32 results on '"Armellin M"'
Search Results
2. Risolvere i problemi alla primaria. Attività per allenare il ragionamento con il Metodo Euristico Riflessivo
- Author
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Antonietti, Alessandro, Antonietti, C., Armellin, M. N., Gagliardi, C., and Germagnoli, S.
- Subjects
problem solving ,problem finding ,Settore M-PSI/01 - PSICOLOGIA GENERALE - Published
- 2021
3. Dendritic Targeting of mRNAs for Plasticity Genes in Experimental Models of Temporal Lobe Epilepsy
- Author
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Simonato, M., Bregola, G., Armellin, M., Del Piccolo, P., Rodi, D., Zucchini, S., and Tongiorgi, E.
- Published
- 2002
4. Retrograde response of the rat facial motor nucleus to muscle inflammation elicited by phytohaemagglutinin
- Author
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Mariotti, R., Tongiorgi, E., Bressan, C., Armellin, M., Kristensson, K., and Bentivoglio, M.
- Published
- 2001
5. EXPRESSION AND DENDRITIC MRNA LOCALISATION OF GABAC RECEPTOR rho1 AND rho2 SUBUNITS IN DEVELOPING RAT BRAIN AND SPINAL CORD
- Author
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Rozzo, A, Armellin, M, Franzot, J, Chiaruttini, C, Nistri, A, Tongiorgi, Enrico, Rozzo, A, Armellin, M, Franzot, J, Chiaruttini, C, Nistri, A, and Tongiorgi, Enrico
- Published
- 2002
6. Retrograde response of the rat facial motor nucleus to muscle inflammation elicited by phytohemagglutinin
- Author
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MARIOTTI R, BRESSAN C, ARMELLIN M, KRISTENSSON K, BENTIVOGLIO M., TONGIORGI, Enrico, Mariotti, R, Tongiorgi, Enrico, Bressan, C, Armellin, M, Kristensson, K, and Bentivoglio, M.
- Published
- 2001
7. Retrograde response of the rat facial motor nucleus to muscle inflammation elicited by phytohemagglutinin
- Author
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Mariotti, Raffaella, Tongiorgi, E., Armellin, M., Kristensson, K., and BENTIVOGLIO FALES, Marina
- Published
- 2001
8. Priming enhances motoneuron vulnerability
- Author
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Mariotti, Raffaella, Tongiorgi, E., Armellin, M., Kristensson, K., and BENTIVOGLIO FALES, Marina
- Published
- 1999
9. 238 ZEB1 and Aberrant DNA Methylation Sustain Mesenchymal-stem Phenotype and the Resistance to EGFR Inhibitors in Breast Cancer
- Author
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Borgna, S., primary, di Gennaro, A., additional, Armellin, M., additional, Maestro, R., additional, and Santarosa, M., additional
- Published
- 2012
- Full Text
- View/download PDF
10. Fra2 is an antagonist of p53
- Author
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Piccinin, S., primary, Grizzo, A., additional, Bertoja, A. Zambon, additional, Garziera, M., additional, Armellin, M., additional, and Maestro, R., additional
- Published
- 2008
- Full Text
- View/download PDF
11. Differential somato-dendritic localization of TrkA, TrkB, TrkC and p75 mRNAs in vivo
- Author
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Tongiorgi, E, primary, Armellin, M, additional, and Cattaneo, A, additional
- Published
- 2000
- Full Text
- View/download PDF
12. Differential somatodendritic localization of TrkA TrkB TrkC and p75 mRNAs in vivo
- Author
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Tongiorgi, E, Armellin, M, and Cattaneo, A
- Abstract
TrkB mRNA was shown to be localized in the somatodendritic compartment in vitrobut no data are currently available on the subcellular distribution of the neurotrophin receptors mRNAs in vivo. Here we describe the subcellular distribution of TrkA, TrkB, TrkC and p75 mRNAs in the adult rat basal forebrain. We find that TrkA, TrkC and p75 mRNAs are restricted to the cell soma but in addition, p75 mRNA labelling extends in average for 8 μm within the proximal dendrites of 34 of the labelled neurons. TrkB mRNA has a somatodendritic distribution in 95 of the labelled neurons reaching variable distances in different neurons (23–84.5 μm) and forebrain regions (mean: 40, 51 and 55 μm for diagonal band, septum and ventral pallidum).
- Published
- 2000
13. Alterations of β-Catenin Pathway in Non-Melanoma Skin Tumors: Loss of α-ABC Nuclear Reactivity Correlates with the Presence of β-Catenin Gene Mutation
- Author
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Doglioni, C., Piccinin, S., Demontis, S., Cangi, M. G., Pecciarini, L., Chiarelli, C., Armellin, M., Vukosavljevic, T., Boiocchi, M., and Roberta Maestro
14. Interference of p53:Twist1 interaction through competing nanobodies
- Author
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Sara Piccinin, Michela Armellin, Serena D'Agostino, Ario de Marco, Roberta Maestro, Elisa Mazzega, Katja Praček, Sara Fortuna, Flavia Pivetta, D'Agostino, S., Mazzega, E., Pracek, K., Piccinin, S., Pivetta, F., Armellin, M., Fortuna, S., Maestro, R., and de Marco, A.
- Subjects
Models, Molecular ,p53 ,animal structures ,Protein Conformation ,Immunoprecipitation ,Panning strategies ,Cell ,VHH ,Binding, Competitive ,Panning strategie ,Biochemistry ,Cell Line ,law.invention ,Epitopes ,Structure-Activity Relationship ,Intrabodies ,Structural Biology ,law ,medicine ,Humans ,Nanobody ,Twist1 ,Protein Interaction Domains and Motifs ,Viability assay ,Intrabodie ,Molecular Biology ,Chemistry ,Twist-Related Protein 1 ,Wild type ,General Medicine ,Single-Domain Antibodies ,Recombinant Proteins ,In vitro ,Cell biology ,medicine.anatomical_structure ,Docking (molecular) ,Recombinant DNA ,Tumor Suppressor Protein p53 ,Protein Binding ,P53 binding - Abstract
Twist1 promote the bypass of p53 response by interacting with p53 and facilitating its MDM2-mediated degradation. We reasoned that reagents able to interfere with the p53:Twist1 complex might alleviate Twist1 inhibitory effect over p53, thus representing potential therapeutic tools in p53 wild type tumors. From a pre-immune library of llama nanobodies (VHH), we isolated binders targeting the p53 C-terminal region (p53-CTD) involved in the interaction with Twist1 by using recombinant Twist1 as an epitope-specific competitor during elution. Positive hits were validated by proving their capacity to immunoprecipitate p53 and to inhibit Twist1:p53 binding in vitro. Molecular modeling confirmed a preferential docking of positive hits with p53-CTD. D11 VHH activity was validated in human cell models, succeeded in immunoprecipitating endogenous p53 and, similarly to Twist1 knock-down, interfered with p53 turnover, p53 phosphorylation at Serine 392 and affected cell viability. Despite the limited functional effect determined by D11 expression in target cells, our results provide the proof of principle that nanobodies ectopically expressed within a cell, have the capacity to target the assembly of the pro-tumorigenic Twist1:p53 complex. These results disclose novel tools for dissecting p53 biology and lay down the grounds for the development of innovative targeted therapeutic approaches.
- Published
- 2022
15. Brain-derived neurotrophic factor mRNA and protein are targeted to discrete dendritic laminas by events that trigger epileptogenesis
- Author
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Piero Giulio Giulianini, Michele Simonato, M. Armellin, Beatrice Paradiso, Enrico Tongiorgi, Oswald Steward, Silvia Zucchini, Antonino Cattaneo, Gianni Bregola, Tongiorgi, E, Armellin, M, Giulianini, Pg, Bregola, G, Zucchini, S, Paradiso, B, Steward, O, Cattaneo, Antonino, Simonato, M., Tongiorgi, Enrico, Armellin, M., Giulianini, PIERO GIULIO, Bregola, G., Zucchini, S., Paradiso, B., Steward, O., and Cattaneo, A.
- Subjects
Male ,rat hippocampus ,Kainate receptor ,Convulsants ,AMPA receptor ,Hippocampal formation ,neurotrophins ,Epileptogenesis ,NMDA receptors ,Hippocampus ,Receptors, N-Methyl-D-Aspartate ,Rats, Sprague-Dawley ,Epilepsy ,Status Epilepticus ,Postsynaptic potential ,Seizures ,Neurobiology of Disease ,muscarinic acetylcholine receptors ,medicine ,Kindling, Neurologic ,Animals ,RNA, Messenger ,AMPA receptors ,Brain-derived neurotrophic factor ,Electroshock ,Kainic Acid ,biology ,General Neuroscience ,Brain-Derived Neurotrophic Factor ,Pilocarpine ,Biological Transport ,Dendrites ,medicine.disease ,Cell Compartmentation ,Rats ,Protein Transport ,epilepsy ,plasticity ,mRNA trafficking ,nervous system ,Synapses ,biology.protein ,neurotrophins, rat hippocampus, epilepsy, plasticity, mRNA trafficking, AMPA receptors, NMDA receptors, muscarinic acetylcholine receptors ,Dizocilpine Maleate ,Neuroscience ,Neurotrophin - Abstract
Dendritic targeting of mRNA and local protein synthesis are mechanisms that enable neurons to deliver proteins to specific postsynaptic sites. Here, we demonstrate that epileptogenic stimuli induce a dramatic accumulation of BDNF mRNA and protein in the dendrites of hippocampal neuronsin vivo. BDNF mRNA and protein accumulate in dendrites in all hippocampal subfields after pilocarpine seizures and in selected subfields after other epileptogenic stimuli (kainate and kindling). BDNF accumulates selectively in discrete dendritic laminas, suggesting targeting to synapses that are active during seizures. Dendritic targeting of BDNF mRNA occurs during the time when the cellular changes that underlie epilepsy are occurring and is not seen after intense stimuli that are non-epileptogenic, including electroconvulsive seizures and high-frequency stimulation. MK801, an NMDA receptor antagonist that can prevent epileptogenesis but not acute seizures, prevents the dendritic accumulation of BDNF mRNA, indicating that dendritic targeting is mediated via NMDA receptor activation. Together, these results suggest that dendritic accumulation of BDNF mRNA and protein play a critical role in the cellular changes leading to epilepsy.
- Published
- 2004
16. A p53/miR-30a/ZEB2 axis controls triple negative breast cancer aggressiveness
- Author
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Tiziana Perin, Antonella Zucchetto, Alessandra di Gennaro, Herman P. Spaink, Michela Armellin, Valentina Damiano, Manuela Santarosa, Roberta Maestro, B. Ewa Snaar-Jagalska, Claudio Doglioni, Michela Guardascione, Giulia Brisotto, Di Gennaro, A., Damiano, V., Brisotto, G., Armellin, M., Perin, T., Zucchetto, A., Guardascione, M., Spaink, H. P., Doglioni, C., Snaar-Jagalska, B. E., Santarosa, M., and Maestro, R.
- Subjects
0301 basic medicine ,In silico ,Triple Negative Breast Neoplasms ,Drug resistance ,Biology ,Article ,03 medical and health sciences ,0302 clinical medicine ,Transcription (biology) ,Cell Line, Tumor ,microRNA ,medicine ,Humans ,Epigenetics ,Molecular Biology ,Lymph node ,Transcription factor ,Triple-negative breast cancer ,Zinc Finger E-box Binding Homeobox 2 ,Correction ,Cell Biology ,Middle Aged ,MicroRNAs ,030104 developmental biology ,medicine.anatomical_structure ,030220 oncology & carcinogenesis ,Cancer research ,Female ,Tumor Suppressor Protein p53 - Abstract
Inactivation of p53 contributes significantly to the dismal prognosis of breast tumors, most notably triple-negative breast cancers (TNBCs). How the relief from p53 tumor suppressive functions results in tumor cell aggressive behavior is only partially elucidated. In an attempt to shed light on the implication of microRNAs in this context, we discovered a new signaling axis involving p53, miR-30a and ZEB2. By an in silico approach we identified miR-30a as a putative p53 target and observed that in breast tumors reduced miR-30a expression correlated with p53 inactivation, lymph node positivity and poor prognosis. We demonstrate that p53 binds the MIR30A promoter and induces the transcription of both miRNA strands 5p and 3p. Both miR-30a-5p and -3p showed the capacity of targeting ZEB2, a transcription factor involved in epithelial-mesenchymal transition (EMT), tumor cell migration and drug resistance. Intriguingly, we found that p53 does restrain ZEB2 expression via miR-30a. Finally, we provide evidence that the new p53/miR-30a/ZEB2 axis controls tumor cell invasion and distal spreading and impinges upon miR-200c expression. Overall, this study highlights the existence of a novel axis linking p53 to EMT via miR-30a, and adds support to the notion that miRNAs represent key elements of the complex network whereby p53 inactivation affects TNBC clinical behavior.
- Published
- 2018
17. Dendritic targeting of mRNAs for plasticity genes in experimental models of temporal lobe epilepsy
- Author
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Gianni Bregola, Enrico Tongiorgi, P. Del Piccolo, Michele Simonato, Donata Rodi, Silvia Zucchini, M. Armellin, Simonato, M, Bregola, G, Armellin, M, DEL PICCOLO, P, Rodi, D, Zucchini, S, and Tongiorgi, Enrico
- Subjects
Male ,Convulsants ,Tropomyosin receptor kinase B ,Hippocampal formation ,Biology ,Epileptogenesis ,Rats, Sprague-Dawley ,Reference Values ,Seizures ,Neurotrophic factors ,Ca2+/calmodulin-dependent protein kinase ,Kindling, Neurologic ,Animals ,Protein Isoforms ,Receptor, trkB ,RNA, Messenger ,Brain-derived neurotrophic factor ,Neuronal Plasticity ,Brain-Derived Neurotrophic Factor ,musculoskeletal, neural, and ocular physiology ,Dentate gyrus ,Pilocarpine ,Dendrites ,Rats ,Disease Models, Animal ,Epilepsy, Temporal Lobe ,nervous system ,Neurology ,Calcium-Calmodulin-Dependent Protein Kinases ,Gene Targeting ,biology.protein ,Neurology (clinical) ,Calcium-Calmodulin-Dependent Protein Kinase Type 2 ,Neuroscience ,Subcellular Fractions ,Neurotrophin - Abstract
Summary: Purpose: To analyze whether the subcellular localization of the messenger RNAs (mRNAs) coding for the neurotrophin brain-derived neurotrophic factor (BDNF), its receptor TrkB, and the α and β subunits of calcium-calmodulin–dependent kinase II (CaMKII) are modified after pilocarpine and kindled seizures. Methods: Epilepsy models: pilocarpine and kindling. Analysis of mRNA levels in the dendrites: high-resolution, nonradioactive in situ hybridization. Results: Nonstimulated rats: BDNF, TrkB, and CaMKII-β mRNAs localized in the soma and in the proximal dendrites of hippocampal pyramidal cells, and in the soma only of dentate gyrus (DG) granule cells; CaMKII-α mRNA localized throughout the dendritic length in neurons of all hippocampal subfields. Pilocarpine seizures: increased staining levels of CaMKII-α mRNA throughout the whole dendritic length in all hippocampal subfields; induction of CaMKII-β, BDNF, and TrkB mRNAs dendritic targeting in CA1, CA3, and DG neurons. Class 2 kindled seizures: increase in dendritic staining intensity for CaMKII-α in CA1, CA3, and DG neurons; induction of dendritic localization of CaMKII-β, BDNF, and TrkB mRNAs in CA3 neurons. Fully kindled seizures: no change in the subcellular distribution of BDNF, TrkB and CaMKII-β mRNAs; reduction of CaMKII-α mRNA dendritic staining, as compared with unstimulated kindled animals. Conclusions: Data provide evidence that BDNF, TrkB, and CaMKII-α and -β mRNAs are accumulated in the dendrites of specific hippocampal neurons during pilocarpine seizures and kindling development. The dendritic targeting of these genes may be causally involved in epileptogenesis and thus may represent a new therapeutic target for some forms of partial epilepsy.
- Published
- 2002
18. Differential somato-dendritic localization of TrkA, TrkB, TrkC and p75 mRNAs in vivo
- Author
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Enrico Tongiorgi, M. Armellin, Antonino Cattaneo, Tongiorgi, Enrico, Armellin, M, Cattaneo, A., Tongiorgi, E, and Cattaneo, Antonino
- Subjects
Male ,animal structures ,Tropomyosin receptor kinase B ,Biology ,Tropomyosin receptor kinase A ,Globus Pallidus ,Receptor, Nerve Growth Factor ,Tropomyosin receptor kinase C ,Prosencephalon ,Animals ,Receptor, trkB ,Low-affinity nerve growth factor receptor ,Receptor, trkC ,RNA, Messenger ,Rats, Wistar ,Receptor, trkA ,In Situ Hybridization ,Basal forebrain ,General Neuroscience ,Dendrites ,Cell Compartmentation ,Rats ,Cell biology ,Somatodendritic compartment ,nervous system ,Forebrain ,biology.protein ,Septal Nuclei ,Neuroscience ,Neurotrophin - Abstract
TrkB mRNA was shown to be localized in the somatodendritic compartment in vitro but no data are currently available on the subcellular distribution of the neurotrophin receptors mRNAs in vivo. Here we describe the subcellular distribution of TrkA, TrkB, TrkC and p75 mRNAs in the adult rat basal forebrain. We find that TrkA, TrkC and p75 mRNAs are restricted to the cell soma but in addition, p75 mRNA labelling extends in average for 8 microm within the proximal dendrites of 34% of the labelled neurons. TrkB mRNA has a somatodendritic distribution in 95% of the labelled neurons reaching variable distances in different neurons (23-84.5 microm) and forebrain regions (mean: 40, 51 and 55 microm for diagonal band, septum and ventral pallidum).
19. Effectiveness of rehabilitation intervention in persons with Friedreich ataxia.
- Author
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Paparella G, Stragà C, Vavla M, Pesenti N, Merotto V, Martorel GA, Zalunardo S, Armellin M, Comiotto J, and Martinuzzi A
- Abstract
Introduction: The relevance of rehabilitation in progressive neurological disorders, such as Friedreich's Ataxia (FRDA), has yet to be convincingly proven. FRDA is characterized by ataxia, loss of gait, scoliosis, cardiomyopathy, dysarthria and dysphagia, with reduced life expectancy. The disease onset is usually in adolescence, leading to progressive disability. Omaveloxolone has been recently approved as the first pharmacological treatment for FRDA in adults and adolescents aged 16 years and older. Regarding non-pharmacological therapies, neurorehabilitation is a valuable aid in addressing the symptoms and in maintaining the residual functioning. We performed a prospective observational cohort study to evaluate the efficacy of inpatient rehabilitation (IR) for people with FRDA., Methods: A total of 42 individuals (29 adults and 13 children) with FRDA were recruited. There were 27 ambulant and 15 non-ambulant participants. The patients underwent IR of 3 and 4 weeks in children and adults, respectively. The IR treatment was designed to be applied within a multidisciplinary setting, so FRDA patients underwent, in addition to physiotherapy, also occupational therapy, practical manual activities and psychological support aiming to enhance transferable skills useful in the activities of daily living. The primary outcome was the Scale for the Assessment and Rating of Ataxia (SARA). Other measures were: Friedreich Ataxia Rating Scale (FARS) and Nine Hole Peg Test (NHPT). Furthermore, we used the 6 Minute Walk Test (6MWT), the Timed Up and Go (TUG) and the Berg Balance Scale (BBS) only on ambulant subjects. Outcomes were evaluated at baseline and at the end of the treatment., Results: We report that the IR significantly improves motor performance and ataxia symptoms in patients with FRDA. Our study shows significant functional improvement in all the outcome measures used, except for NHPT bilaterally. FARS and SARA scores post-IR are significatively reduced when compared ( p < 0.001)., Discussion: We demonstrate that IR programs in FRDA can provide a meaningful clinical improvement in terms of outcome measures. These findings could be useful when approaching progressive neurological disorders., Competing Interests: NP collaborates with Revelo Datalabs Srl. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision., (Copyright © 2023 Paparella, Stragà, Vavla, Pesenti, Merotto, Martorel, Zalunardo, Armellin, Comiotto and Martinuzzi.)
- Published
- 2023
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- View/download PDF
20. Optimization of Anthocyanin Production in Tobacco Cells.
- Author
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Carpi A, Rahim MA, Marin A, Armellin M, Brun P, Miotto G, Dal Monte R, and Trainotti L
- Subjects
- Antioxidants pharmacology, Chlorogenic Acid pharmacology, Plant Cells, Flavonols, Nicotiana genetics, Anthocyanins
- Abstract
Plant cell cultures have emerged as a promising tool for producing active molecules due to their numerous advantages over traditional agricultural methods. Flavonols, and anthocyanin pigments in particular, together with other phenolic compounds such as chlorogenic acid, are known for their beneficial health properties, mainly due to their antioxidant, antimicrobial, and anti-inflammatory activities. The synthesis of these molecules is finely regulated in plant cells and controlled at the transcriptional level by specific MYB and bHLH transcription factors that coordinate the transcription of structural biosynthetic genes. The co-expression of peach PpMYB10.1 and PpbHLH3 in tobacco was used to develop tobacco cell lines showing high expression of both the peach transgenes and the native flavonol structural genes. These cell lines were further selected for fast growth. High production levels of chlorogenic acid, anthocyanins (mainly cyanidin 3-rutinoside), and other phenolics were also achieved in pre-industrial scale-up trials. A single-column-based purification protocol was developed to produce a lyophile called ANT-CA, which was stable over time, showed beneficial effects on cell viability, and had antioxidant, anti-inflammatory, antibacterial, and wound-healing activities. This lyophile could be a valuable ingredient for food or cosmetic applications.
- Published
- 2023
- Full Text
- View/download PDF
21. In Silico Identification of a BRCA1:miR-29:DNMT3 Axis Involved in the Control of Hormone Receptors in BRCA1-Associated Breast Cancers.
- Author
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Santarosa M, Baldazzi D, Armellin M, and Maestro R
- Subjects
- Humans, Genes, BRCA1, DNA Methylation, Receptors, Progesterone genetics, Receptors, Progesterone metabolism, DNA metabolism, Gene Expression Regulation, Neoplastic, MicroRNAs genetics, MicroRNAs metabolism, Neoplasms genetics, Triple Negative Breast Neoplasms pathology
- Abstract
Germline inactivating mutations in the BRCA1 gene lead to an increased lifetime risk of ovarian and breast cancer (BC). Most BRCA1-associated BC are triple-negative tumors (TNBC), aggressive forms of BC characterized by a lack of expression of estrogen and progesterone hormone receptors (HR) and HER2. How BRCA1 inactivation may favor the development of such a specific BC phenotype remains to be elucidated. To address this question, we focused on the role of miRNAs and their networks in mediating BRCA1 functions. miRNA, mRNA, and methylation data were retrieved from the BRCA cohort of the TCGA project. The cohort was divided into a discovery set (Hi-TCGA) and a validation set (GA-TCGA) based on the platform used for miRNA analyses. The METABRIC, GSE81002, and GSE59248 studies were used as additional validation data sets. BCs were differentiated into BRCA1-like and non-BRCA1-like based on an established signature of BRCA1 pathway inactivation. Differential expression of miRNAs, gene enrichment analysis, functional annotation, and methylation correlation analyses were performed. The miRNAs downregulated in BRCA1-associated BC were identified by comparing the miRNome of BRCA1-like with non-BRCA1-like tumors from the Hi-TCGA discovery cohort. miRNAs:gene-target anticorrelation analyses were then performed. The target genes of miRNAs downregulated in the Hi-TCGA series were enriched in the BRCA1-like tumors from the GA-TCGA and METABRIC validation data sets. Functional annotation of these genes revealed an over-representation of several biological processes ascribable to BRCA1 activity. The enrichment of genes related to DNA methylation was particularly intriguing, as this is an aspect of BRCA1 functions that has been poorly explored. We then focused on the miR-29:DNA methyltransferase network and showed that the miR-29 family, which was downregulated in BRCA1-like tumors, was associated with poor prognosis in these BCs and inversely correlated with the expression of the DNA methyltransferases DNMT3A and DNMT3B. This, in turn, correlated with the methylation extent of the promoter of HR genes. These results suggest that BRCA1 may control the expression of HR via a miR-29:DNMT3:HR axis and that disruption of this network may contribute to the receptor negative phenotype of tumors with dysfunctional BRCA1.
- Published
- 2023
- Full Text
- View/download PDF
22. Efficacy of Trichoderma longibrachiatum Trichogin GA IV Peptaibol analogs against the Black Rot Pathogen Xanthomonas campestris pv. campestris and other Phytopathogenic Bacteria.
- Author
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Caracciolo R, Sella L, De Zotti M, Bolzonello A, Armellin M, Trainotti L, Favaron F, and Tundo S
- Abstract
Black rot caused by the Gram-negative bacterial pathogen Xanthomonas campestris pv. campestris (Xcc) is considered one of the most destructive diseases affecting crucifers. Xcc is a seedborne pathogen able to infect the host at any growth stage. The management of the pathogen mainly relies on the use of copper-based products with possible negative effects on human health and the environment. Searching for protection alternatives is crucial for achieving a sustainable management of Xcc. Trichoderma spp. has been largely used as a biocontrol agent against several phytopathogens. Among Trichoderma species, Trichoderma longibrachiatum produces the peptaibol trichogin GA IV, a secondary metabolite with antimicrobial activity against Gram-positive bacteria, as well as filamentous and yeast-like fungi. In this work, we tested, at micromolar concentrations, 25 synthetic analogs of the peptaibol trichogin GA IV for their bacteriostatic and bactericidal activity toward the bacterium Xcc. One of the most effective peptides (4r) was also tested against the Gram-negative bacteria Xanthomonas arboricola , Pseudomonas corrugata , Pseudomonas savastanoi pv. savastanoi , Agrobacterium tumefaciens , Ralstonia solanacearum , and Erwinia carotovora subsp. carotovora , as well as the Gram-positive bacterium Bacillus subtilis . The peptide 4r reduced black rot symptoms on cauliflower plants when administered both before and 24 h after inoculation with Xcc. The cytotoxic activity of the peptide 4r was also evaluated towards suspensions of tobacco cells by Evans Blue assay.
- Published
- 2023
- Full Text
- View/download PDF
23. Interference of p53:Twist1 interaction through competing nanobodies.
- Author
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D'Agostino S, Mazzega E, Praček K, Piccinin S, Pivetta F, Armellin M, Fortuna S, Maestro R, and de Marco A
- Subjects
- Binding, Competitive, Cell Line, Epitopes chemistry, Epitopes immunology, Humans, Models, Molecular, Protein Binding, Protein Conformation, Protein Interaction Domains and Motifs, Recombinant Proteins, Structure-Activity Relationship, Tumor Suppressor Protein p53 metabolism, Twist-Related Protein 1 metabolism, Single-Domain Antibodies chemistry, Tumor Suppressor Protein p53 chemistry, Twist-Related Protein 1 chemistry
- Abstract
Twist1 promote the bypass of p53 response by interacting with p53 and facilitating its MDM2-mediated degradation. We reasoned that reagents able to interfere with the p53:Twist1 complex might alleviate Twist1 inhibitory effect over p53, thus representing potential therapeutic tools in p53 wild type tumors. From a pre-immune library of llama nanobodies (VHH), we isolated binders targeting the p53 C-terminal region (p53-CTD) involved in the interaction with Twist1 by using recombinant Twist1 as an epitope-specific competitor during elution. Positive hits were validated by proving their capacity to immunoprecipitate p53 and to inhibit Twist1:p53 binding in vitro. Molecular modeling confirmed a preferential docking of positive hits with p53-CTD. D11 VHH activity was validated in human cell models, succeeded in immunoprecipitating endogenous p53 and, similarly to Twist1 knock-down, interfered with p53 turnover, p53 phosphorylation at Serine 392 and affected cell viability. Despite the limited functional effect determined by D11 expression in target cells, our results provide the proof of principle that nanobodies ectopically expressed within a cell, have the capacity to target the assembly of the pro-tumorigenic Twist1:p53 complex. These results disclose novel tools for dissecting p53 biology and lay down the grounds for the development of innovative targeted therapeutic approaches., (Copyright © 2021 Elsevier B.V. All rights reserved.)
- Published
- 2022
- Full Text
- View/download PDF
24. Correction to: A p53/miR-30a/ZEB2 axis controls triple negative breast cancer aggressiveness.
- Author
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di Gennaro A, Damiano V, Brisotto G, Armellin M, Perin T, Zucchetto A, Guardascione M, Spaink HP, Doglioni C, Snaar-Jagalska BE, Santarosa M, and Maestro R
- Abstract
Since publication of the article, the authors were notified by ATCC that the cell line HCC1395 (ATCC® CRL-2324™ Lot 62235652) suffered a "low level of cell line cross-contamination" with another cell line.
- Published
- 2019
- Full Text
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25. A p53/miR-30a/ZEB2 axis controls triple negative breast cancer aggressiveness.
- Author
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di Gennaro A, Damiano V, Brisotto G, Armellin M, Perin T, Zucchetto A, Guardascione M, Spaink HP, Doglioni C, Snaar-Jagalska BE, Santarosa M, and Maestro R
- Subjects
- Cell Line, Tumor, Female, Humans, Middle Aged, MicroRNAs metabolism, Triple Negative Breast Neoplasms metabolism, Triple Negative Breast Neoplasms pathology, Tumor Suppressor Protein p53 metabolism, Zinc Finger E-box Binding Homeobox 2 metabolism
- Abstract
Inactivation of p53 contributes significantly to the dismal prognosis of breast tumors, most notably triple-negative breast cancers (TNBCs). How the relief from p53 tumor suppressive functions results in tumor cell aggressive behavior is only partially elucidated. In an attempt to shed light on the implication of microRNAs in this context, we discovered a new signaling axis involving p53, miR-30a and ZEB2. By an in silico approach we identified miR-30a as a putative p53 target and observed that in breast tumors reduced miR-30a expression correlated with p53 inactivation, lymph node positivity and poor prognosis. We demonstrate that p53 binds the MIR30A promoter and induces the transcription of both miRNA strands 5p and 3p. Both miR-30a-5p and -3p showed the capacity of targeting ZEB2, a transcription factor involved in epithelial-mesenchymal transition (EMT), tumor cell migration and drug resistance. Intriguingly, we found that p53 does restrain ZEB2 expression via miR-30a. Finally, we provide evidence that the new p53/miR-30a/ZEB2 axis controls tumor cell invasion and distal spreading and impinges upon miR-200c expression. Overall, this study highlights the existence of a novel axis linking p53 to EMT via miR-30a, and adds support to the notion that miRNAs represent key elements of the complex network whereby p53 inactivation affects TNBC clinical behavior.
- Published
- 2018
- Full Text
- View/download PDF
26. Epigenetic silencing of miR-200c in breast cancer is associated with aggressiveness and is modulated by ZEB1.
- Author
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Damiano V, Brisotto G, Borgna S, di Gennaro A, Armellin M, Perin T, Guardascione M, Maestro R, and Santarosa M
- Subjects
- Apoptosis, Blotting, Western, Cell Movement, Cell Proliferation, Combined Modality Therapy, DNA Methylation, Epithelial-Mesenchymal Transition, Female, Follow-Up Studies, Humans, Immunoenzyme Techniques, Lymphatic Metastasis, Middle Aged, Neoplasm Grading, Neoplasm Invasiveness, Neoplasm Staging, Prognosis, RNA, Messenger genetics, Real-Time Polymerase Chain Reaction, Retrospective Studies, Reverse Transcriptase Polymerase Chain Reaction, Survival Rate, Triple Negative Breast Neoplasms pathology, Triple Negative Breast Neoplasms therapy, Tumor Cells, Cultured, Zinc Finger E-box-Binding Homeobox 1 genetics, Biomarkers, Tumor genetics, Epigenesis, Genetic genetics, Gene Expression Regulation, Neoplastic, Gene Silencing, MicroRNAs genetics, Triple Negative Breast Neoplasms genetics, Zinc Finger E-box-Binding Homeobox 1 metabolism
- Abstract
Loss of expression of miR-200 family members has been implicated in cellular plasticity, a phenomenon that accounts for epithelial-to-mesenchymal transition (EMT) and stem-like features of many carcinomas and is considered a major cause of tumor aggressiveness and drug resistance. Nevertheless, the mechanisms of miR-200 downregulation in breast cancer are still largely unknown. Here we show that miR-200c expression inversely correlates with miR-200c/miR-141 locus methylation in triple-negative breast tumors (TNBC). Importantly, low levels of miR-200c expression and high levels of miR-200c/miR-141 locus methylation associated with lymph node metastasis. Moreover, miR-200c/miR-141 locus methylation was significantly related to high expression of ZEB1 in two independent TNBC series. Silencing of ZEB1 in vitro reduced miR-200c/miR-141 DNA methylation and, concurrently, decreased histone H3K9 trimethylation. This chromatin modifications were paralleled by an increase in the expression of both miR-200c and E-cadherin. Similar effects were achieved by treatment with a demethylating agent. Our data suggest that gene methylation is an important element in the regulation of the miR-200c/ZEB1 axis and that chromatin remodeling of the miR-200c/miR-141 locus is affected by ZEB1 and, thus, contributes to ZEB1-induced cellular plasticity. © 2016 Wiley Periodicals, Inc., (© 2016 Wiley Periodicals, Inc.)
- Published
- 2017
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27. An improved sequencing-based strategy to estimate locus-specific DNA methylation.
- Author
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Brisotto G, di Gennaro A, Damiano V, Armellin M, Perin T, Maestro R, and Santarosa M
- Subjects
- Breast Neoplasms genetics, Cell Line, Tumor, Female, Humans, MicroRNAs genetics, Promoter Regions, Genetic, DNA Methylation, Genetic Loci, Sequence Analysis, DNA methods
- Abstract
Background: DNA methylation is an important epigenetic mechanism of transcriptional control that plays an essential role in several cellular functions. Aberrant DNA methylation in cancer has been frequently associated with downregulation of microRNAs and protein coding genes, such as miR-200c/miR-141 cluster and E-cadherin. Current strategies to assess DNA methylation, including bisulfite treatment-based assays, tend to be time-consuming and may be quite expensive when a precise appraisal is required. The Sanger-sequencing of the amplified bisulfite-treated DNA (BSP) might represent a practical option to measure DNA methylation at single CpG resolution. However, this strategy often produces noisy data, which affects accurate quantification. Here we propose an improved, reliable and cost-effective BSP-based protocol that allows proper DNA methylation assessment., Methods: Our strategy, named normalized-BSP (NBSP), takes advantage of tailed C-balanced primers and a normalization procedure based on C/T ratio to overcome BSP-associated noise problems and nucleotide signal unbalance. NBSP was applied to estimate miR-200c/miR-141 locus methylation in serial dilution experiments and was compared to conventional methods. Besides, it was applied in the analysis of FFPE breast cancer samples and further validated in the context of the E-cadherin promoter., Results: NBSP strategy outperformed conventional BSP in the estimate of the fraction of methylated cytosine in serial dilution experiments, providing data in agreement with the widely used but cumbersome cloning-based protocol. This held true for both miR-200c/miR-141 locus and E-cadherin promoter analyses. Moreover, the miR-200c/miR-141 locus methylation reflected the decrease in miRNA expression both in breast cancer cell lines and in the FFPE samples., Conclusions: NBSP is a rapid and economical method to estimate the extent of methylation at each CpG of a given locus. Notably, NBSP works efficiently on FFPE samples, thus disclosing the perspective of its application also in the diagnostic setting.
- Published
- 2015
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28. Mesenchymal traits are selected along with stem features in breast cancer cells grown as mammospheres.
- Author
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Borgna S, Armellin M, di Gennaro A, Maestro R, and Santarosa M
- Subjects
- Aldehyde Dehydrogenase 1 Family, Biomarkers, Tumor metabolism, Breast Neoplasms metabolism, Breast Neoplasms pathology, Cadherins metabolism, Cell Line, Tumor, Epithelial-Mesenchymal Transition, Female, Gene Expression Regulation, Neoplastic, Humans, Isoenzymes metabolism, MCF-7 Cells, Phenotype, Receptor, ErbB-2 metabolism, Retinal Dehydrogenase metabolism, Vimentin metabolism, Mesenchymal Stem Cells metabolism, Neoplastic Stem Cells metabolism
- Abstract
Increasing evidence indicates that invasive properties of breast cancers rely on gain of mesenchymal and stem features, which has suggested that the dual targeting of these phenotypes may represent an appealing therapeutic strategy. It is known that the fraction of stem cells can be enriched by culturing breast cancer cells as mammospheres (MS), but whether these pro-stem conditions favor also the expansion of cells provided of mesenchymal features is still undefined. In the attempt to shed light on this issue, we compared the phenotypes of a panel of 10 breast cancer cell lines representative of distinct subtypes (luminal, HER2-positive, basal-like and claudin-low), grown in adherent conditions and as mammospheres. Under MS-proficient conditions, the increment in the fraction of stem-like cells was associated to upregulation of the mesenchymal marker Vimentin and downregulation of the epithelial markers expressed by luminal cells (E-cadherin, KRT18, KRT19, ESR1). Luminal cells tended also to upregulate the myoepithelial marker CD10. Taken together, our data indicate that MS-proficient conditions do favor mesenchymal/myoepithelial features, and indicate that the use of mammospheres as an in vitro tumor model may efficiently allow the exploitation of therapeutic approaches aimed at targeting aggressive tumors that have undergone epithelial-to-mesenchymal transition
- Published
- 2012
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29. Brain-derived neurotrophic factor mRNA and protein are targeted to discrete dendritic laminas by events that trigger epileptogenesis.
- Author
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Tongiorgi E, Armellin M, Giulianini PG, Bregola G, Zucchini S, Paradiso B, Steward O, Cattaneo A, and Simonato M
- Subjects
- Animals, Biological Transport, Brain-Derived Neurotrophic Factor genetics, Cell Compartmentation, Convulsants toxicity, Dendrites ultrastructure, Dizocilpine Maleate pharmacology, Electroshock, Epilepsy chemically induced, Epilepsy prevention & control, Hippocampus metabolism, Hippocampus pathology, Kainic Acid toxicity, Kindling, Neurologic, Male, Pilocarpine toxicity, Protein Transport, Rats, Rats, Sprague-Dawley, Receptors, N-Methyl-D-Aspartate antagonists & inhibitors, Receptors, N-Methyl-D-Aspartate physiology, Seizures chemically induced, Seizures metabolism, Seizures prevention & control, Status Epilepticus chemically induced, Status Epilepticus metabolism, Status Epilepticus pathology, Synapses physiology, Brain-Derived Neurotrophic Factor metabolism, Dendrites metabolism, Epilepsy metabolism, Hippocampus cytology, RNA, Messenger metabolism
- Abstract
Dendritic targeting of mRNA and local protein synthesis are mechanisms that enable neurons to deliver proteins to specific postsynaptic sites. Here, we demonstrate that epileptogenic stimuli induce a dramatic accumulation of BDNF mRNA and protein in the dendrites of hippocampal neurons in vivo. BDNF mRNA and protein accumulate in dendrites in all hippocampal subfields after pilocarpine seizures and in selected subfields after other epileptogenic stimuli (kainate and kindling). BDNF accumulates selectively in discrete dendritic laminas, suggesting targeting to synapses that are active during seizures. Dendritic targeting of BDNF mRNA occurs during the time when the cellular changes that underlie epilepsy are occurring and is not seen after intense stimuli that are non-epileptogenic, including electroconvulsive seizures and high-frequency stimulation. MK801, an NMDA receptor antagonist that can prevent epileptogenesis but not acute seizures, prevents the dendritic accumulation of BDNF mRNA, indicating that dendritic targeting is mediated via NMDA receptor activation. Together, these results suggest that dendritic accumulation of BDNF mRNA and protein plays a critical role in the cellular changes leading to epilepsy.
- Published
- 2004
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30. Alterations of beta-catenin pathway in non-melanoma skin tumors: loss of alpha-ABC nuclear reactivity correlates with the presence of beta-catenin gene mutation.
- Author
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Doglioni C, Piccinin S, Demontis S, Cangi MG, Pecciarini L, Chiarelli C, Armellin M, Vukosavljevic T, Boiocchi M, and Maestro R
- Subjects
- Antibodies, Monoclonal, Axin Protein, Cytoskeletal Proteins immunology, DNA Mutational Analysis, Genes, APC, Humans, Immunohistochemistry, Skin metabolism, Trans-Activators immunology, beta Catenin, Cell Nucleus metabolism, Cytoskeletal Proteins genetics, Cytoskeletal Proteins metabolism, Mutation, Skin Neoplasms metabolism, Trans-Activators genetics, Trans-Activators metabolism
- Abstract
To determine the role of beta-catenin pathway in human skin carcinogenesis, 135 non-melanoma skin tumors were analyzed for beta-catenin expression and gene mutations. Intense nucleo-cytoplasmic immunoreactivity for C terminus beta-catenin antibodies was observed in all pilomatricomas and in single cases of trichoepithelioma and squamous cell carcinoma showing peculiar signs of matrical differentiation. Moderate increase of beta-catenin nuclear staining was detected in a significant proportion of basal cell carcinomas, Bowen disease, spiroadenomas, and occasionally also in squamous cell carcinomas, but in these neoplasms only a limited fraction of tumor cells accumulated beta-catenin. Molecular analysis revealed that beta-catenin gene mutations are a peculiar feature of skin tumors with matrical differentiation and correlate with a pattern of intense and diffuse beta-catenin nuclear expression. In contrast, adenomatous polyposis coli (APC) and AXIN2 mutations were not involved in skin tumorigenesis. Analysis of Wnt pathway revealed that TCF-1 and MITF-M were selectively induced in the tumor types harboring beta-catenin mutations, indicating that a Wnt/beta-catenin pathway involving TCF-1 and MITF-M is activated in these tumors. Interestingly, high expression levels of TCF-3 were found in basal cell carcinomas and spiroadenomas. TCF-3 is reported to act as a negative modulator of beta-catenin degradation pathway. Thus, the moderate increase of beta-catenin nuclear staining detected in these tumor types might, at least in part, be due to a TCF-3-dependent mechanism. Finally, we found that the presence of beta-catenin mutations significantly correlated with loss of nuclear immunoreactivity for an antibody raised against the N terminus of beta-catenin (alphaABC). Thus, a combined analysis with C terminus-beta-catenin antibodies and alphaABC Ab may represent a powerful investigative approach for the detection of beta-catenin structural alterations.
- Published
- 2003
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31. Expression and dendritic mRNA localization of GABAC receptor rho1 and rho2 subunits in developing rat brain and spinal cord.
- Author
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Rozzo A, Armellin M, Franzot J, Chiaruttini C, Nistri A, and Tongiorgi E
- Subjects
- Aging metabolism, Animals, Animals, Newborn, Brain cytology, Brain metabolism, Dendrites ultrastructure, GABA Antagonists pharmacology, Hippocampus cytology, Hippocampus growth & development, Hippocampus metabolism, Immunohistochemistry, Membrane Potentials drug effects, Membrane Potentials physiology, Motor Neurons drug effects, Motor Neurons metabolism, Rats, Rats, Wistar, Receptors, GABA metabolism, Sodium Channel Blockers pharmacology, Spinal Cord cytology, Spinal Cord metabolism, Synaptic Transmission physiology, gamma-Aminobutyric Acid pharmacology, Brain growth & development, Dendrites metabolism, Gene Expression Regulation, Developmental physiology, Neural Inhibition physiology, RNA, Messenger metabolism, Receptors, GABA genetics, Spinal Cord growth & development, gamma-Aminobutyric Acid metabolism
- Abstract
The cellular distribution of GABAC receptor rho1 and rho2 subunits in the rat central nervous system remains controversial. We investigated how these subunits were distributed in cerebellum, hippocampus and spinal cord at postnatal day 1, 7 or in adult life. We found that in the adult cerebellum rho1 and rho2 mRNAs were expressed in Purkinje cells and basket-like cells only. In the hippocampus both subunits were expressed throughout the CA1 pyramidal layer, dentate gyrus and scattered interneurons with maximum staining intensity at P7. In the adult hippocampus in situ staining was predominantly found on interneurons. GABAC antibody labelling in P7 and adult hippocampus was largely overlapping with the in situ staining. Western blot analysis showed GABAC receptor in retina, ovary and testis. In the spinal cord the rho2 signal was consistently stronger than rho1 with overlapping expression patterns. At P1, the most intensely labelled cells were the motoneurons while on P7 and adult sections, interneurons and motoneurons were likewise labelled. On spinal neurons both rho1 and rho2 mRNAs showed somatodendritic localization, extending out for >100 microm with punctate appearance especially in adult cells. A similar spinal distribution pattern was provided with polyclonal antibody labelling, suggesting close correspondence between mRNA and protein compartmentalization. Electrophysiological experiments indicated that P1 spinal motoneurons did possess functional GABAC receptors even though GABAC receptors played little role in evoked synaptic transmission. Our results suggest a pattern of rho1 and rho2 subunit distribution more widespread than hitherto suspected with strong developmental regulation of subunit occurrence.
- Published
- 2002
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32. Loss of heterozygosity at 10q in tumors of the upper respiratory tract is associated with poor prognosis.
- Author
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Gasparotto D, Vukosavljevic T, Piccinin S, Barzan L, Sulfaro S, Armellin M, Boiocchi M, and Maestro R
- Subjects
- Blotting, Southern methods, Carcinoma, Squamous Cell mortality, Carcinoma, Squamous Cell pathology, Carcinoma, Squamous Cell surgery, Chromosome Mapping, Genetic Markers, Head and Neck Neoplasms mortality, Head and Neck Neoplasms pathology, Head and Neck Neoplasms surgery, Humans, Mucous Membrane pathology, Polymerase Chain Reaction methods, Predictive Value of Tests, Prognosis, Respiratory Tract Neoplasms mortality, Respiratory Tract Neoplasms pathology, Respiratory Tract Neoplasms surgery, Survival Analysis, Time Factors, Carcinoma, Squamous Cell genetics, Chromosomes, Human, Pair 10, Head and Neck Neoplasms genetics, Loss of Heterozygosity, Polymorphism, Single-Stranded Conformational, Respiratory Tract Neoplasms genetics
- Abstract
Frequent loss of a specific chromosomic region in cancers is often associated with inactivation of a tumor-suppressor gene. The long arm of chromosome 10 is deleted in several types of tumor, among them squamous-cell carcinomas of the head and neck (HNSCC). To determine the role of 10q deletions in the tumorigenesis of the upper respiratory tract, 47 HNSCCs were examined for loss of heterozygosity (LOH) at 10q: 43% of the cases analyzed showed LOH at 10q, and 2 distinct hot spots of deletion were identified, at 10q22-23 and 10q25-26. The possible involvement of pTEN/MMAC1, a tumor-suppressor gene mapped at 10q23, was also evaluated. No mutation, homozygous deletion or loss of expression of pTEN/MMAC1 was detected, indicating that inactivation of this gene plays a minor role in HNSCC development. Interestingly, the frequency of deletion at 10q was greater in invasive carcinoma than in adjacent carcinoma in situ, and a significant association between LOH and poor prognosis was observed. Taken together, our results suggest the presence in the long arm of chromosome 10 of (a) tumor-suppressor gene(s) other than pTEN/MMAC1 and presumably involved in the malignant progression of tumors of the upper respiratory tract. Int. J. Cancer (Pred. Oncol.) 84:432-436, 1999., (Copyright 1999 Wiley-Liss, Inc.)
- Published
- 1999
- Full Text
- View/download PDF
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