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41 results on '"Scatolini, Maria"'

1. Non-Small Cell Lung Cancer Testing on Reference Specimens: An Italian Multicenter Experience

Author

Pepe, Francesco, Russo, Gianluca, Venuta, Alessandro, Scimone, Claudia, Nacchio, Mariantonia, Pisapia, Pasquale, Goteri, Gaia, Barbisan, Francesca, Chiappetta, Caterina, Pernazza, Angelina, Campagna, Domenico, Giordano, Marco, Perrone, Giuseppe, Sabarese, Giovanna, Altimari, Annalisa, de Biase, Dario, Tallini, Giovanni, Calistri, Daniele, Chiadini, Elisa, Capelli, Laura, Santinelli, Alfredo, Gulini, Anna Elisa, Pierpaoli, Elisa, Badiali, Manuela, Murru, Stefania, Murgia, Riccardo, Guerini Rocco, Elena, Venetis, Konstantinos, Fusco, Nicola, Morotti, Denise, Gianatti, Andrea, Furlan, Daniela, Rossi, Giulio, Melocchi, Laura, Russo, Maria, De Luca, Caterina, Palumbo, Lucia, Simonelli, Saverio, Maffè, Antonella, Francia di Celle, Paola, Venesio, Tiziana, Scatolini, Maria, Grosso, Enrico, Orecchia, Sara, Fassan, Matteo, Balistreri, Mariangela, Zulato, Elisabetta, Reghellin, Daniela, Lazzari, Elena, Santacatterina, Maria, Piredda, Maria Liliana, Riccardi, Manuela, Laurino, Licia, Roz, Elena, Longo, Domenico, Romeo, Daniela Petronilla, Fazzari, Carmine, Moreno-Manuel, Andrea, Puglia, Giuseppe Diego, Prjibelski, Andrey D., Shafranskaya, Daria, Righi, Luisella, Listì, Angela, Vitale, Domenico, Iaccarino, Antonino, Malapelle, Umberto, and Troncone, Giancarlo

Published
2024
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3. Identification of a minimum number of genes to predict triple-negative breast cancer subgroups from gene expression profiles

Author

Akhouayri, Laila, Ostano, Paola, Mello-Grand, Maurizia, Gregnanin, Ilaria, Crivelli, Francesca, Laurora, Sara, Liscia, Daniele, Leone, Francesco, Santoro, Angela, Mulè, Antonino, Guarino, Donatella, Maggiore, Claudia, Carlino, Angela, Magno, Stefano, Scatolini, Maria, Di Leone, Alba, Masetti, Riccardo, and Chiorino, Giovanna

Published
2022
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6. THU616 Analysis Of Germline Mutations In Patients With Sporadic Adrenocortical Carcinoma

Author

Terzolo, Massimo, primary, Grisanti, Salvatore, additional, Scatolini, Maria, additional, Tomaiuolo, Pasquale, additional, Grosso, Enrico, additional, Basile, Vittoria, additional, Cosentini, Deborah, additional, Puglisi, Soraya, additional, Laganà, Marta, additional, Perotti, Paola, additional, Saba, Laura, additional, Rossini, Elisa, additional, Sigala, Sandra, additional, Volante, Marco, additional, and Berruti, Alfredo, additional

Published
2023
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9. Analysis of germline mutations in patients with non-syndromic adrenocortical carcinoma

Author

Terzolo, Massimo, primary, Grisanti, Salvatore, additional, Scatolini, Maria, additional, Tomaiuolo, Pasquale, additional, Grosso, Enrico, additional, Basile, Vittoria, additional, Cosentini, Deborah, additional, Puglisi, Soraya, additional, Lagana, Marta, additional, Perotti, Paola, additional, Rossini, Elisa, additional, Sigala, Sandra, additional, Volante, Marco, additional, and Berruti, Alfredo, additional

Published
2023
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10. Supplementary Figures S1, S2, S3, S4, S5 from Targeting p63 Upregulation Abrogates Resistance to MAPK Inhibitors in Melanoma

Author

Patel, Ankit, primary, Garcia, Lucia Fraile, primary, Mannella, Viviana, primary, Gammon, Luke, primary, Borg, Tiffanie-Marie, primary, Maffucci, Tania, primary, Scatolini, Maria, primary, Chiorino, Giovanna, primary, Vergani, Elisabetta, primary, Rodolfo, Monica, primary, Maurichi, Andrea, primary, Posch, Christian, primary, Matin, Rubeta N., primary, Harwood, Catherine A., primary, and Bergamaschi, Daniele, primary

Published
2023
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11. Data from Targeting p63 Upregulation Abrogates Resistance to MAPK Inhibitors in Melanoma

Author

Patel, Ankit, primary, Garcia, Lucia Fraile, primary, Mannella, Viviana, primary, Gammon, Luke, primary, Borg, Tiffanie-Marie, primary, Maffucci, Tania, primary, Scatolini, Maria, primary, Chiorino, Giovanna, primary, Vergani, Elisabetta, primary, Rodolfo, Monica, primary, Maurichi, Andrea, primary, Posch, Christian, primary, Matin, Rubeta N., primary, Harwood, Catherine A., primary, and Bergamaschi, Daniele, primary

Published
2023
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14. Ribociclib Cytotoxicity Alone or Combined With Progesterone and/or Mitotane in in Vitro Adrenocortical Carcinoma Cells

Author

Abate, Andrea, primary, Rossini, Elisa, additional, Tamburello, Mariangela, additional, Laganà, Marta, additional, Cosentini, Deborah, additional, Grisanti, Salvatore, additional, Fiorentini, Chiara, additional, Tiberio, Guido A M, additional, Scatolini, Maria, additional, Grosso, Enrico, additional, Hantel, Constanze, additional, Memo, Maurizio, additional, Berruti, Alfredo, additional, and Sigala, Sandra, additional

Published
2021
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15. Thrombospondin-1 is part of a Slug-independent motility and metastatic program in cutaneous melanoma, in association with VEGFR-1 and FGF-2

Author

Borsotti, Patrizia, Ghilardi, Carmen, Ostano, Paola, Silini, Antonietta, Dossi, Romina, Pinessi, Denise, Foglieni, Chiara, Scatolini, Maria, Lacal, Pedro M., Ferrari, Raffaele, Moscatelli, Davide, Sangalli, Fabio, DʼAtri, Stefania, Giavazzi, Raffaella, Bani, Maria Rosa, Chiorino, Giovanna, and Taraboletti, Giulia

Published
2015
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21. Malignant struma ovarii: next-generation sequencing of six cases revealed Nras, Braf, and Jak3 mutations

Author

Poli, Roberta, primary, Scatolini, Maria, additional, Grosso, Enrico, additional, Maletta, Francesca, additional, Gallo, Marco, additional, Liscia, Daniele, additional, Nelva, Anna, additional, Cesario, Flora, additional, Forte, Giuseppe, additional, Metovic, Jasna, additional, Volante, Marco, additional, Arvat, Emanuela, additional, and Papotti, Mauro, additional

Published
2020
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23. Targeting p63 Upregulation Abrogates Resistance to MAPK Inhibitors in Melanoma

Author

Patel, Ankit, primary, Garcia, Lucia Fraile, additional, Mannella, Viviana, additional, Gammon, Luke, additional, Borg, Tiffanie-Marie, additional, Maffucci, Tania, additional, Scatolini, Maria, additional, Chiorino, Giovanna, additional, Vergani, Elisabetta, additional, Rodolfo, Monica, additional, Maurichi, Andrea, additional, Posch, Christian, additional, Matin, Rubeta N., additional, Harwood, Catherine A., additional, and Bergamaschi, Daniele, additional

Published
2020
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25. Ribociclib Cytotoxicity Alone or Combined With Progesterone and/or Mitotane in in Vitro Adrenocortical Carcinoma Cells.

Author

Abate, Andrea, Rossini, Elisa, Tamburello, Mariangela, Laganà, Marta, Cosentini, Deborah, Grisanti, Salvatore, Fiorentini, Chiara, Tiberio, Guido A M, Scatolini, Maria, Grosso, Enrico, Hantel, Constanze, Memo, Maurizio, Berruti, Alfredo, and Sigala, Sandra

Abstract

Mitotane is the only approved drug for treating adrenocortical carcinoma (ACC). The regimen added to mitotane is chemotherapy with etoposide, doxorubicin, and cisplatin. This pharmacological approach, however, has a limited efficacy and significant toxicity. Target-therapy agents represent a new promising approach to cancer therapy. Among these, a preeminent role is played by agents that interfere with cell-cycle progression, such as CDK4/6-inhibitors. Here, we investigate whether ribociclib could induce a cytotoxic effect both in ACC cell line and patient-derived primary cell cultures, alone or in combined settings. Cell viability was determined by 3-(4,5-dimethyl-2-thiazol)-2,5-diphenyl-2H-tetrazolium bromide assay, whereas cell proliferation was evaluated by direct count. Binary combination experiments were performed using Chou and Talalay method. Gene expression was analyzed by quantitative RT-PCR, whereas protein expression was evaluated by immunofluorescence. A double staining assay revealed that ribociclib induced a prevalent apoptotic cell death. Cell-cycle analysis was performed to evaluate the effect of ribociclib treatment on cell-cycle progression in ACC cell models. Our results indicate that ribociclib was cytotoxic and reduced the cell proliferation rate. The effect on cell viability was enhanced when ribociclib was combined with progesterone and/or mitotane. The effect of ribociclib on cell-cycle progression revealed a drug-induced cell accumulation in G2 phase. The positive relationship underlined by our results between ribociclib, progesterone, and mitotane strengthen the clinical potential of this combination. [ABSTRACT FROM AUTHOR]

Published
2022
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26. Assessment of a High Sensitivity Method for Identification of IDH1 R132x Mutations in Tumors and Plasma of Intrahepatic Cholangiocarcinoma Patients

Author

Peraldo-Neia, Caterina, primary, Scatolini, Maria, additional, Grosso, Enrico, additional, Lombardi, Pasquale, additional, Filippi, Roberto, additional, Raggi, Chiara, additional, Marchiò, Caterina, additional, Cavalloni, Giuliana, additional, Aglietta, Massimo, additional, and Leone, Francesco, additional

Published
2019
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27. Truncating mutations of TP53AIP1 gene predispose to cutaneous melanoma

Author

Benfodda, Meriem, primary, Gazal, Steven, additional, Descamps, Vincent, additional, Basset-Seguin, Nicole, additional, Deschamps, Lydia, additional, Thomas, Luc, additional, Lebbe, Celeste, additional, Saiag, Philippe, additional, Zanetti, Roberto, additional, Sacchetto, Lidia, additional, Chiorino, Giovanna, additional, Scatolini, Maria, additional, Grandchamp, Bernard, additional, Bensussan, Armand, additional, and Soufir, Nadem, additional

Published
2018
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30. Thrombospondin‐1 is part of a Slug‐independent motility and metastatic program in cutaneous melanoma, in association with VEGFR‐1 and FGF‐2

Author

Borsotti, Patrizia, primary, Ghilardi, Carmen, additional, Ostano, Paola, additional, Silini, Antonietta, additional, Dossi, Romina, additional, Pinessi, Denise, additional, Foglieni, Chiara, additional, Scatolini, Maria, additional, Lacal, Pedro M., additional, Ferrari, Raffaele, additional, Moscatelli, Davide, additional, Sangalli, Fabio, additional, D'Atri, Stefania, additional, Giavazzi, Raffaella, additional, Bani, Maria Rosa, additional, Chiorino, Giovanna, additional, and Taraboletti, Giulia, additional

Published
2014
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31. p63 is an alternative p53 repressor in melanoma that confers chemoresistance and a poor prognosis

Author

Matin, Rubeta N., primary, Chikh, Anissa, additional, Pak Chong, Stephanie Law, additional, Mesher, David, additional, Graf, Manuela, additional, Sanza, Paolo, additional, Senatore, Valentina, additional, Scatolini, Maria, additional, Moretti, Francesca, additional, Leigh, Irene M., additional, Proby, Charlotte M., additional, Costanzo, Antonio, additional, Chiorino, Giovanna, additional, Cerio, Rino, additional, Harwood, Catherine A., additional, and Bergamaschi, Daniele, additional

Published
2013
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33. Nicotinamide phosphoribosyltransferase (NAMPT) is over-expressed in melanoma lesions

Author

Maldi, Elena, primary, Travelli, Cristina, additional, Caldarelli, Antonio, additional, Agazzone, Nicolò, additional, Cintura, Sara, additional, Galli, Ubaldina, additional, Scatolini, Maria, additional, Ostano, Paola, additional, Miglino, Benedetta, additional, Chiorino, Giovanna, additional, Boldorini, Renzo, additional, and Genazzani, Armando A., additional

Published
2012
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34. Abstract C21: LincRNA expression data analysis identifies prostate tumor subtypes with distinct biological processes

Author

Mello-Grand, Maurizia, primary, Singh, Vijay K., additional, Ghimenti, Chiara, additional, Scatolini, Maria, additional, Longoni, Nicole, additional, Curti, Laura, additional, Zitella, Andrea, additional, Gontero, Paolo, additional, Catapano, Carlo V., additional, Carbone, Giuseppina M., additional, and Chiorino, Giovanna, additional

Published
2012
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35. Altered molecular pathways in melanocytic lesions

Author

Scatolini, Maria, primary, Grand, Maurizia Mello, additional, Grosso, Enrico, additional, Venesio, Tiziana, additional, Pisacane, Alberto, additional, Balsamo, Antonella, additional, Sirovich, Roberta, additional, Risio, Mauro, additional, and Chiorino, Giovanna, additional

Published
2009
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36. The epithelial–mesenchymal transition induced by keratinocyte growth conditions is overcome by E6 and E7 from HPV16, but not HPV8 and HPV38: Characterization of global transcription profiles

Author

Azzimonti, Barbara, primary, Dell'Oste, Valentina, additional, Borgogna, Cinzia, additional, Mondini, Michele, additional, Gugliesi, Francesca, additional, De Andrea, Marco, additional, Chiorino, Giovanna, additional, Scatolini, Maria, additional, Ghimenti, Chiara, additional, Landolfo, Santo, additional, and Gariglio, Marisa, additional

Published
2009
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39. p63 is an alternative p53 repressor in melanoma that confers chemoresistance and a poor prognosis

Author

Matin, Rubeta N., Chikh, Anissa, Law Pak Chong, Stephanie, Mesher, David, Graf, Manuela, Sanza’, Paolo, Senatore, Valentina, Scatolini, Maria, Moretti, Francesca, Leigh, Irene M., Proby, Charlotte M., Costanzo, Antonio, Chiorino, Giovanna, Cerio, Rino, Harwood, Catherine A., and Bergamaschi, Daniele

Abstract

The role of apoptosis in melanoma pathogenesis and chemoresistance is poorly characterized. Mutations in TP53 occur infrequently, yet the TP53 apoptotic pathway is often abrogated. This may result from alterations in TP53 family members, including the TP53 homologue TP63. Here we demonstrate that TP63 has an antiapoptotic role in melanoma and is responsible for mediating chemoresistance. Although p63 was not expressed in primary melanocytes, up-regulation of p63 mRNA and protein was observed in melanoma cell lines and clinical samples, providing the first evidence of significant p63 expression in this lineage. Upon genotoxic stress, endogenous p63 isoforms were stabilized in both nuclear and mitochondrial subcellular compartments. Our data provide evidence of a physiological interaction between p63 with p53 whereby translocation of p63 to the mitochondria occurred through a codependent process with p53, whereas accumulation of p53 in the nucleus was prevented by p63. Using RNA interference technology, both isoforms of p63 (TA and ΔNp63) were demonstrated to confer chemoresistance, revealing a novel oncogenic role for p63 in melanoma cells. Furthermore, expression of p63 in both primary and metastatic melanoma clinical samples significantly correlated with melanoma-specific deaths in these patients. Ultimately, these observations provide a possible explanation for abrogation of the p53-mediated apoptotic pathway in melanoma, implicating novel approaches aimed at sensitizing melanoma to therapeutic agents.

Published
2013
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40. In melanocytic lesions the fraction of BRAFV600Ealleles is associated with sun exposure but unrelated to ERK phosphorylation

Author

Venesio, Tiziana, Chiorino, Giovanna, Balsamo, Antonella, Zaccagna, Alessandro, Petti, Consalvo, Scatolini, Maria, Pisacane, Alberto, Sarotto, Ivana, Picciotto, Franco, and Risio, Mauro

Abstract

BRAFV600Emutation has been frequently reported in different types of melanocytic lesions, but its role in melanomagenesis is poorly understood, having been associated with either the proliferative-induced MAPK pathway activation or the acquisition of oncogene-driven senescence. The presence of BRAF alterations has been related to sun exposure, although the molecular mechanisms underlying this event are only partly known. To elucidate the relationships among BRAF/NRAS alterations, MAPK pathway activation, and sun exposure, we examined 22 acquired nevi and 18 cutaneus melanomas from 38 patients. Microdissected tissues from each lesion were subjected to BRAF/NRAS mutation analysis by sequencing, allele-specific PCR and pyrosequencing assay. The same lesions were also examined for the expression of phosphorylated ERK1/2. Phototype and an accurate history of sun exposure were evaluated for each patient. BRAFV600Emutation was detected in 50% of the acquired nevi and in 70% of the cutaneus melanomas in the absence of NRAS alterations. The fraction of alleles carrying BRAFV600Esubstitution was variable but strongly associated with sun exposure. In contrast, no relationship was evidenced between the presence of this mutation and patients' phototype, phosphorylated ERK1/2 expression, or Clark's level. Our findings indicate that in melanocytic lesions, BRAFV600Emutation can affect a subset of the cells and is associated with the type and quantity of sun exposure. This mutation is independent of the nevo-melanoma progression and unrelated to ERK phosphorylation, suggesting that alternative mechanisms to the MAPK activation are also involved in this type of transformation.Modern Pathology (2008) 21, 716–726; doi:10.1038/modpathol.2008.41; published online 11 April 2008

Published
2008
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41. Regulation of aromatase expression in breast cancer treated with anastrozole neoadjuvant therapy.

Author

Ghimenti C, Mello-Grand M, Grosso E, Scatolini M, Regolo L, Zambelli A, and Chiorino G

Abstract

Aromatase inhibitors (AIs), such as anastrozole, are established in the treatment of hormone-dependent breast cancer. However, ∼20% of patients with hormone receptor-positive breast tumors treated with anastrozole do not respond and it remains impossible to accurately predict sensitivity. Since polymorphisms in the aromatase gene may influence the response to inhibitory drugs, we evaluated the presence of rs6493497 and rs7176005 polymorphisms (mapping in the 5'-flanking region of the CYP19A1 gene coding for the aromatase protein) in a cohort of 37 patients with postmenopausal breast cancer who received three-month neoadjuvant treatment with anastrozole. We then investigated any association of the polymorphisms with changes in aromatase mRNA expression change and/or response to treatment. We also analyzed five miRNAs computationally predicted to target aromatase, to observe any association between their expression and sensitivity to anastrozole. Three samples carried the two polymorphisms and the remaining samples were wild-type for both, however, no association with response or with aromatase mRNA basal expression level or expression difference after therapy was observed. Polymorphic samples that were resistant to anastrozole showed no change or decrease in aromatase expression following AI treatment, whereas an increase in expression was observed for the polymorphic responsive samples. No statistically significant correlation was observed between miRNA and aromatase mRNA expression, or with response to anastrozole neoadjuvant treatment. These data indicate that the polymorphisms analyzed are not involved in aromatase activity and that other epigenetic mechanisms may regulate aromatase protein expression.

Published
2013
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