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11 results on '"Piccirillo, S. g."'

3. Bone morphogenetic proteins inhibit the tumorigenic potential of human brain tumour-initiating cells

Author

Piccirillo, S. G. M., Reynolds, B. A., Zanetti, N., Lamorte, G., Binda, E., Broggi, G., Brem, H., Olivi, A., Dimeco, F., and Vescovi, A. L.

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): S. G. M. Piccirillo [1, 2]; B. A. Reynolds [3]; N. Zanetti [2]; G. Lamorte [2]; E. Binda [4]; G. Broggi [5]; H. Brem [6]; A. Olivi [6]; F. [...]

Published
2006
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6. Distinct pools of cancer stem-like cells coexist within human glioblastomas and display different tumorigenicity and independent genomic evolution.

Author

Piccirillo, S. g., Combi, L., Cajola, L., Patrizi, A., Redaelli, S., Bentivegna, A., Baronchelli, S., Maira, Giulio, Pollo, B., Mangiola, Annunziato, Dimeco, F., Dalprà, L., Vescovi, A. l., Piccirillo , S.g., Combi , L., Cajola , L., Patrizi , A., Redaelli , S., Bentivegna , A., Baronchelli , S., Maira , Giulio, Pollo , B., Mangiola, Annunziato (ORCID:0000-0002-1378-4524), Dimeco , F., Dalprà , L., Vescovi , A.l., Piccirillo, S. g., Combi, L., Cajola, L., Patrizi, A., Redaelli, S., Bentivegna, A., Baronchelli, S., Maira, Giulio, Pollo, B., Mangiola, Annunziato, Dimeco, F., Dalprà, L., Vescovi, A. l., Piccirillo , S.g., Combi , L., Cajola , L., Patrizi , A., Redaelli , S., Bentivegna , A., Baronchelli , S., Maira , Giulio, Pollo , B., Mangiola, Annunziato (ORCID:0000-0002-1378-4524), Dimeco , F., Dalprà , L., and Vescovi , A.l.

Published
2009

8. Abstracts from the 2011 BNOS Conference, June 29 - July 1, 2011, Homerton College, Cambridge

Author

Ammoun, S., primary, Zhou, L., additional, Barczyk, M., additional, Hilton, D., additional, Hafizi, S., additional, Hanemann, C., additional, Lehnus, K. S., additional, Donovan, L. K., additional, Pilkington, G. J., additional, An, Q., additional, Anderson, I. A., additional, Thomson, S., additional, Bailey, M., additional, Lekka, E., additional, Law, J., additional, Davis, C., additional, Banfill, K., additional, Loughrey, C., additional, Hatfield, P., additional, Bax, D., additional, Elliott, R., additional, Bishop, R., additional, Taylor, K., additional, Marshall, L., additional, Gaspar, N., additional, Viana-Pereira, M., additional, Reis, R., additional, Renshaw, J., additional, Ashworth, A., additional, Lord, C., additional, Jones, C., additional, Bellamy, C., additional, Shaw, L., additional, Alder, J., additional, Shorrocks, A., additional, Lea, R., additional, Birks, S., additional, Burnet, M., additional, Pilkington, G., additional, Bruch, J. D., additional, Ho, J., additional, Watts, C., additional, Price, S. J., additional, Camp, S., additional, Apostolopoulos, V., additional, Mehta, A., additional, Roncaroli, F., additional, Nandi, D., additional, Clark, B., additional, Mackinnon, M., additional, MacLeod, N., additional, Stewart, W., additional, Chalmers, A., additional, Cole, A., additional, Hanna, G., additional, Bailie, K., additional, Conkey, D., additional, Harney, J., additional, Darlow, C., additional, Chapman, S., additional, Mohsen, L., additional, Price, S., additional, Donovan, L., additional, Dyer, H., additional, Lord, H., additional, Fletcher, K., additional, das Nair, R., additional, MacNiven, J., additional, Basu, S., additional, Byrne, P., additional, Glancz, L., additional, Critchley, G., additional, Grech-Sollars, M., additional, Saunders, D., additional, Phipps, K., additional, Clayden, J., additional, Clark, C., additional, Greco, A., additional, Acquati, S., additional, Marino, S., additional, Hammouche, S., additional, Wilkins, S. P., additional, Smith, T., additional, Brodbelt, A., additional, Clark, S., additional, Wong, A. H. L., additional, Eldridge, P., additional, Farah, J. O., additional, Bruch, J., additional, Lamb, G., additional, Smith, S., additional, James, A., additional, Glegg, M., additional, Jeffcote, T., additional, Boulos, S., additional, Robbins, P., additional, Knuckey, N., additional, Banigo, A., additional, Brodbelt, A. R., additional, Jenkinson, M. D., additional, Jeyapalan, J. N., additional, Mumin, M. A., additional, Forshew, T., additional, Lawson, A. R., additional, Tatevossian, R. G., additional, Jacques, T. S., additional, Sheer, D., additional, Kilday, J., additional, Wright, K., additional, Leavy, S., additional, Lowe, J., additional, Schwalbe, E., additional, Clifford, S., additional, Gilbertson, R., additional, Coyle, B., additional, Grundy, R., additional, Kinsella, P., additional, Clynes, M., additional, Amberger-Murphy, V., additional, Barron, N., additional, Lambert, S. R., additional, Jones, D., additional, Pearson, D., additional, Ichimura, I., additional, Collins, V., additional, Steele, L., additional, Sinha, P., additional, Chumas, P., additional, Tyler, J., additional, Ogawa, D., additional, Chiocca, E., additional, DeLay, M., additional, Bronisz, A., additional, Nowicki, M., additional, Godlewski, J., additional, Lawler, S., additional, Lee, M. K., additional, Javadpour, M., additional, Abel, P., additional, Dawson, T., additional, Lea, B., additional, Lim, C. S.-K., additional, Grundy, P. L., additional, Pendleton, M., additional, Williamson, A., additional, Merve, A., additional, Zhang, X., additional, Miller, S., additional, Rogers, H. A., additional, Lyon, P., additional, Rand, V., additional, Adamowicz-Brice, M., additional, Clifford, S. C., additional, Hayden, J. T., additional, Dyer, S., additional, Pfister, S., additional, Korshunov, A., additional, Brundler, M.-A., additional, Grundy, R. G., additional, Nankivell, M., additional, Mulvenna, P., additional, Barton, R., additional, Wilson, P., additional, Faivre-Finn, C., additional, Pugh, C., additional, Langley, R., additional, Ngoga, D., additional, Tennant, D., additional, Williams, A., additional, Moss, P., additional, Cruickshank, G., additional, Owusu-Agyemang, K., additional, Bell, S., additional, St.George, J., additional, Piccirillo, S. G., additional, Qadri, S., additional, Pirola, E., additional, Jenkinson, M., additional, Rahman, R., additional, Rahman, C., additional, MacArthur, D., additional, Rose, F., additional, Shakesheff, K., additional, Carroll, C., additional, Watson, P., additional, Hawkins, M., additional, Spoudeas, H., additional, Walker, D., additional, Holland, T., additional, Ring, H., additional, Rooney, A., additional, McNamara, S., additional, Fraser, M., additional, Rampling, R., additional, Carson, A., additional, Grant, R., additional, Royds, J., additional, Al Nadaf, S., additional, Ahn, A., additional, Chen, Y.-J., additional, Wiles, A., additional, Jellinek, D., additional, Braithwaite, A., additional, Baguley, B., additional, MacFarlane, M., additional, Hung, N., additional, Slatter, T., additional, Rusbridge, S., additional, Walmsley, N., additional, Griffiths, S., additional, Wilford, P., additional, Rees, J., additional, Ryan, D., additional, Liu, P., additional, Galavotti, S., additional, Shaked-Rabi, M., additional, Tulchinsky, E., additional, Brandner, S., additional, Salomoni, P., additional, Schulte, A., additional, Gunther, H. S., additional, Zapf, S., additional, Riethdorf, S., additional, Westphal, M., additional, Lamszus, K., additional, Selvanathan, S. K., additional, Salminen, H. J., additional, Setua, S., additional, Welland, M. E., additional, Shevtsov, M., additional, Khachatryan, W., additional, Kim, A., additional, Samochernych, K., additional, Pozdnyakov, A., additional, Guzhova, I. V., additional, Romanova, I. V., additional, Margulis, B., additional, Barrow, J., additional, Macarthur, D., additional, Long, A., additional, Maherally, Z., additional, Smith, J. R., additional, Dickson, L., additional, Prabhu, S., additional, Harris, F., additional, Snape, T. J., additional, Sussman, M., additional, Wilne, S., additional, Whitehouse, W., additional, Chow, G., additional, Liu, J.-F., additional, Snape, T., additional, Karakoula, A., additional, Rowther, F., additional, Warr, T., additional, Zisakis, A., additional, Varsos, V., additional, Panteli, A., additional, Karypidou, O., additional, Zampethanis, A., additional, Fotovati, A., additional, Abu-Ali, S., additional, Wang, P.-S., additional, Deleyrolle, L., additional, Lee, C., additional, Triscott, J., additional, Chen, J. Y., additional, Franciosi, S., additional, Nakamura, Y., additional, Sugita, Y., additional, Uchiumi, T., additional, Kuwano, M., additional, Leavitt, B. R., additional, Singh, S. K., additional, Jury, A., additional, Wakimoto, H., additional, Reynolds, B. A., additional, Pallen, C. J., additional, Dunn, S. E., additional, Shepherd, S., additional, Scott, S., additional, Bowyer, D., additional, Wallace, L., additional, Hacking, B., additional, Jena, R., additional, Gillard, J., additional, Verraeult, M., additional, Reynolds, B., additional, Dunham, C., additional, Bally, M., additional, Hukin, J., additional, Singhal, S., additional, Singh, S., additional, and Dunn, S., additional

Published
2011
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9. Bone Morphogenetic Proteins Regulate Tumorigenicity in Human Glioblastoma Stem Cells.

Author

Wiestler, O. D., Haendler, B., Mumberg, D., Piccirillo, S. G. M., and Vescovi, A. L.

Abstract

Human glioblastomas appear to be established and expanded by cancer stem cells, which are endowed with tumour-initiating and perpetuating ability. We report that bone morphogenetic proteins (BMPs), amongst which BMP4 elicits the strongest effect, activate their cognate receptors (BMPRs) and trigger the Smad but not the MAP38 kinase signalling cascade in cells isolated from human glioblastomas (GBMs). This is followed by a reduction in proliferation and increased expression of differentiated neural markers, without affecting cell viability. The concomitant reduction in the clonogenic ability, both in the size of the CD133+ side population and in the growth kinetics of GBM cells, indicates that BMP4 triggers a reduction in the in vitro cancer stem cell (CSC) pool. Accordingly, transient ex vivo exposure to BMP4 abolishes the capacity of transplanted GBM cells to establish intracerebral GBMs. Most important, in vivo delivery of BMP4 effectively blocks the tumour growth and associated mortality which occur in 100% of control mice in less than 12 weeks, following intracerebral grafting of human GBM cells. These findings show that the BMP-BMPR signalling system, which controls the activity of normal brain stem cells, may also act as a key inhibitory regulator of cancer-initiating, GBM stem-like cells and identifies BMP4 as a novel, non-cytotoxic therapeutic effector, which may be used to prevent growth and recurrence of GBMs in humans. [ABSTRACT FROM AUTHOR]

Published
2007
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10. Evolutionary dynamics of residual disease in human glioblastoma.

Author

Spiteri, I, Caravagna, G, Cresswell, G D, Vatsiou, A, Nichol, D, Acar, A, Ermini, L, Chkhaidze, K, Werner, B, Mair, R, Brognaro, E, Verhaak, R G W, Sanguinetti, G, Piccirillo, S G M, Watts, C, and Sottoriva, A

Subjects
*DISEASES, *CANCER cells, *CANCER
Abstract

Background Glioblastoma is the most common and aggressive adult brain malignancy against which conventional surgery and chemoradiation provide limited benefit. Even when a good treatment response is obtained, recurrence inevitably occurs either locally (∼80%) or distally (∼20%), driven by cancer clones that are often genomically distinct from those in the primary tumour. Glioblastoma cells display a characteristic infiltrative phenotype, invading the surrounding tissue and often spreading across the whole brain. Cancer cells responsible for relapse can reside in two compartments of residual disease that are left behind after treatment: the infiltrated normal brain parenchyma and the sub-ventricular zone. However, these two sources of residual disease in glioblastoma are understudied because of the difficulty in sampling these regions during surgery. Patient and methods Here, we present the results of whole-exome sequencing of 69 multi-region samples collected using fluorescence-guided resection from 11 patients, including the infiltrating tumour margin and the sub-ventricular zone for each patient, as well as matched blood. We used a phylogenomic approach to dissect the spatio-temporal evolution of each tumour and unveil the relation between residual disease and the main tumour mass. We also analysed two patients with paired primary-recurrence samples with matched residual disease. Results Our results suggest that infiltrative subclones can arise early during tumour growth in a subset of patients. After treatment, the infiltrative subclones may seed the growth of a recurrent tumour, thus representing the 'missing link' between the primary tumour and recurrent disease. Conclusions These results are consistent with recognised clinical phenotypic behaviour and suggest that more specific therapeutic targeting of cells in the infiltrated brain parenchyma may improve patient's outcome. [ABSTRACT FROM AUTHOR]

Published
2019
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11. Single-nucleus and spatial landscape of the sub-ventricular zone in human glioblastoma.

Author

Licón-Muñoz Y, Avalos V, Subramanian S, Granger B, Martinez F, Varela S, Moore D, Perkins E, Kogan M, Berto S, Chohan MO, Bowers CA, and Piccirillo SGM

Abstract

The sub-ventricular zone (SVZ) is the most well-characterized neurogenic area in the mammalian brain. We previously showed that in 65% of patients with glioblastoma (GBM), the SVZ is a reservoir of cancer stem-like cells that contribute to treatment resistance and emergence of recurrence. Here, we built a single-nucleus RNA-sequencing-based microenvironment landscape of the tumor mass (T_Mass) and the SVZ (T_SVZ) of 15 GBM patients and 2 histologically normal SVZ (N_SVZ) samples as controls. We identified a mesenchymal signature in the T_SVZ of GBM patients: tumor cells from the T_SVZ relied on the ZEB1 regulatory network, whereas tumor cells in the T_Mass relied on the TEAD1 regulatory network. Moreover, the T_SVZ microenvironment was predominantly characterized by tumor-supportive microglia, which spatially co-exist and establish heterotypic interactions with tumor cells. Lastly, differential gene expression analyses, predictions of ligand-receptor and incoming/outgoing interactions, and functional assays revealed that the IL-1β/IL-1RAcP and Wnt-5a/Frizzled-3 pathways are therapeutic targets in the T_SVZ microenvironment. Our data provide insights into the biology of the SVZ in GBM patients and identify specific targets of this microenvironment.

Published
2024
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