: FGFR-TACC, found in different tumor types, is characterized by the fusion of a member of fibroblast grown factor receptor (FGFR) tyrosine kinase (TK) family to a member of the transforming acidic coiled-coil (TACC) proteins. Because chromosome numerical ... ...

Abstract	FGFR-TACC, found in different tumor types, is characterized by the fusion of a member of fibroblast grown factor receptor (FGFR) tyrosine kinase (TK) family to a member of the transforming acidic coiled-coil (TACC) proteins. Because chromosome numerical alterations, hallmarks of FGFR-TACC fusions are present in many hematological disorders and there are no data on the prevalence, we studied a series of patients with acute myeloid leukemia and myelodysplastic syndrome who presented numerical alterations using cytogenetic traditional analysis. None of the analyzed samples showed FGFR3-TACC3 gene fusion, so screening for this mutation at diagnosis is not recommended.
MeSH term(s)	Chromosome Aberrations ; Gene Rearrangement ; Hematologic Neoplasms/genetics ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Leukemia, Myeloid, Acute/genetics ; Microtubule-Associated Proteins/genetics ; Myelodysplastic Syndromes/genetics ; Oncogene Proteins, Fusion/genetics ; Receptor, Fibroblast Growth Factor, Type 3/genetics
Chemical Substances	Microtubule-Associated Proteins ; Oncogene Proteins, Fusion ; TACC3 protein, human ; FGFR3 protein, human (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 3 (EC 2.7.10.1)
Language	English
Publishing date	2020-03-16
Publishing country	England
Document type	Letter
ZDB-ID	2651893-4
ISSN	1658-3876
ISSN	1658-3876
DOI	10.1016/j.hemonc.2020.02.005
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Article ; Online: Retinoic acid and arsenic trioxide sensitize acute promyelocytic leukemia cells to ER stress.

Masciarelli, S / Capuano, E / Ottone, T / Divona, M / De Panfilis, S / Banella, C / Noguera, N I / Picardi, A / Fontemaggi, G / Blandino, G / Lo-Coco, F / Fazi, F

Leukemia

2017 Volume 32, Issue 2, Page(s) 285–294

Abstract: Retinoic acid (RA) in association with chemotherapy or with arsenic trioxide (ATO) results in high cure rates of acute promyelocytic leukemia (APL). We show that RA-induced differentiation of human leukemic cell lines and primary blasts dramatically ... ...

Abstract	Retinoic acid (RA) in association with chemotherapy or with arsenic trioxide (ATO) results in high cure rates of acute promyelocytic leukemia (APL). We show that RA-induced differentiation of human leukemic cell lines and primary blasts dramatically increases their sensitivity to endoplasmic reticulum (ER) stress-inducing drugs at doses that are not toxic in the absence of RA. In addition, we demonstrate that the PERK pathway, triggered in response to ER stress, has a major protective role. Moreover, low amounts of pharmacologically induced ER stress are sufficient to strongly increase ATO toxicity. Indeed, in the presence of ER stress, ATO efficiently induced apoptosis in RA-sensitive and RA-resistant APL cell lines, at doses ineffective in the absence of ER stress. Our findings identify the ER stress-related pathways as potential targets in the search for novel therapeutic strategies in AML.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Arsenic Trioxide/pharmacology ; Cell Differentiation/drug effects ; Cell Line ; Cell Line, Tumor ; Endoplasmic Reticulum Stress/drug effects ; HEK293 Cells ; Humans ; Leukemia, Promyelocytic, Acute/drug therapy ; Tretinoin/pharmacology
Chemical Substances	Antineoplastic Agents ; Tretinoin (5688UTC01R) ; Arsenic Trioxide (S7V92P67HO)
Language	English
Publishing date	2017-08-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/leu.2017.231
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Article ; Online: PML nuclear body disruption impairs DNA double-strand break sensing and repair in APL.

di Masi, A / Cilli, D / Berardinelli, F / Talarico, A / Pallavicini, I / Pennisi, R / Leone, S / Antoccia, A / Noguera, N I / Lo-Coco, F / Ascenzi, P / Minucci, S / Nervi, C

Cell death & disease

2016 Volume 7, Page(s) e2308

Abstract: Proteins involved in DNA double-strand break (DSB) repair localize within the promyelocytic leukemia nuclear bodies (PML-NBs), whose disruption is at the root of the acute promyelocytic leukemia (APL) pathogenesis. All-trans-retinoic acid (RA) treatment ... ...

Abstract	Proteins involved in DNA double-strand break (DSB) repair localize within the promyelocytic leukemia nuclear bodies (PML-NBs), whose disruption is at the root of the acute promyelocytic leukemia (APL) pathogenesis. All-trans-retinoic acid (RA) treatment induces PML-RARα degradation, restores PML-NB functions, and causes terminal cell differentiation of APL blasts. However, the precise role of the APL-associated PML-RARα oncoprotein and PML-NB integrity in the DSB response in APL leukemogenesis and tumor suppression is still lacking. Primary leukemia blasts isolated from APL patients showed high phosphorylation levels of H2AX (γ-H2AX), an initial DSBs sensor. By addressing the consequences of ionizing radiation (IR)-induced DSB response in primary APL blasts and RA-responsive and -resistant myeloid cell lines carrying endogenous or ectopically expressed PML-RARα, before and after treatment with RA, we found that the disruption of PML-NBs is associated with delayed DSB response, as revealed by the impaired kinetic of disappearance of γ-H2AX and 53BP1 foci and activation of ATM and of its substrates H2AX, NBN, and CHK2. The disruption of PML-NB integrity by PML-RARα also affects the IR-induced DSB response in a preleukemic mouse model of APL in vivo. We propose the oncoprotein-dependent PML-NB disruption and DDR impairment as relevant early events in APL tumorigenesis.
MeSH term(s)	Animals ; Ataxia Telangiectasia Mutated Proteins/genetics ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Nucleus/drug effects ; Cell Nucleus/metabolism ; Cell Nucleus/radiation effects ; Cell Nucleus/ultrastructure ; Checkpoint Kinase 2/genetics ; Checkpoint Kinase 2/metabolism ; DNA/genetics ; DNA/metabolism ; DNA Breaks, Double-Stranded/radiation effects ; Disease Models, Animal ; Gamma Rays ; Gene Expression Regulation, Leukemic ; Granulocyte Precursor Cells/drug effects ; Granulocyte Precursor Cells/metabolism ; Granulocyte Precursor Cells/pathology ; Granulocyte Precursor Cells/radiation effects ; Histones/genetics ; Histones/metabolism ; Humans ; Leukemia, Promyelocytic, Acute/genetics ; Leukemia, Promyelocytic, Acute/metabolism ; Leukemia, Promyelocytic, Acute/pathology ; Mice ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Oncogene Proteins, Fusion/genetics ; Oncogene Proteins, Fusion/metabolism ; Signal Transduction ; Tretinoin/pharmacology ; Tumor Suppressor p53-Binding Protein 1/genetics ; Tumor Suppressor p53-Binding Protein 1/metabolism
Chemical Substances	Cell Cycle Proteins ; H2AX protein, human ; Histones ; NBN protein, human ; Nuclear Proteins ; Oncogene Proteins, Fusion ; TP53BP1 protein, human ; Tumor Suppressor p53-Binding Protein 1 ; promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein ; Tretinoin (5688UTC01R) ; DNA (9007-49-2) ; Checkpoint Kinase 2 (EC 2.7.1.11) ; ATM protein, human (EC 2.7.11.1) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; CHEK2 protein, human (EC 2.7.11.1)
Language	English
Publishing date	2016-07-28
Publishing country	England
Document type	Journal Article
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/cddis.2016.115
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Article: Triplication (/alphaalphaalpha anti3.7) or deletion (-alpha3.7/) association in Argentinian beta-thalassemic carriers.

Bragós, I M / Noguera, N I / Raviola, M P / Milani, A C

Annals of hematology

2003 Volume 82, Issue 11, Page(s) 696–698

Abstract: Prevalence of alpha gene triplication or deletion in beta-thalassemia carriers was studied in 109 unrelated individuals in Rosario, Argentina. In different populations -alpha(3.7) allele presents a higher prevalence than alphaalphaalpha(anti3.7); thus, ... ...

Abstract	Prevalence of alpha gene triplication or deletion in beta-thalassemia carriers was studied in 109 unrelated individuals in Rosario, Argentina. In different populations -alpha(3.7) allele presents a higher prevalence than alphaalphaalpha(anti3.7); thus, alpha-thalassemia associated with beta-thalassemia is more frequently observed. Nevertheless, this event was detected in only one case (0.9%), while the association with alpha triplication was present in two subjects (1.8%).
MeSH term(s)	Adult ; Alleles ; Argentina/epidemiology ; Blood Cell Count ; Child ; Female ; Gene Deletion ; Gene Duplication ; Globins/genetics ; Hemoglobins/metabolism ; Heterozygote ; Humans ; Infant ; Male ; Prevalence ; alpha-Thalassemia/blood ; alpha-Thalassemia/epidemiology ; alpha-Thalassemia/genetics
Chemical Substances	Hemoglobins ; Globins (9004-22-2)
Language	English
Publishing date	2003-11
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1064950-5
ISSN	1432-0584 ; 0939-5555 ; 0945-8077
ISSN (online)	1432-0584
ISSN	0939-5555 ; 0945-8077
DOI	10.1007/s00277-003-0738-6
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Article ; Online: Nucleophosmin/B26 regulates PTEN through interaction with HAUSP in acute myeloid leukemia.

Noguera, N I / Song, M S / Divona, M / Catalano, G / Calvo, K L / García, F / Ottone, T / Florenzano, F / Faraoni, I / Battistini, L / Colombo, E / Amadori, S / Pandolfi, P P / Lo-Coco, F

Leukemia

2013 Volume 27, Issue 5, Page(s) 1037–1043

Abstract: PTEN (phosphatase and tensin homolog deleted in chromosome 10) is a bona fide dual lipid and protein phosphatase with cytoplasmic (Cy) and nuclear localization. PTEN nuclear exclusion has been associated with tumorigenesis. Nucleophosmin (NPM1) is ... ...

Abstract	PTEN (phosphatase and tensin homolog deleted in chromosome 10) is a bona fide dual lipid and protein phosphatase with cytoplasmic (Cy) and nuclear localization. PTEN nuclear exclusion has been associated with tumorigenesis. Nucleophosmin (NPM1) is frequently mutated in acute myeloid leukemia (AML) and displays Cy localization in mutated nucleophosmin (NPMc+) AML. Here we show that NPM1 directly interacts with herpes virus-associated ubiquitin specific protease (HAUSP), which is known as a PTEN deubiquitinating enzyme. Strikingly, PTEN is aberrantly localized in AML carrying NPMc+. Mechanistically, NPM1 in the nucleus opposes HAUSP-mediated deubiquitination and this promotes the shuttle of PTEN to the cytoplasm. In the cytoplasm, NPMc+ prevents HAUSP from deubiquitinating PTEN, causing the latter to stay in the cytoplasm where it is polyubiquitinated and degraded. Our findings delineate a new NPM1-HAUSP molecular interaction controlling PTEN deubiquitination and trafficking.
MeSH term(s)	Cell Line, Tumor ; HEK293 Cells ; Humans ; Leukemia, Myeloid, Acute/metabolism ; Nuclear Proteins/physiology ; PTEN Phosphohydrolase/analysis ; PTEN Phosphohydrolase/metabolism ; Protein Transport ; Ubiquitin Thiolesterase/physiology ; Ubiquitin-Specific Peptidase 7 ; Ubiquitination
Chemical Substances	Nuclear Proteins ; nucleophosmin (117896-08-9) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; PTEN protein, human (EC 3.1.3.67) ; USP7 protein, human (EC 3.4.19.12) ; Ubiquitin Thiolesterase (EC 3.4.19.12) ; Ubiquitin-Specific Peptidase 7 (EC 3.4.19.12)
Language	English
Publishing date	2013-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/leu.2012.314
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Article: Modified salting-out method for DNA isolation from newborn cord blood nucleated cells.

Noguera, N I / Tallano, C E / Bragós, I M / Milani, A C

Journal of clinical laboratory analysis

2000 Volume 14, Issue 6, Page(s) 280–283

Abstract: The present work describes modification of a widely used salting-out procedure to rapidly extract DNA suitable for PCR, using the ARMS method to amplify a target sequence in the beta-globin gene. The salting-out DNA extraction procedure did not ... ...

Abstract	The present work describes modification of a widely used salting-out procedure to rapidly extract DNA suitable for PCR, using the ARMS method to amplify a target sequence in the beta-globin gene. The salting-out DNA extraction procedure did not completely remove or decrease the presence of inhibitors to PCR in a considerable number of cord blood samples. By introducing a simple phenol/chloroform step, before ethanol precipitation of the nucleic acid, to certain samples, we were able to eliminate or substantially reduce the presence of inhibitors to PCR without having to re-extract the samples.
MeSH term(s)	Blood Cells/chemistry ; Chemical Precipitation ; Chloroform ; DNA/blood ; Electrophoresis, Agar Gel ; Ethanol ; Ethidium ; Fetal Blood/cytology ; Globins/genetics ; Humans ; Indicators and Reagents ; Infant, Newborn ; Phenol ; Polymerase Chain Reaction ; Spectrophotometry
Chemical Substances	Indicators and Reagents ; Phenol (339NCG44TV) ; Ethanol (3K9958V90M) ; Chloroform (7V31YC746X) ; Globins (9004-22-2) ; DNA (9007-49-2) ; Ethidium (EN464416SI)
Language	English
Publishing date	2000
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	645095-7
ISSN	1098-2825 ; 0887-8013
ISSN (online)	1098-2825
ISSN	0887-8013
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Article: Most frequent mutations of beta-thalassemia in Rosario, Argentina.

Bragós, I M / Noguera, N I / Morisoli, L / Milani, A C

Haematologica

2000 Volume 85, Issue 1, Page(s) 101–102

MeSH term(s)	Amino Acid Substitution ; Argentina/epidemiology ; DNA Mutational Analysis ; Family Health ; Gene Frequency ; Greece/ethnology ; Heterozygote ; Humans ; Italy/ethnology ; Mutation/genetics ; Spain/ethnology ; beta-Thalassemia/epidemiology ; beta-Thalassemia/ethnology ; beta-Thalassemia/genetics
Language	English
Publishing date	2000-01
Publishing country	Italy
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	2333-4
ISSN	1592-8721 ; 0390-6078 ; 0017-6567
ISSN (online)	1592-8721
ISSN	0390-6078 ; 0017-6567
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Article: Screening for hemoglobinopathies in neonates in Argentina.

Noguera, N I / Bragós, I M / Morisoli, L / Milani, A C

Haematologica

1999 Volume 84, Issue 5, Page(s) 468–470

MeSH term(s)	Argentina ; Hemoglobinopathies/diagnosis ; Humans ; Infant, Newborn ; Neonatal Screening/methods
Language	English
Publishing date	1999-05
Publishing country	Italy
Document type	Letter
ZDB-ID	2333-4
ISSN	1592-8721 ; 0390-6078 ; 0017-6567
ISSN (online)	1592-8721
ISSN	0390-6078 ; 0017-6567
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