Search

Your search keyword '"Sciot, R"' showing total 1,083 results
Start Over Author "Sciot, R"
1,083 results on '"Sciot, R"'

4. Activity and safety of crizotinib in patients with alveolar soft part sarcoma with rearrangement of TFE3: European Organization for Research and Treatment of Cancer (EORTC) phase II trial 90101 ‘CREATE’

Author

Schöffski, P., Wozniak, A., Kasper, B., Aamdal, S., Leahy, M.G., Rutkowski, P., Bauer, S., Gelderblom, H., Italiano, A., Lindner, L.H., Hennig, I., Strauss, S., Zakotnik, B., Anthoney, A., Albiges, L., Blay, J.-Y., Reichardt, P., Sufliarsky, J., van der Graaf, W.T.A., Debiec-Rychter, M., Sciot, R., Van Cann, T., Marréaud, S., Raveloarivahy, T., Collette, S., and Stacchiotti, S.

Published
2018
Full Text
View/download PDF

7. Activity and safety of crizotinib in patients with advanced clear-cell sarcoma with MET alterations: European Organization for Research and Treatment of Cancer phase II trial 90101 ‘CREATE’

Author

Schöffski, P, Wozniak, A, Stacchiotti, S, Rutkowski, P, Blay, J -Y, Lindner, L H, Strauss, S J, Anthoney, A, Duffaud, F, Richter, S, Grünwald, V, Leahy, M G, Reichardt, P, Sufliarsky, J, van der Graaf, W T, Sciot, R, Debiec-Rychter, M, van Cann, T, Marréaud, S, Lia, M, Raveloarivahy, T, Collette, L, and Bauer, S

Published
2017
Full Text
View/download PDF

9. ALK-positive histiocytosis: a new clinicopathologic spectrum highlighting neurologic involvement and responses to ALK inhibition

Author

Kemps, P.G., Picarsic, J., Durham, B.H., Hélias-Rodzewicz, Z., Hiemcke-Jiwa, L., Bos, Cor van den, Wetering, M.D. van de, Noesel, C.J. van, Laar, Jacob M. van, Verdijk, R.M., Flucke, U.E., Hogendoorn, P.C., Woei, A.J.F., Sciot, R., Beilken, A., Feuerhake, F., Ebinger, M., Möhle, R., Fend, F., Bornemann, A., Wiegering, V., Ernestus, K., Méry, T., Gryniewicz-Kwiatkowska, O., Dembowska-Baginska, B., Evseev, D.A., Potapenko, V., Baykov, V.V., Gaspari, S., Rossi, S., Gessi, M., Tamburrini, G., Héritier, S., Donadieu, J., Bonneau-Lagacherie, J., Lamaison, C., Farnault, L., Fraitag, S., Jullié, M.L., Haroche, J., Collin, M., Allotey, J., Madni, M., Turner, K., Picton, S., Barbaro, P.M., Poulin, A., Tam, I.S., Demellawy, D. El, Empringham, B., Whitlock, J.A., Raghunathan, A., Swanson, A.A., Suchi, M., Brandt, J.M., Yaseen, N.R., Weinstein, J.L., Eldem, I., Sisk, B.A., Sridhar, V., Atkinson, M., Massoth, L.R., Hornick, J.L., Alexandrescu, S., Yeo, K.K., Petrova-Drus, K., Peeke, S.Z., Muñoz-Arcos, L.S., Leino, D.G., Grier, D.D., Lorsbach, R., Roy, S., Kumar, A.R., Garg, S., Tiwari, N., Schafernak, K.T., Henry, M.M., Halteren, A.G. van, Abla, O., Diamond, E.L., Emile, J.F., Kemps, P.G., Picarsic, J., Durham, B.H., Hélias-Rodzewicz, Z., Hiemcke-Jiwa, L., Bos, Cor van den, Wetering, M.D. van de, Noesel, C.J. van, Laar, Jacob M. van, Verdijk, R.M., Flucke, U.E., Hogendoorn, P.C., Woei, A.J.F., Sciot, R., Beilken, A., Feuerhake, F., Ebinger, M., Möhle, R., Fend, F., Bornemann, A., Wiegering, V., Ernestus, K., Méry, T., Gryniewicz-Kwiatkowska, O., Dembowska-Baginska, B., Evseev, D.A., Potapenko, V., Baykov, V.V., Gaspari, S., Rossi, S., Gessi, M., Tamburrini, G., Héritier, S., Donadieu, J., Bonneau-Lagacherie, J., Lamaison, C., Farnault, L., Fraitag, S., Jullié, M.L., Haroche, J., Collin, M., Allotey, J., Madni, M., Turner, K., Picton, S., Barbaro, P.M., Poulin, A., Tam, I.S., Demellawy, D. El, Empringham, B., Whitlock, J.A., Raghunathan, A., Swanson, A.A., Suchi, M., Brandt, J.M., Yaseen, N.R., Weinstein, J.L., Eldem, I., Sisk, B.A., Sridhar, V., Atkinson, M., Massoth, L.R., Hornick, J.L., Alexandrescu, S., Yeo, K.K., Petrova-Drus, K., Peeke, S.Z., Muñoz-Arcos, L.S., Leino, D.G., Grier, D.D., Lorsbach, R., Roy, S., Kumar, A.R., Garg, S., Tiwari, N., Schafernak, K.T., Henry, M.M., Halteren, A.G. van, Abla, O., Diamond, E.L., and Emile, J.F.

Abstract

Item does not contain fulltext, ALK-positive histiocytosis is a rare subtype of histiocytic neoplasm first described in 2008 in 3 infants with multisystemic disease involving the liver and hematopoietic system. This entity has subsequently been documented in case reports and series to occupy a wider clinicopathologic spectrum with recurrent KIF5B-ALK fusions. The full clinicopathologic and molecular spectra of ALK-positive histiocytosis remain, however, poorly characterized. Here, we describe the largest study of ALK-positive histiocytosis to date, with detailed clinicopathologic data of 39 cases, including 37 cases with confirmed ALK rearrangements. The clinical spectrum comprised distinct clinical phenotypic groups: infants with multisystemic disease with liver and hematopoietic involvement, as originally described (Group 1A: 6/39), other patients with multisystemic disease (Group 1B: 10/39), and patients with single-system disease (Group 2: 23/39). Nineteen patients of the entire cohort (49%) had neurologic involvement (7 and 12 from Groups 1B and 2, respectively). Histology included classic xanthogranuloma features in almost one-third of cases, whereas the majority displayed a more densely cellular, monomorphic appearance without lipidized histiocytes but sometimes more spindled or epithelioid morphology. Neoplastic histiocytes were positive for macrophage markers and often conferred strong expression of phosphorylated extracellular signal-regulated kinase, confirming MAPK pathway activation. KIF5B-ALK fusions were detected in 27 patients, whereas CLTC-ALK, TPM3-ALK, TFG-ALK, EML4-ALK, and DCTN1-ALK fusions were identified in single cases. Robust and durable responses were observed in 11/11 patients treated with ALK inhibition, 10 with neurologic involvement. This study presents the existing clinicopathologic and molecular landscape of ALK-positive histiocytosis and provides guidance for the clinical management of this emerging histiocytic entity.

Published
2022

18. An Unusual Course of Donor-Transmitted Angiosarcoma after Lung Transplantation

Author

Bos, S., primary, Daniëls, L., additional, Michaux, L., additional, Bempt, I. Vanden, additional, Vermeer, S., additional, Woei-A-Jin, S., additional, Schöffski, P., additional, Weynand, B., additional, Sciot, R., additional, Declercq, S., additional, Van Raemdonck, D.E., additional, Ceulemans, L.J., additional, Dupont, L.J., additional, Verleden, G.M., additional, and Vos, R., additional

Published
2021
Full Text
View/download PDF

20. Corrigendum to “Clinical Presentation, Natural History, and Therapeutic Approach in Patients with Solitary Fibrous Tumor: A Retrospective Analysis”

Author

Schöffski, P., primary, Timmermans, I., additional, Hompes, D., additional, Stas, M., additional, Boecxstaens, Veerle, additional, Sinnaeve, F., additional, De Leyn, P., additional, Coosemans, W., additional, Van Raemdonck, D., additional, Hauben, E., additional, Sciot, R., additional, Clement, P., additional, Bechter, O., additional, Beuselinck, B., additional, Woei-A-Jin, F. J. S. H., additional, Dumez, H., additional, Nafteux, P., additional, and Wessels, T., additional

Published
2021
Full Text
View/download PDF

25. Elevated risk for MPNST in NF1 microdeletion patients. (Report)

Author

De Raedt, T., Brems, H., Wolkenstein, P., Vidaud, D., Pilotti, S., Perrone, F., Mautner, V., Frahm, S., Sciot, R., and Legius, E.

Subjects
Genetic disorders -- Research, Human genetics -- Research, Neurofibromatosis -- Genetic aspects, Biological sciences
Published
2003

31. Clinical Presentation, Natural History, and Therapeutic Approach in Patients with Solitary Fibrous Tumor: A Retrospective Analysis

Author

Schöffski, P., primary, Timmermans, I., additional, Hompes, D., additional, Stas, M., additional, Sinnaeve, F., additional, De Leyn, P., additional, Coosemans, W., additional, Van Raemdonck, D., additional, Hauben, E., additional, Sciot, R., additional, Clement, P., additional, Bechter, O., additional, Beuselinck, B., additional, Woei-A-Jin, F. J. S. H., additional, Dumez, H., additional, Nafteux, P., additional, and Wessels, T., additional

Published
2020
Full Text
View/download PDF

35. Consensus meeting for the management of gastrointestinal stromal tumors Report of the GIST Consensus Conference of 20–21 March 2004, under the auspices of ESMO

Author

Blay, J.-Y., Bonvalot, S., Casali, P., Choi, H., Debiec-Richter, M., Dei Tos, A.P., Emile, J.-F., Gronchi, A., Hogendoorn, P.C.W., Joensuu, H., Le Cesne, A., Mac Clure, J., Maurel, J., Nupponen, N., Ray-Coquard, I., Reichardt, P., Sciot, R., Stroobants, S., van Glabbeke, M., van Oosterom, A., and Demetri, G.D.

Published
2005
Full Text
View/download PDF

50. Molecular Comparison of Imatinib-Naive and Resistant Gastrointestinal Stromal Tumors: Differentially Expressed microRNAs and mRNAs

Author

Amirnasr, A. (Azadeh), Gits, C.M.M. (Caroline), Kuijk, P.F. (Patricia) van, Smid, M. (Marcel), Vriends, A.L.M. (Anne), Rutkowski, P. (Piotr), Sciot, R. (Raf), Schoffski, P, Debiec-Rychter, M. (Maria), Sleijfer, S. (Stefan), Wiemer, E.A.C. (Erik), Amirnasr, A. (Azadeh), Gits, C.M.M. (Caroline), Kuijk, P.F. (Patricia) van, Smid, M. (Marcel), Vriends, A.L.M. (Anne), Rutkowski, P. (Piotr), Sciot, R. (Raf), Schoffski, P, Debiec-Rychter, M. (Maria), Sleijfer, S. (Stefan), and Wiemer, E.A.C. (Erik)

Abstract

Despite the success of imatinib in advanced gastrointestinal stromal tumor (GIST) patients, 50% of the patients experience resistance within two years of treatment underscoring the need to get better insight into the mechanisms conferring imatinib resistance. Here the microRNA and mRNA expression profiles in primary (imatinib-naïve) and imatinib-resistant GIST were examined. Fifty-three GIST samples harboring primary KIT mutations (exon 9; n = 11/exon 11; n = 41/exon 17; n = 1) and comprising imatinib-naïve (IM-n) (n = 33) and imatinib-resistant (IM-r) (n = 20) tumors, were analyzed. The microRNA expression profiles were determined and from a subset (IM-n, n = 14; IM-r, n = 15) the mRNA expression profile was established. Ingenuity pathway analyses were used to unravel biochemical pathways and gene networks in IM-r GIST. Thirty-five differentially expressed miRNAs between IM-n and IM-r GIST samples were identified. Additionally, miRNAs distinguished IM-r samples with and without secondary KIT mutations. Furthermore 352 aberrantly expressed genes were found in IM-r samples. Pathway and network analyses revealed an association of differentially expressed genes with cell cycle progression and cellular proliferation, thereby implicating genes and pathways involved in imatinib resistance in GIST. Differentially expressed miRNAs and mRNAs between IM-n and IM-r GIST were identified. Bioinformatic analyses provided insight into the genes and biochemical pathways involved in imatinib-resistance and highlighted key genes that may be putative treatment targets.

Published
2019
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results