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376 results on '"Mottolese, Marcella"'

1. p53 and BLC2 Immunohistochemical Expression Across Molecular Subtypes in 1099 Early Breast Cancer Patients With Long-Term Follow-up: An Observational Study

Author

Fabi, Alessandra, Mottolese, Marcella, Di Benedetto, Anna, Sperati, Francesca, Ercolani, Cristiana, Buglioni, Simonetta, Nisticò, Cecilia, Ferretti, Gianluigi, Vici, Patrizia, Perracchio, Letizia, Malaguti, Paola, Russillo, Michelangelo, Botti, Claudio, Pescarmona, Edoardo, Cognetti, Francesco, and Terrenato, Irene

Published
2020
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2. TRF2 and VEGF-A: an unknown relationship with prognostic impact on survival of colorectal cancer patients

Author

Dinami, Roberto, Porru, Manuela, Amoreo, Carla Azzurra, Sperduti, Isabella, Mottolese, Marcella, Buglioni, Simonetta, Marinelli, Daniele, Maugeri-Saccà, Marcello, Sacconi, Andrea, Blandino, Giovanni, Leonetti, Carlo, Di Rocco, Giuliana, Verdina, Alessandra, Spinella, Francesca, Fiorentino, Francesco, Ciliberto, Gennaro, Biroccio, Annamaria, and Zizza, Pasquale

Published
2020
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6. The Dilemma of HER2 Double-equivocal Breast Carcinomas: Genomic Profiling and Implications for Treatment

Author

Marchiò, Caterina, Dell’Orto, Patrizia, Annaratone, Laura, Geyer, Felipe C., Venesio, Tiziana, Berrino, Enrico, Verdun di Cantogno, Ludovica, Garofoli, Andrea, Rangel, Nelson, Casorzo, Laura, dell’Aglio, Carmine, Gugliotta, Patrizia, Trisolini, Elena, Beano, Alessandra, Pietribiasi, Francesca, Orlassino, Renzo, Cassoni, Paola, Pich, Achille, Montemurro, Filippo, Mottolese, Marcella, Vincent-Salomon, Anne, Penault-Llorca, Frédérique, Medico, Enzo, Ng, Charlotte K.Y., Viale, Giuseppe, and Sapino, Anna

Published
2018
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9. Functional and prognostic significance of the genomic amplification of frizzled 6 (FZD6) in breast cancer

Author

Corda, Gabriele, Sala, Gianluca, Lattanzio, Rossano, Iezzi, Manuela, Sallese, Michele, Fragassi, Giorgia, Lamolinara, Alessia, Mirza, Hasan, Barcaroli, Daniela, Ermler, Sibylle, Silva, Elisabete, Yasaei, Hemad, Newbold, Robert F, Vagnarelli, Paola, Mottolese, Marcella, Natali, Pier Giorgio, Perracchio, Letizia, Quist, Jelmar, Grigoriadis, Anita, Marra, Pierfrancesco, Tutt, Andrew N, Piantelli, Mauro, Iacobelli, Stefano, De Laurenzi, Vincenzo, and Sala, Arturo

Published
2017
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13. Outcomes of HER2-positive early breast cancer patients in the pre-trastuzumab and trastuzumab eras: a real-world multicenter observational analysis. The RETROHER study

Author

Vici, Patrizia, Pizzuti, Laura, Natoli, Clara, Moscetti, Luca, Mentuccia, Lucia, Vaccaro, Angela, Sergi, Domenico, Di Lauro, Luigi, Trenta, Patrizia, Seminara, Patrizia, Santini, Daniele, Iezzi, Laura, Tinari, Nicola, Bertolini, Ilaria, Sini, Valentina, Mottolese, Marcella, Giannarelli, Diana, Giotta, Francesco, Maugeri-Saccà, Marcello, Barba, Maddalena, Marchetti, Paolo, Michelotti, Andrea, Sperduti, Isabella, and Gamucci, Teresa

Published
2014
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16. A comparative biomarker study of 514 matched cases of male and female breast cancer reveals gender-specific biological differences

Author

Shaaban, Abeer M., Ball, Graham R., Brannan, Rebecca A., Cserni, Gabor, Benedetto, Anna Di, Dent, Jo, Fulford, Laura, Honarpisheh, Helen, Jordan, Lee, Jones, J. Louise, Kanthan, Rani, Maraqa, Loaie, Litwiniuk, Maria, Mottolese, Marcella, Pollock, Steven, Provenzano, Elena, Quinlan, Philip R., Reall, Georgina, Shousha, Sami, Stephens, Mark, Verghese, Eldo T., Walker, Rosemary A., Hanby, Andrew M., and Speirs, Valerie

Published
2012
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18. Increased overall survival independent of RECIST response in metastatic breast cancer patients continuing trastuzumab treatment: evidence from a retrospective study

Author

Campiglio, Manuela, Bufalino, Rosaria, Sandri, Marco, Ferri, Elisa, Aiello, Rosa Anna, De Matteis, Andrea, Mottolese, Marcella, De Placido, Sabino, Querzoli, Patrizia, Jirillo, Antonio, Bottini, Alberto, Fantini, Manuela, Bonetti, Andrea, Pedani, Fulvia, Mauri, Maria, Molino, Annamaria, Ferro, Antonella, Pupa, Serenella M., Sasso, Marianna, Ménard, Sylvie, Balsari, Andrea, and Tagliabue, Elda

Published
2011
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21. Endothelial NOS, estrogen receptor [beta], and HIFs cooperate in the activation of a prognostic transcriptional pattern in aggressive human prostate cancer

Author

Nanni, Simona, Benvenuti, Valentina, Grasselli, Annalisa, Priolo, Carmen, Aiello, Aurora, Mattiussi, Stefania, Colussi, Claudia, Lirangi, Vittoria, Illi, Barbara, D'Eletto, Manuela, Cianciulli, Anna Maria, Gallucci, Michele, De Carli, Piero, Sentinelli, Steno, Mottolese, Marcella, Carlini, Paolo, Strigari, Lidia, Finn, Stephen, Mueller, Elke, Arcangeli, Giorgio, Gaetano, Carlo, Capogrossi, Maurizio C., Donnorso, Raffaele Perrone, Bacchetti, Silvia, Sacchi, Ada, Pontecorvi, Alfredo, Loda, Massimo, and Farsetti, Antonella

Subjects
DNA binding proteins -- Physiological aspects, DNA binding proteins -- Research, Prostate cancer -- Diagnosis, Prostate cancer -- Prognosis, Prostate cancer -- Care and treatment, Prostate cancer -- Genetic aspects, Prostate cancer -- Research, Estrogen -- Receptors, Estrogen -- Physiological aspects, Estrogen -- Genetic aspects, Estrogen -- Research
Abstract

The identification of biomarkers that distinguish between aggressive and indolent forms of prostate cancer (PCa) is crucial for diagnosis and treatment. In this study, we used cultured cells derived from prostate tissue from patients with PCa to define a molecular mechanism underlying the most aggressive form of PCa that involves the functional activation of eNOS and HIFs in association with estrogen receptor [beta] (ER[beta]). Cells from patients with poor prognosis exhibited a constitutively hypoxic phenotype and increased NO production. Upon estrogen treatment, formation of ER[beta]/eNOS, ER[beta]/HIF-1[alpha], or ER[beta]/HIF-2[alpha] combinatorial complexes led to chromatin remodeling and transcriptional induction of prognostic genes. Tissue microarray analysis, using an independent cohort of patients, established a hierarchical predictive power for these proteins, with expression of eNOS plus ER[beta] and nuclear eNOS plus HIF-2[alpha] being the most relevant indicators of adverse clinical outcome. Genetic or pharmacologic modulation of eNOS expression and activity resulted in reciprocal conversion of the transcriptional signature in cells from patients with bad or good outcome, respectively, highlighting the relevance of eNOS in PCa progression. Our work has considerable clinical relevance, since it may enable the earlier diagnosis of aggressive PCa through routine biopsy assessment of eNOS, ER[beta], and HIF-2[alpha] expression. Furthermore, proposing eNOS as a therapeutic target fosters innovative therapies for PCa with NO inhibitors, which are employed in preclinical trials in non-oncological diseases., Introduction In the clinical management of prostate cancer (PCa), the second most common neoplasia in men worldwide (1), the ability to distinguish between aggressive and indolent forms of the disease [...]

Published
2009

25. Telomere damage induced by the G-quadruplex ligand RHPS4 has an antitumor effect

Author

Salvati, Erica, Leonetti, Carlo, Rizzo, Angela, Scarsella, Marco, Mottolese, Marcella, Galati, Rossella, Sperduti, Isabella, Stevens, Malcolm F.G., D'Incalci, Maurizio, Blasco, Maria, Chiorino, Giovanna, Bauwens, Serge, Horard, Beatrice, Gilson, Eric, Stoppacciaro, Antonella, Zupi, Gabriella, and Biroccio, Annamaria

Abstract

Functional telomeres are required for the replicability of cancer cells. The G-rich strand of telomeric DNA can fold into a 4-stranded structure known as the G-quadruplex (G4), whose stabilization alters [...]

Published
2007

26. High-mobility group A1 inhibits p53 by cytoplasmic relocalization of its proapoptotic activator HIPK2

Author

Pierantoni, Giovanna Maria, Rinaldo, Cinzia, Mottolese, Marcella, Benedetto, Anna Di, Esposito, Francesco, Soddu, Silvia, and Fusco, Alfredo

Subjects
Antibody diversity -- Research, Protein kinases -- Research, Proteins -- Research, Chromosomes, Cytoplasm
Abstract

High-mobility group A1 (HMGA1) overexpression and gene rearrangement are frequent events in human cancer, but the molecular basis of HMGA1 oncogenic activity remains unclear. Here we describe a mechanism through [...]

Published
2007

27. KRAS gene amplification in colorectal cancer and impact on response to EGFR-targeted therapy

Author

Valtorta, Emanuele, Misale, Sandra, Sartore-Bianchi, Andrea, Nagtegaal, Iris D., Paraf, François, Lauricella, Calogero, Dimartino, Valentina, Hobor, Sebastijan, Jacobs, Bart, Ercolani, Cristiana, Lamba, Simona, Scala, Elisa, Veronese, Silvio, Laurent-Puig, Pierre, Siena, Salvatore, Tejpar, Sabine, Mottolese, Marcella, Punt, Cornelis J.A., Gambacorta, Marcello, Bardelli, Alberto, and Di Nicolantonio, Federica

Published
2013
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34. EGFR Molecular Profiling in Advanced NSCLC: A Prospective Phase II Study in Molecularly/Clinically Selected Patients Pretreated with Chemotherapy

Author

Milella, Michele, Nuzzo, Carmen, Bria, Emilio, Sperduti, Isabella, Visca, Paolo, Buttitta, Fiamma, Antoniani, Barbara, Merola, Roberta, Gelibter, Alain, Cuppone, Federica, D’Alicandro, Valerio, Ceribelli, Anna, Rinaldi, Massimo, Cianciulli, Anna, Felicioni, Lara, Malatesta, Sara, Marchetti, Antonio, Mottolese, Marcella, and Cognetti, Francesco

Published
2012
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38. Endothelial NOS, estrogen receptor β, and HIFs cooperate in the activation of a prognostic transcriptional pattern in aggressive human prostate cancer

Author

Nanni, Simona, Benvenuti, Valentina, Grasselli, Annalisa, Priolo, Carmen, Aiello, Aurora, Mattiussi, Stefania, Colussi, Claudia, Lirangi, Vittoria, Illi, Barbara, D’Eletto, Manuela, Cianciulli, Anna Maria, Gallucci, Michele, De Carli, Piero, Sentinelli, Steno, Mottolese, Marcella, Carlini, Paolo, Strigari, Lidia, Finn, Stephen, Mueller, Elke, Arcangeli, Giorgio, Gaetano, Carlo, Capogrossi, Maurizio C., Donnorso, Raffaele Perrone, Bacchetti, Silvia, Sacchi, Ada, Pontecorvi, Alfredo, Loda, Massimo, and Farsetti, Antonella

Published
2009

41. Does Granulocyte Colony-Stimulating Factor Worsen Anemia in Early Breast Cancer Patients Treated With Epirubicin and Cyclophosphamide?

Author

Papaldo, Paola, Ferretti, Gianluigi, Di Cosimo, Serena, Giannarelli, Diana, Marolla, Paolo, Lopez, Massimo, Cortesi, Enrico, Antimi, Mauro, Terzoli, Edmondo, Carlini, Paolo, Vici, Patrizia, Botti, Claudio, Di Lauro, Luigi, Naso, Giuseppe, Nisticò, Cecilia, Mottolese, Marcella, Di Filippo, Franco, Ruggeri, Enzo Maria, Ceribelli, Anna, and Cognetti, Francesco

Published
2006
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48. Caspase-8 contributes to angiogenesis and chemotherapy resistance in glioblastoma

Author

Fianco, Giulia, Mongiardi, Maria Patrizia, Levi, Andrea, Luca, Teresa De, Desideri, Marianna, Trisciuoglio, Daniela, Bufalo, Donatella Del, Cinà, Irene, Benedetto, Anna Di, Mottolese, Marcella, Gentile, Antonietta, Centonze, Diego, Ferrè, Fabrizio, Barilà, Daniela, Fianco, Giulia, Mongiardi, Maria Patrizia, Levi, Andrea, Luca, Teresa De, Desideri, Marianna, Trisciuoglio, Daniela, Bufalo, Donatella Del, Cinã , Irene, Benedetto, Anna Di, Mottolese, Marcella, Gentile, Antonietta, Centonze, Diego, Ferrè, Fabrizio, and Barilà , Daniela

Subjects
Vascular Endothelial Growth Factor A, 0301 basic medicine, Angiogenesis, Immunology and Microbiology (all), Neovascularization, angiogenesis, cell biology, Biology (General), cancer biology, Caspase 8, Neovascularization, Pathologic, General Neuroscience, NF-kappa B, General Medicine, Prognosis, Vascular endothelial growth factor A, cell death, Cytokines, Medicine, Settore MED/26 - Neurologia, medicine.symptom, signal transduction, medicine.drug, QH301-705.5, Science, Short Report, Biology, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, medicine, Humans, cancer, Neoplastic transformation, human, mouse, Temozolomide, Neuroscience (all), Biochemistry, Genetics and Molecular Biology (all), General Immunology and Microbiology, Microarray analysis techniques, Gene Expression Profiling, Cancer, angiogenesi, Microarray Analysis, medicine.disease, Gene expression profiling, Settore BIO/18 - Genetica, cell proliferation, 030104 developmental biology, Drug Resistance, Neoplasm, Immunology, Cancer research, Glioblastoma
Abstract

Caspase-8 is a key player in extrinsic apoptosis and its activity is often downregulated in cancer. However, human Caspase-8 expression is retained in some tumors, including glioblastoma (GBM), suggesting that it may support cancer growth in these contexts. GBM, the most aggressive of the gliomas, is characterized by extensive angiogenesis and by an inflammatory microenvironment that support its development and resistance to therapies. We have recently shown that Caspase-8 sustains neoplastic transformation in vitro in human GBM cell lines. Here, we demonstrate that Caspase-8, through activation of NF-kB, enhances the expression and secretion of VEGF, IL-6, IL-8, IL-1beta and MCP-1, leading to neovascularization and increased resistance to Temozolomide. Importantly, the bioinformatics analysis of microarray gene expression data derived from a set of high-grade human gliomas, shows that high Caspase-8 expression levels correlate with a worse prognosis. DOI: http://dx.doi.org/10.7554/eLife.22593.001, eLife digest Cancer cells are different to normal cells in various ways. Most cancer cells, for example, delete or switch off the gene for a protein called Caspase-8. This is because this protein is best known for promoting cell death and stopping tumor cells from growing. However, some cancers keep the gene for Caspase-8 switched on including glioblastoma, the most aggressive type of brain cancer in adults. This begged the question whether this protein may in fact promote the development of tumors under certain circumstances. Glioblastomas are often highly resistant to chemotherapy and can communicate with nearby cells using proteins called cytokines to promote the formation of new blood vessels. The new blood vessel allows the tumor to readily spread into healthy brain tissue, which in turn makes it difficult for surgeons to remove all the cancerous cells. As a result, glioblastomas almost always return after surgery, and so there is strong need for new effective treatments for this type of cancer. Fianco et al. have now investigated whether Caspase-8 helps glioblastomas to grow and form new blood vessels. One common method to study human cancer cells is to inject them into mice and watch how they grow, because these experiments mimic how tumors develop in the human body. When mice were injected with human glioblastoma cells with experimentally reduced levels of Caspase-8, the cells grew poorly and did not form as many new blood vessels as unaltered glioblastoma cells. Further experiments showed that, when grown in the laboratory, glioblastoma cells with less Caspase-8 were more sensitive to a chemotherapeutic drug called temozolomide. These findings confirm that Caspase-8 does boost the growth and drug resistance of at least one cancer. When Fianco et al. analyzed clinical data from patients affected by glioblastoma, they also observed that those patients with high levels of Caspase-8 often had the worse outcomes. Previous studies conducted in white blood cells showed that Caspase-8 activated a protein complex called NF-kB, which in turn led to the cells releasing cytokines. Fianco et al. have now verified that Caspase-8 promotes NF-kB activity also in glioblastoma cells, and that this causes the cancer cells to release more cytokines. As such, these findings reveal a clear link between Caspase-8 and the formation of new blood vessels by glioblastomas. Future studies are now needed to understand why Caspase-8 promotes cell death in some cancers but the formation of new blood vessels in others. Indeed, Caspase-8 might become a target for new anticancer drugs if it is possible to inhibit its cancer-boosting activity without interfering with its ability to promote cell death. DOI: http://dx.doi.org/10.7554/eLife.22593.002

Published
2017

50. Claspin as a biomarker of human papillomavirus-related high grade lesions of uterine cervix

Author

Benevolo Maria, Musio Antonio, Vocaturo Amina, Donà Maria, Rollo Francesca, Terrenato Irene, Carosi Mariantonia, Pescarmona Edoardo, Vocaturo Giuseppe, and Mottolese Marcella

Subjects
Claspin, Human papillomavirus, Uterine cervix, Biomarker, Medicine
Abstract

Abstract Background Claspin is a nuclear protein involved in DNA replication and damage response and is a key mediator for the S-phase checkpoint. Claspin expression is significantly high in several human solid tumors. Furthermore, high levels of claspin have been found in cervical cancer cell lines. Nevertheless, no data are available regarding claspin expression in cervical tissues. Methods In order to investigate whether claspin immunoreactivity is related to the lesion severity and High-Risk (HR) HPV infection, we analyzed claspin expression by immunohistochemistry in a series of cervical biopsies which represent the steps occurring during cervical carcinogenesis (normal tissues, Cervical Intraepithelial Neoplasias 1, 2 and 3, Squamous Cell Carcinomas). All patients also had a cervico-vaginal sample for HPV testing, collected immediately before the colposcopy-guided biopsy. The HR-HPV DNA detection was performed by the HR-HPV Hybrid Capture 2 test. HPV genotyping was performed using the Linear Array HPV Genotyping Test. Results Our results evidenced a constant and significant increase of the rate of claspin positivity from the normal tissues to carcinomas (pχ2trend 2 Conclusions Our findings indicate that in vivo claspin expression is significantly related to HR-HPV infection and lesion grade both in histological and cytological samples. Therefore, the analysis of claspin expression could be clinically relevant in the diagnosis of HPV-related cervical lesions, in particular when applied to cervico-vaginal cytology. Moreover, giving information on the proliferation rate of each lesion, claspin immunostaining may contribute to the evaluation of progression risk, thus being helpful in patient management. Nevertheless, only large prospective studies may clarify the true clinical usefulness of claspin expression in distinguishing lesions with different progression potential.

Published
2012
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