16 results on '"Pullano V"'
Search Results
2. Endogenous growth hormone secretion does not correlate with growth in patients with Turner's syndrome
- Author
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luciano cavallo, Gurrado, R., Bernasconi, S., Bona, G., Buzi, F., Cacciari, E., Mazzanti, L., Luca, F., Sanctis, V., Einaudi, S., Gabrielli, O., Guarneri, M. P., Manzoni, P., Morabito, F., Pasquino, A. M., Pullano, V., Radetti, G., Ragusa, M. C., Rigon, F., Saggese, G., Cinquanta, L., Salerno, M. C., Severi, F., Larizza, D., Sposito, M., Stoppoloni, G., Tatò, L., Tonini, G., Cavallo, L., Gurrado, R., Bernasconi, S., Bona, G., Buzi, F., Cacciari, E., Mozzanti, L., De Luca, F., De Sanctis, V., Einaudi, S., Gabrielli, O., Guarnieri, M. P., Manzoni, P., Morabito, F., Pasquino, A. M., Pullano, V., Radetti, G., Ragusa, M. C., Rigon, F., Saggese, G., Cinquanta, L., Salerno, Mariacarolina, Severi, F., Larizza, D., Sposito, M., Stoppoloni, G., Tatò, L., and Tonini, G.
- Subjects
Endogenous growth hormone secretion,growth, Turner Syndrome, Italian Study Group for Turner Syndrome - Abstract
We investigated in Turner's syndrome patients whether the decrease in growth hormone (GH) secretion is frequent or sporadic, whether or not reduced GH secretion contributes to insufficient growth, and whether age, spontaneous presence of telarche and/or pubarche, karyotype and weight influence GH secretion decrease. We evaluated GH reserve in 301 patients by classical stimulation tests and in 68 of these patients mean nocturnal spontaneous secretion was also measured. Spontaneous telarche and/or pubarche were present in 33% of girls aged > 9 years. In 11% of patients, weight was more than 20% above levels appropriate for height. In 36.2% of patients (low-responders), we observed a reduction of the GH reserve (peak < or = 10 micrograms/l during two stimulation tests). Moreover, we noted reduced mean nocturnal spontaneous secretion (< or = 3.3 micrograms/l) in 61.8% of patients. Karyotype and the presence/absence of spontaneous telarche and/or pubarche did not influence either GH reserve or mean nocturnal spontaneous secretion. GH secretion (both GH reserve and mean nocturnal spontaneous secretion) did not influence height, yet low-responders had a significantly higher chronological age than normal-responders. Obese Turner's girls were low-responders and showed reduced mean nocturnal spontaneous secretion more frequently than normal weight girls; body mass index was significantly higher in patients with reduced GH secretion when compared to patients with normal GH secretion. We conclude that impairment of GH secretion is frequent in Turner's syndrome patients, especially if obese; that GH secretion impairment is not related to karyotype or spontaneous telarche and/or pubarche; that GH secretion is irrelevant to growth in these, patients and, therefore, its evaluation is unnecessary.
- Published
- 1999
3. Modeling effects of impulse noise on Application-Layer FEC in DSL channels
- Author
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Pullano, V., primary, Skupin, R., additional, Corazza, G.E., additional, Hellge, C., additional, and Schierl, T., additional
- Published
- 2013
- Full Text
- View/download PDF
4. GH/IGF-I axis in aging: multicenter study in 152 healthy elderly subjects with different degrees of physical activity: Italian association for research on brain aging (AIRIC) multicenter study group
- Author
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Ambrosio, Mr, DEGLI UBERTI, E, Arvat, E, Camanni, F, Ghigo, E, Gianotti, L, Baumann, G, Ceda, Gp, Valenti, G, Cella, Sg, Muller, Ee, Rigamonti, A, Cifani, S, Torri, V, Corradini, C, Fonzi, S, Giordano, F, Minuto, F, Murialdo, G, Polleri, A, Gasperi, Maurizio, Macchia, E, Martino, E, Pinchera, A, Ghidinelli, S, Maestri, P, Pullano, V, Riondino, G, Strollo, F, and Rizzi, G.
- Published
- 1997
5. Function of GH/IGF-I axis in aging: Multicenter study in 152 healthy elderly subjects with different degrees of physical activity: Italian Association for Research on Brain Aging (AIRIC) Multicenter Study Group
- Author
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Ambrosio, M. R., Degli Uberti, E. C., Arvat, E., Camanni, F., Ghigo, E., Gianotti, L., Baumann, G., Ceda, G. P., Valenti, G., Cella, S. G., Müller, E. E., Rigamonti, A., Cifani, S., Torri, V., COSTANTINO CORRADINI, Fonzi, S., Giordano, F., Minuto, F., Murialdo, G., Polleri, A., Gasperi, M., Macchia, E., Martino, E., Pinchera, A., Ghidinelli, S., Maestri, P., Pullano, V., Riondino, G., Strollo, F., and Rizzi, G.
6. Final height in non-growth hormone deficient children treated with growth hormone
- Author
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Bernasconi, S., Maria Elisabeth Street, Volta, C., Mazzardo, G., Bartolotta, E., Benso, L., Bona, G., Borrelli, P., Buzi, F., Cappa, M., Chiabotto, P., Luca, F., Sanctis, V., Klain, U., Loche, S., Morabito, F., Pietta, R., Pullano, V., Radetti, G., Rigon, F., Sartorio, A., and Tonini, G.
7. DNA methylation analysis in patients with neurodevelopmental disorders improves variant interpretation and reveals complexity.
- Author
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Trajkova S, Kerkhof J, Rossi Sebastiano M, Pavinato L, Ferrero E, Giovenino C, Carli D, Di Gregorio E, Marinoni R, Mandrile G, Palermo F, Carestiato S, Cardaropoli S, Pullano V, Rinninella A, Giorgio E, Pippucci T, Dimartino P, Rzasa J, Rooney K, McConkey H, Petlichkovski A, Pasini B, Sukarova-Angelovska E, Campbell CM, Metcalfe K, Jenkinson S, Banka S, Mussa A, Ferrero GB, Sadikovic B, and Brusco A
- Subjects
- Humans, Male, Female, Transcription Factors genetics, Child, Epigenesis, Genetic, Child, Preschool, DNA-Binding Proteins genetics, Mutation, Adolescent, DNA Methylation genetics, Neurodevelopmental Disorders genetics, Neurodevelopmental Disorders diagnosis
- Abstract
Analysis of genomic DNA methylation by generating epigenetic signature profiles (episignatures) is increasingly being implemented in genetic diagnosis. Here we report our experience using episignature analysis to resolve both uncomplicated and complex cases of neurodevelopmental disorders (NDDs). We analyzed 97 NDDs divided into (1) a validation cohort of 59 patients with likely pathogenic/pathogenic variants characterized by a known episignature and (2) a test cohort of 38 patients harboring variants of unknown significance or unidentified variants. The expected episignature was obtained in most cases with likely pathogenic/pathogenic variants (53/59 [90%]), a revealing exception being the overlapping profile of two SMARCB1 pathogenic variants with ARID1A/B:c.6200, confirmed by the overlapping clinical features. In the test cohort, five cases showed the expected episignature, including (1) novel pathogenic variants in ARID1B and BRWD3; (2) a deletion in ATRX causing MRXFH1 X-linked mental retardation; and (3) confirmed the clinical diagnosis of Cornelia de Lange (CdL) syndrome in mutation-negative CdL patients. Episignatures analysis of the in BAF complex components revealed novel functional protein interactions and common episignatures affecting homologous residues in highly conserved paralogous proteins (SMARCA2 M856V and SMARCA4 M866V). Finally, we also found sex-dependent episignatures in X-linked disorders. Implementation of episignature profiling is still in its early days, but with increasing utilization comes increasing awareness of the capacity of this methodology to help resolve the complex challenges of genetic diagnoses., Competing Interests: Declaration of interests B.S. is a shareholder in EpiSign Inc, company involved in commercialization of EpiSign technology., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)
- Published
- 2024
- Full Text
- View/download PDF
8. Identification of the DNA methylation signature of Mowat-Wilson syndrome.
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Caraffi SG, van der Laan L, Rooney K, Trajkova S, Zuntini R, Relator R, Haghshenas S, Levy MA, Baldo C, Mandrile G, Lauzon C, Cordelli DM, Ivanovski I, Fetta A, Sukarova E, Brusco A, Pavinato L, Pullano V, Zollino M, McConkey H, Tartaglia M, Ferrero GB, Sadikovic B, and Garavelli L
- Subjects
- Humans, Female, Male, Child, Child, Preschool, Adolescent, CpG Islands, DNA Methylation, Intellectual Disability genetics, Intellectual Disability diagnosis, Intellectual Disability pathology, Zinc Finger E-box Binding Homeobox 2 genetics, Zinc Finger E-box Binding Homeobox 2 metabolism, Microcephaly genetics, Microcephaly diagnosis, Microcephaly pathology, Hirschsprung Disease genetics, Hirschsprung Disease diagnosis, Hirschsprung Disease pathology, Homeodomain Proteins genetics, Repressor Proteins genetics, Facies
- Abstract
Mowat-Wilson syndrome (MOWS) is a rare congenital disease caused by haploinsufficiency of ZEB2, encoding a transcription factor required for neurodevelopment. MOWS is characterized by intellectual disability, epilepsy, typical facial phenotype and other anomalies, such as short stature, Hirschsprung disease, brain and heart defects. Despite some recognizable features, MOWS rarity and phenotypic variability may complicate its diagnosis, particularly in the neonatal period. In order to define a novel diagnostic biomarker for MOWS, we determined the genome-wide DNA methylation profile of DNA samples from 29 individuals with confirmed clinical and molecular diagnosis. Through multidimensional scaling and hierarchical clustering analysis, we identified and validated a DNA methylation signature involving 296 differentially methylated probes as part of the broader MOWS DNA methylation profile. The prevalence of hypomethylated CpG sites agrees with the main role of ZEB2 as a transcriptional repressor, while differential methylation within the ZEB2 locus supports the previously proposed autoregulation ability. Correlation studies compared the MOWS cohort with 56 previously described DNA methylation profiles of other neurodevelopmental disorders, further validating the specificity of this biomarker. In conclusion, MOWS DNA methylation signature is highly sensitive and reproducible, providing a useful tool to facilitate diagnosis., (© 2024. The Author(s).)
- Published
- 2024
- Full Text
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9. Genetic variants in DDX53 contribute to Autism Spectrum Disorder associated with the Xp22.11 locus.
- Author
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Scala M, Bradley CA, Howe JL, Trost B, Salazar NB, Shum C, Reuter MS, MacDonald JR, Ko SY, Frankland PW, Granger L, Anadiotis G, Pullano V, Brusco A, Keller R, Parisotto S, Pedro HF, Lusk L, McDonnell PP, Helbig I, Mullegama SV, Douine ED, Russell BE, Nelson SF, Zara F, and Scherer SW
- Abstract
Autism Spectrum Disorder (ASD) exhibits an ~4:1 male-to-female sex bias and is characterized by early-onset impairment of social/communication skills, restricted interests, and stereotyped behaviors. Disruption of the Xp22.11 locus has been associated with ASD in males. This locus includes the three-exon PTCHD1 gene, an adjacent multi-isoform long noncoding RNA (lncRNA) named PTCHD1-AS (spanning ~1Mb), and a poorly characterized single-exon RNA helicase named DDX53 that is intronic to PTCHD1-AS . While the relationship between PTCHD1/PTCHD1-AS and ASD is being studied, the role of DDX53 has not been examined, in part because there is no apparent functional murine orthologue. Through clinical testing, here, we identified 6 males and 1 female with ASD from 6 unrelated families carrying rare, predicted-damaging or loss-of-function variants in DDX53 . Then, we examined databases, including the Autism Speaks MSSNG and Simons Foundation Autism Research Initiative, as well as population controls. We identified 24 additional individuals with ASD harboring rare, damaging DDX53 variations, including the same variants detected in two families from the original clinical analysis. In this extended cohort of 31 participants with ASD (28 male, 3 female), we identified 25 mostly maternally-inherited variations in DDX53 , including 18 missense changes, 2 truncating variants, 2 in-frame variants, 2 deletions in the 3' UTR and 1 copy number deletion. Our findings in humans support a direct link between DDX53 and ASD, which will be important in clinical genetic testing. These same autism-related findings, coupled with the observation that a functional orthologous gene is not found in mouse, may also influence the design and interpretation of murine-modelling of ASD., Competing Interests: Competing interests At the time of this study and its publication, S.W.S. served on the Scientific Advisory Committee of Population Bio. Intellectual property from aspects of his research held at The Hospital for Sick Children are licensed to Athena Diagnostics and Population Bio. These relationships did not influence data interpretation or presentation during this study but are disclosed for potential future considerations. SVM is an employee of GeneDx, LLC. HFP is on the research advisory boards and speaker bureau for Takeda Pharmaceutical, AvroBio, Amicus Therapeutics, Sanofi, Alexion Therapeutics, Denali Therapeutics and Acer Therapeutics. All other authors declare no conflict of interest.
- Published
- 2023
- Full Text
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10. Skewed X-chromosome inactivation in unsolved neurodevelopmental disease cases can guide re-evaluation For X-linked genes.
- Author
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Giovenino C, Trajkova S, Pavinato L, Cardaropoli S, Pullano V, Ferrero E, Sukarova-Angelovska E, Carestiato S, Salmin P, Rinninella A, Battaglia A, Bertoli L, Fadda A, Palermo F, Carli D, Mussa A, Dimartino P, Bruselles A, Froukh T, Mandrile G, Pasini B, De Rubeis S, Buxbaum JD, Pippucci T, Tartaglia M, Rossato M, Delledonne M, Ferrero GB, and Brusco A
- Subjects
- Female, Humans, Male, Mothers, Alleles, Chromosomes, Chromosomes, Human, X genetics, Neoplasm Proteins genetics, X Chromosome Inactivation, Genes, X-Linked
- Abstract
Despite major advances in genome technology and analysis, >50% of patients with a neurodevelopmental disorder (NDD) remain undiagnosed after extensive evaluation. A point in case is our clinically heterogeneous cohort of NDD patients that remained undiagnosed after FRAXA testing, chromosomal microarray analysis and trio exome sequencing (ES). In this study, we explored the frequency of non-random X chromosome inactivation (XCI) in the mothers of male patients and affected females, the rationale being that skewed XCI might be masking previously discarded genetic variants found on the X chromosome. A multiplex fluorescent PCR-based assay was used to analyse the pattern of XCI after digestion with HhaI methylation-sensitive restriction enzyme. In families with skewed XCI, we re-evaluated trio-based ES and identified pathogenic variants and a deletion on the X chromosome. Linkage analysis and RT-PCR were used to further study the inactive X chromosome allele, and Xdrop long-DNA technology was used to define chromosome deletion boundaries. We found skewed XCI (>90%) in 16/186 (8.6%) mothers of NDD males and in 12/90 (13.3%) NDD females, far beyond the expected rate of XCI in the normal population (3.6%, OR = 4.10; OR = 2.51). By re-analyzing ES and clinical data, we solved 7/28 cases (25%) with skewed XCI, identifying variants in KDM5C, PDZD4, PHF6, TAF1, OTUD5 and ZMYM3, and a deletion in ATRX. We conclude that XCI profiling is a simple assay that targets a subgroup of patients that can benefit from re-evaluation of X-linked variants, thus improving the diagnostic yield in NDD patients and identifying new X-linked disorders., (© 2023. The Author(s), under exclusive licence to European Society of Human Genetics.)
- Published
- 2023
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11. Deleterious, protein-altering variants in the transcriptional coregulator ZMYM3 in 27 individuals with a neurodevelopmental delay phenotype.
- Author
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Hiatt SM, Trajkova S, Sebastiano MR, Partridge EC, Abidi FE, Anderson A, Ansar M, Antonarakis SE, Azadi A, Bachmann-Gagescu R, Bartuli A, Benech C, Berkowitz JL, Betti MJ, Brusco A, Cannon A, Caron G, Chen Y, Cochran ME, Coleman TF, Crenshaw MM, Cuisset L, Curry CJ, Darvish H, Demirdas S, Descartes M, Douglas J, Dyment DA, Elloumi HZ, Ermondi G, Faoucher M, Farrow EG, Felker SA, Fisher H, Hurst ACE, Joset P, Kelly MA, Kmoch S, Leadem BR, Lyons MJ, Macchiaiolo M, Magner M, Mandrile G, Mattioli F, McEown M, Meadows SK, Medne L, Meeks NJL, Montgomery S, Napier MP, Natowicz M, Newberry KM, Niceta M, Noskova L, Nowak CB, Noyes AG, Osmond M, Prijoles EJ, Pugh J, Pullano V, Quélin C, Rahimi-Aliabadi S, Rauch A, Redon S, Reymond A, Schwager CR, Sellars EA, Scheuerle AE, Shukarova-Angelovska E, Skraban C, Stolerman E, Sullivan BR, Tartaglia M, Thiffault I, Uguen K, Umaña LA, van Bever Y, van der Crabben SN, van Slegtenhorst MA, Waisfisz Q, Washington C, Rodan LH, Myers RM, and Cooper GM
- Subjects
- Humans, Male, Female, Phenotype, Gene Expression Regulation, Face, Nuclear Proteins genetics, Histone Demethylases genetics, Neurodevelopmental Disorders genetics, Intellectual Disability genetics, Nervous System Malformations
- Abstract
Neurodevelopmental disorders (NDDs) result from highly penetrant variation in hundreds of different genes, some of which have not yet been identified. Using the MatchMaker Exchange, we assembled a cohort of 27 individuals with rare, protein-altering variation in the transcriptional coregulator ZMYM3, located on the X chromosome. Most (n = 24) individuals were males, 17 of which have a maternally inherited variant; six individuals (4 male, 2 female) harbor de novo variants. Overlapping features included developmental delay, intellectual disability, behavioral abnormalities, and a specific facial gestalt in a subset of males. Variants in almost all individuals (n = 26) are missense, including six that recurrently affect two residues. Four unrelated probands were identified with inherited variation affecting Arg441, a site at which variation has been previously seen in NDD-affected siblings, and two individuals have de novo variation resulting in p.Arg1294Cys (c.3880C>T). All variants affect evolutionarily conserved sites, and most are predicted to damage protein structure or function. ZMYM3 is relatively intolerant to variation in the general population, is widely expressed across human tissues, and encodes a component of the KDM1A-RCOR1 chromatin-modifying complex. ChIP-seq experiments on one variant, p.Arg1274Trp, indicate dramatically reduced genomic occupancy, supporting a hypomorphic effect. While we are unable to perform statistical evaluations to definitively support a causative role for variation in ZMYM3, the totality of the evidence, including 27 affected individuals, recurrent variation at two codons, overlapping phenotypic features, protein-modeling data, evolutionary constraint, and experimentally confirmed functional effects strongly support ZMYM3 as an NDD-associated gene., Competing Interests: Declaration of interests J.L.B., Y.C., B.R.L., M.P.N., A.G.N., and H.Z.E. are employees of GeneDx, LLC. S.E.A. is a cofounder and CEO of MediGenome, the Swiss Institute of Genomic Medicine. All other authors declare no competing interests., (Copyright © 2022 American Society of Human Genetics. Published by Elsevier Inc. All rights reserved.)
- Published
- 2023
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- View/download PDF
12. Successful treatment with MEK-inhibitor in a patient with NRAS-related cutaneous skeletal hypophosphatemia syndrome.
- Author
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Carli D, Cardaropoli S, Tessaris D, Coppo P, La Selva R, Cesario C, Lepri FR, Pullano V, Palumbo M, Ramenghi U, Brusco A, Medico E, De Sanctis L, Ferrero GB, and Mussa A
- Subjects
- DNA, GTP Phosphohydrolases genetics, Humans, Membrane Proteins genetics, Mitogen-Activated Protein Kinase Kinases, Phosphates, Phosphatidylinositol 3-Kinases, Syndrome, Chylothorax, Hamartoma, Hypophosphatemia diagnosis, Hypophosphatemia genetics, Nevus, Nevus, Pigmented diagnosis, Nevus, Pigmented genetics, Nevus, Pigmented metabolism, Rickets, Hypophosphatemic genetics, Skin Neoplasms genetics
- Abstract
Cutaneous skeletal hypophosphatemia syndrome (CSHS) is caused by somatic mosaic NRAS variants and characterized by melanocytic/sebaceous naevi, eye, and brain malformations, and FGF23-mediated hypophosphatemic rickets. The MEK inhibitor Trametinib, acting on the RAS/MAPK pathway, is a candidate for CSHS therapy. A 4-year-old boy with seborrheic nevus, eye choristoma, multiple hamartomas, brain malformation, pleural lymphangioma and chylothorax developed severe hypophosphatemic rickets unresponsive to phosphate supplementation. The c.182A > G;p.(Gln61Arg) somatic NRAS variant found in DNA from nevus biopsy allowed diagnosing CSHS. We administered Trametinib for 15 months investigating the transcriptional effects at different time points by whole blood RNA-seq. Treatment resulted in prompt normalization of phosphatemia and phosphaturia, catch-up growth, chylothorax regression, improvement of bone mineral density, reduction of epidermal nevus and hamartomas. Global RNA sequencing on peripheral blood mononucleate cells showed transcriptional changes under MEK inhibition consisting in a strong sustained downregulation of signatures related to RAS/MAPK, PI3 kinase, WNT and YAP/TAZ pathways, reverting previously defined transcriptomic signatures. CSHS was effectively treated with a MEK inhibitor with almost complete recovery of rickets and partial regression of the phenotype. We identified "core" genes modulated by MEK inhibition potentially serving as surrogate markers of Trametinib action., (© 2022 The Authors. Genes, Chromosomes and Cancer published by Wiley Periodicals LLC.)
- Published
- 2022
- Full Text
- View/download PDF
13. IDH2 inhibition enhances proteasome inhibitor responsiveness in hematological malignancies.
- Author
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Bergaggio E, Riganti C, Garaffo G, Vitale N, Mereu E, Bandini C, Pellegrino E, Pullano V, Omedè P, Todoerti K, Cascione L, Audrito V, Riccio A, Rossi A, Bertoni F, Deaglio S, Neri A, Palumbo A, and Piva R
- Subjects
- Animals, Apoptosis, Cell Proliferation, Cytokines antagonists & inhibitors, Cytokines genetics, Hematologic Neoplasms genetics, Hematologic Neoplasms pathology, Humans, Isocitrate Dehydrogenase genetics, Mice, Mice, Inbred NOD, Mice, SCID, Nicotinamide Phosphoribosyltransferase antagonists & inhibitors, Nicotinamide Phosphoribosyltransferase genetics, RNA, Small Interfering genetics, Sirtuin 3 antagonists & inhibitors, Sirtuin 3 genetics, Tumor Cells, Cultured, Xenograft Model Antitumor Assays, Drug Resistance, Neoplasm, Hematologic Neoplasms drug therapy, Isocitrate Dehydrogenase antagonists & inhibitors, Oligopeptides pharmacology, Proteasome Inhibitors pharmacology
- Abstract
Proteasome inhibitors (PI) are extensively used for the therapy of multiple myeloma (MM) and mantle cell lymphoma. However, patients continuously relapse or are intrinsically resistant to this class of drugs. Here, to identify targets that synergize with PI, we carried out a functional screening in MM cell lines using a short hairpin RNA library against cancer driver genes. Isocitrate dehydrogenase 2 ( IDH2) was identified as a top candidate, showing a synthetic lethal activity with the PI carfilzomib (CFZ). Combinations of US Food and Drug Administration-approved PI with a pharmacological IDH2 inhibitor (AGI-6780) triggered synergistic cytotoxicity in MM, mantle cell lymphoma, and Burkitt lymphoma cell lines. CFZ/AGI-6780 treatment increased death of primary CD138
+ cells from MM patients and exhibited a favorable cytotoxicity profile toward peripheral blood mononuclear cells and bone marrow-derived stromal cells. Mechanistically, the CFZ/AGI-6780 combination significantly decreased tricarboxylic acid cycle activity and adenosine triphosphate levels as a consequence of enhanced IDH2 enzymatic inhibition. Specifically, CFZ treatment reduced the expression of nicotinamide phosphoribosyltransferase (NAMPT), thus limiting IDH2 activation through the NAD+ -dependent deacetylase SIRT3. Consistently, combination of CFZ with either NAMPT or SIRT3 inhibitors impaired IDH2 activity and increased MM cell death. Finally, inducible IDH2 knockdown enhanced the therapeutic efficacy of CFZ in a subcutaneous xenograft model of MM, resulting in inhibition of tumor progression and extended survival. Taken together, these findings indicate that NAMPT/SIRT3/IDH2 pathway inhibition enhances the therapeutic efficacy of PI, thus providing compelling evidence for treatments with lower and less toxic doses and broadening the application of PI to other malignancies., (© 2019 by The American Society of Hematology.)- Published
- 2019
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14. Add-On Treatment with Liraglutide Improves Glycemic Control in Patients with Type 2 Diabetes on Metformin Therapy.
- Author
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Chiefari E, Capula C, Vero A, Oliverio R, Puccio L, Liguori R, Pullano V, Greco M, Foti D, Tirinato D, Vero R, and Brunetti A
- Subjects
- Aged, Blood Glucose analysis, Blood Glucose Self-Monitoring, Blood Pressure drug effects, Body Weight drug effects, Diabetes Mellitus, Type 2 blood, Drug Therapy, Combination, Fasting blood, Female, Glycated Hemoglobin analysis, Humans, Male, Middle Aged, Retrospective Studies, Sex Factors, Treatment Outcome, Waist Circumference drug effects, Diabetes Mellitus, Type 2 drug therapy, Hypoglycemic Agents administration & dosage, Liraglutide administration & dosage, Metformin administration & dosage, Sulfonylurea Compounds administration & dosage
- Abstract
Background: Liraglutide is a glucagon-like peptide-1 receptor analog recently approved for the treatment of type 2 diabetes mellitus (T2DM). We aimed to assess the efficacy and safety of liraglutide versus glimepiride, as adjunct treatments to metformin, in achieving glycemic control in Italian patients with T2DM uncontrolled by metformin alone., Subjects and Methods: One hundred seventy-nine diabetes patients treated with metformin plus liraglutide (1.8 mg) or glimepiride (4 mg) were retrospectively assessed at baseline, during, and after 18 months of continuous therapy., Results: Treatment with liraglutide resulted in mean decreases in hemoglobin A1c (HbA1c) of -1.4%, when compared with glimepiride (-0.4%) (P < 0.001), and was followed by a significant reduction (P < 0.001) in fasting plasma glucose. Variations in HbA1c occurred independently from weight loss, which was significantly reduced (P < 0.001) in liraglutide-treated patients. The percentage of subjects reaching HbA1c levels below 7% or ≤ 6.5% was significantly different between the two treated groups (P < 0.001). Treatment with liraglutide reduced waist circumference (WC) (P < 0.001) and decreased both systolic and diastolic blood pressure (BP) (P < 0.001). It is interesting that the study also showed the impact of female gender in predicting a better glycemic response to liraglutide (P = 0.028)., Conclusions: Liraglutide was more effective than glimepiride in reducing HbA1c levels in treated patients with T2DM. This was evident in both genders, but particularly in women. Furthermore, liraglutide reduced body weight, WC, and BP, which are critical risk factors for cardiovascular disease.
- Published
- 2015
- Full Text
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15. Gestational diabetes mellitus: screening and outcomes in southern italian pregnant women.
- Author
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Capula C, Chiefari E, Vero A, Arcidiacono B, Iiritano S, Puccio L, Pullano V, Foti DP, Brunetti A, and Vero R
- Abstract
Recent Italian guidelines exclude women <35 years old, without risk factors for gestational diabetes mellitus (GDM), from screening for GDM. To determine the effectiveness of these measures with respect to the International Association of the Diabetes and Pregnancy Study Groups (IADPSG) criteria, we evaluated 2,448 pregnant women retrospectively enrolled in Calabria, southern Italy. GDM was diagnosed following the IADPSG 2010 criteria. Among 538 women <35 years old, without risk factors, who would have not been tested according to the Italian guidelines, we diagnosed GDM in 171 (31.8%) pregnants (7.0% of total pregnants). Diagnosis was made at baseline (55.6%), 1 hour (39.8%), or 2 hours (4.7%) during OGTT. Despite of appropriate treatment, GDM represented a risk factor for cesarean section, polyhydramnios, increased birth weight, admission to neonatal intensive care units, and large for gestational age. These outcomes were similar to those observed in GDM women at high risk for GDM. In conclusion, Italian recommendations failed to identify 7.0% of women with GDM, when compared to IADPSG criteria. The risk for adverse hyperglycaemic-related outcomes is similar in low-risk and high-risk pregnants with GDM. To limit costs of GDM screening, our data suggest to restrict OGTT to two steps (baseline and 1 hour).
- Published
- 2013
- Full Text
- View/download PDF
16. Predictors of postpartum glucose tolerance testing in italian women with gestational diabetes mellitus.
- Author
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Capula C, Chiefari E, Vero A, Iiritano S, Arcidiacono B, Puccio L, Pullano V, Foti D, Brunetti A, and Vero R
- Abstract
Postpartum screening is critical for early identification of type 2 diabetes in women previously diagnosed with gestational diabetes mellitus (GDM). Nevertheless, its rate remains disappointingly low. Thus, we plan to examine the rate of postpartum glucose tolerance test (ppOGTT) for Italian women with GDM, before and after counseling, and identify demographic, clinical, and/or biochemical predictors of adherence. With these aims, we retrospectively enrolled 1159 women with GDM, in Calabria, Southern Italy, between 2004 and 2011. During the last year, verbal and written counseling on the importance of followup was introduced. Data were analyzed by multiple regression analysis. A significant increase of the return rate was observed following introduction of the counseling [adjusted odds ratio (AOR) 5.17 (95% CI, 3.83-6.97), P < 0.001]. Interestingly, previous diagnosis of polycystic ovary syndrome (PCOS) emerged as the major predictor of postpartum followup [AOR 5.27 (95% CI, 3.51-8.70), P < 0.001], even after stratification for the absence of counseling. Previous diagnosis of GDM, higher educational status, and insulin treatment were also relevant predictors. Overall, our data indicate that counseling intervention is effective, even if many women fail to return, whereas PCOS represents a new strong predictor of adherence to postpartum testing.
- Published
- 2013
- Full Text
- View/download PDF
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