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2. 27MO Integrated digital pathology and single-cell analysis identify the spatial and temporal evolution of immune cells networks in epithelial ovarian cancer

Author

Ghisoni, E., primary, Benedetti, F., additional, Cunnea, P., additional, Fahr, N., additional, Gulhan, D.C., additional, Minasyan, A., additional, Desbuisson, M., additional, Grimm, A., additional, Barras, D., additional, Dagher, J., additional, Fortis, E., additional, Rusakiewicz, S., additional, Tissot, S., additional, Mastroyannis, S.A., additional, Swisher, E., additional, Kandalaft, L., additional, Tanyi, J., additional, Fotopoulou, C., additional, Coukos, G., additional, and Dangaj, D., additional

Published
2022
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3. BiCMOS Variable Gain LNA at C-Band with Ultra Low Power Consumption for WLAN

Author

Ellinger, F., Carta, C., Rodoni, L., von Büren, G., Barras, D., Schmatz, M., Jäckel, H., Hutchison, David, editor, Kanade, Takeo, editor, Kittler, Josef, editor, Kleinberg, Jon M., editor, Mattern, Friedemann, editor, Mitchell, John C., editor, Naor, Moni, editor, Nierstrasz, Oscar, editor, Pandu Rangan, C., editor, Steffen, Bernhard, editor, Sudan, Madhu, editor, Terzopoulos, Demetri, editor, Tygar, Dough, editor, Vardi, Moshe Y., editor, Weikum, Gerhard, editor, de Souza, José Neuman, editor, Dini, Petre, editor, and Lorenz, Pascal, editor

Published
2004
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5. Cell-autonomous inflammation of BRCA1-deficient ovarian cancers drives both tumor-intrinsic immunoreactivity and immune resistance via STING

Author

Bruand, M., Barras, D., Mina, M., Ghisoni, E., Morotti, M., Lanitis, E., Fahr, N., Desbuisson, M., Grimm, A., Zhang, H., Chong, C., Dagher, J., Chee, S., Tsianou, T., Dorier, J., Stevenson, B.J., Iseli, C., Ronet, C., Bobisse, S., Genolet, R., Walton, J., Bassani-Sternberg, M., Kandalaft, L.E., Ren, B., McNeish, I., Swisher, E., Harari, A., Delorenzi, M., Ciriello, G., Irving, M., Rusakiewicz, S., Foukas, P.G., and Martinon, F.

Subjects
BRCA1, CTLA-4, DNA sensing, ICB, PARPi, PD-L1, STING, T cells, VEGF-A, angiogenesis, dual immune checkpoint blockade, ovarian cancer, type I IFN
Abstract

In this study, we investigate mechanisms leading to inflammation and immunoreactivity in ovarian tumors with homologous recombination deficiency (HRD). BRCA1 loss is found to lead to transcriptional reprogramming in tumor cells and cell-intrinsic inflammation involving type I interferon (IFN) and stimulator of IFN genes (STING). BRCA1-mutated (BRCA1 mut ) tumors are thus T cell inflamed at baseline. Genetic deletion or methylation of DNA-sensing/IFN genes or CCL5 chemokine is identified as a potential mechanism to attenuate T cell inflammation. Alternatively, in BRCA1 mut cancers retaining inflammation, STING upregulates VEGF-A, mediating immune resistance and tumor progression. Tumor-intrinsic STING elimination reduces neoangiogenesis, increases CD8 + T cell infiltration, and reverts therapeutic resistance to dual immune checkpoint blockade (ICB). VEGF-A blockade phenocopies genetic STING loss and synergizes with ICB and/or poly(ADP-ribose) polymerase (PARP) inhibitors to control the outgrowth of Trp53 -/- Brca1 -/- but not Brca1 +/+ ovarian tumors in vivo, offering rational combinatorial therapies for HRD cancers.

Published
2021

6. Integrated active pulsed reflector for an indoor local positioning system

Author

Wehrli, S., Gierlich, R., Huttner, J., Barras, D., Ellinger, F., and Jackel, H.

Subjects
Frequency modulation -- Usage, Integrated circuits -- Analysis, Semiconductor chips -- Analysis, Radar systems -- Design and construction, Ultra wideband technology -- Usage, Standard IC, Business, Computers, Electronics, Electronics and electrical industries
Published
2010

8. Cooperation between Constitutive and Inducible Chemokines Enables T Cell Engraftment and Immune Attack in Solid Tumors

Author

Dangaj, D. Bruand, M. Grimm, A.J. Ronet, C. Barras, D. Duttagupta, P.A. Lanitis, E. Duraiswamy, J. Tanyi, J.L. Benencia, F. Conejo-Garcia, J. Ramay, H.R. Montone, K.T. Powell, D.J., Jr. Gimotty, P.A. Facciabene, A. Jackson, D.G. Weber, J.S. Rodig, S.J. Hodi, S.F. Kandalaft, L.E. Irving, M. Zhang, L. Foukas, P. Rusakiewicz, S. Delorenzi, M. Coukos, G.

Subjects
stomatognathic diseases, stomatognathic system, parasitic diseases, virus diseases, hemic and immune systems
Abstract

We investigated the role of chemokines in regulating T cell accumulation in solid tumors. CCL5 and CXCL9 overexpression was associated with CD8+ T cell infiltration in solid tumors. T cell infiltration required tumor cell-derived CCL5 and was amplified by IFN-γ-inducible, myeloid cell-secreted CXCL9. CCL5 and CXCL9 coexpression revealed immunoreactive tumors with prolonged survival and response to checkpoint blockade. Loss of CCL5 expression in human tumors was associated with epigenetic silencing through DNA methylation. Reduction of CCL5 expression caused tumor-infiltrating lymphocyte (TIL) desertification, whereas forced CCL5 expression prevented Cxcl9 expression and TILs loss, and attenuated tumor growth in mice through IFN-γ. The cooperation between tumor-derived CCL5 and IFN-γ-inducible CXCR3 ligands secreted by myeloid cells is key for orchestrating T cell infiltration in immunoreactive and immunoresponsive tumors. Dangaj et al. show that tumor cell-expressed CCL5 and macrophage- and DC-expressed CXCL9 are important for the infiltration of T cells into tumors, a process that also requires recognition of tumor antigens by T cells. CCL5 is often epigenetically silenced in tumor cells but can be reactivated by Decitabine. © 2019 Elsevier Inc.

Published
2019

9. Immunogenicity of BRCA1-deficient ovarian cancers is driven through DNA sensing and is augmented by PARP inhibition

Author

Bruand, M., primary, Barras, D., additional, Mina, M., additional, Lanitis, E., additional, Chong, C., additional, Dorier, J., additional, Walton, J., additional, Bassani-Sternberg, M., additional, Kandalaft, L., additional, McNeish, I.A., additional, Swisher, E., additional, Delorenzi, M., additional, Ren, B., additional, Ciriello, G., additional, Irving, M., additional, Rusakiewicz, S., additional, Foukas, P., additional, Martinon, F., additional, Dangaj, D., additional, and Coukos, G., additional

Published
2019
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12. The SIB Swiss Institute of Bioinformatics' resources: focus on curated databases

Author

Bultet, LA, Aguilar-Rodriguez, J, Ahrens, CH, Ahrne, EL, Ai, N, Aimo, L, Akalin, A, Aleksiev, T, Alocci, D, Altenhoff, A, Alves, I, Ambrosini, G, Pedone, PA, Angelina, P, Anisimova, M, Appel, R, Argoud-Puy, G, Arnold, K, Arpat, B, Artimo, P, Ascencao, K, Auchincloss, A, Axelsen, K, Gerritsen, VB, Bairoch, A, Barisal, P, Baratin, D, Barbato, A, Barbie, V, Barras, D, Barreiro, M, Barret, S, Bastian, F, Batista Neto, TM, Baudis, M, Beaudoing, E, Beckmann, JS, Bekkar, AK, Cammoun, LBH, Benmohammed, S, Bernard, M, Bertelli, C, Bertoni, M, Bienert, S, Bignucolo, O, Bilbao, A, Bilican, A, Blank, D, Blatter, M-C, Blum, L, Bocquet, J, Boeckmann, B, Bolleman, JT, Bordoli, L, Bosshard, L, Boucher, G, Bougueleret, L, Boutet, E, Bovigny, C, Bratulic, S, Breuza, L, Bridge, AJ, Britan, A, Brito, F, Frazao, JB, Bruggmann, R, Bucher, P, Burdet, F, Burger, L, Cabello, EM, Gomez, RMC, Calderon, S, Cannarozzi, G, Carl, S, Casas, CC, Catherinet, S, Perier, RC, Charpilloz, C, Chaskar, PD, Chen, W, Pepe, AC, Chopard, B, Chu, HY, Civic, N, Claassen, M, Clottu, S, Colombo, M, Cosandier, I, Coudert, E, Crespo, I, Creus, M, Cuche, B, Cuendet, MA, Cusin, I, Daga, N, Daina, A, Dauvillier, J, David, F, Davydov, I, Ferreira, MDSRM, de Beer, T, de Castro, E, de Santana, C, Delafontaine, J, Delorenzi, M, Delucinge-Vivier, C, Demirel, O, Derham, R, Dermitzakis, EM, Dib, L, Diene, S, Dilek, N, Dilmi, J, Domagalski, MJ, Dorier, J, Dornevil, D, Dousse, A, Dreos, R, Duchen, P, Roggli, PD, Duperret, ID, Durinx, C, Duvaud, S, Engler, R, Frkek, S, Lopez, PE, Fstreicher, A, Excoffier, L, Fabbretti, R, Falcone, J-L, Falquet, L, Famiglietti, ML, Ferreira, A-M, Feuermann, M, Filliettaz, M, Hegel, V, Foucal, A, Franceschini, A, Fucile, G, Gaidatzis, D, Garcia, V, Gasteiger, E, Gateau, A, Gatti, L, Gaudet, P, Gaudinat, A, Gehant, S, Gfeller, D, Gharib, WH, Ghraichy, M, Gidoin, C, Gil, M, Gleizes, A, Gobeill, J, Gonnet, G, Gos, A, Gotz, L, Gouy, A, Grbic, D, Groux, R, Gruaz-Gumowski, N, Grun, D, Gschwind, A, Guex, N, Gupta, S, Getaz, M, Haake, D, Haas, J, Hatzimanikatis, V, Heckel, G, Gardiol, DFH, Hinard, V, Hinz, U, Homicsko, K, Horlacher, O, Hosseini, S-R, Hotz, H-R, Hulo, C, Hundsrucker, C, Ibberson, M, Ilmjarv, S, Ioannidis, V, Ioannidis, P, Iseli, C, Ivanek, R, Iwaszkiewicz, J, Jacquet, P, Jacquot, M, Jagannathan, V, Jan, M, Jensen, J, Johansson, MU, Johner, N, Jungo, F, Junier, T, Kahraman, A, Katsantoni, M, Keller, G, Kerhornou, A, Khalid, F, Klingbiel, D, Kimljenovic, A, Kriventseva, E, Kryuchkova, N, Kumar, S, Kutalik, Z, Kuznetsov, D, Kuzyakiv, R, Lane, L, Lara, V, Ledesma, L, Leleu, M, Lemercier, P, Lew, D, Lieberherr, D, Liechti, R, Lisacek, F, Fischer, H, Litsios, G, Liu, J, Lombardot, T, Mace, A, Maffioletti, S, Mahi, M-A, Maiolo, M, Majjigapu, SR, Malmstrom, L, Mangold, V, Marek, D, Mariethoz, J, Marin, R, Martin, O, Martin, X, Martin-Campos, T, Mary, C, Masclaux, F, Masson, P, Meier, C, Messina, A, Lenoir, MM, Meyer, X, Michel, P-A, Michielin, O, Milanese, A, Missiaglia, E, Perez, JM, Caria, VM, Moret, P, Moretti, S, Morgat, A, Mottaz, A, Mottin, L, Mouscaz, Y, Mueller, M, Murri, R, Mylonas, R, Neuenschwander, S, Nikitin, F, Niknejad, A, Nouspikel, N, Nso, LN, Okoniewski, M, Omasits, U, Paccaud, B, Pachkov, M, Paesano, SG, Pagni, M, Palagi, PM, Pasche, E, Payne, JL, Pedruzzi, I, Peischl, S, Peitsch, M, Perlini, S, Pilbout, S, Podvinec, M, Pohlmann, R, Polizzi, D, Potter, D, Poux, S, Pozzato, M, Pradervand, S, Praz, V, Pruess, M, Pujadas, E, Racle, J, Raschi, M, Ratib, O, Rausell, A, de Laval, VR, Redaschi, N, Rempfer, C, Ren, G, Vandati, RAR, Rib, L, Grognuz, OR, Altimiras, ER, Rivoire, C, Robin, T, Robinson-Rechavi, M, Rodrigues, J, Roechert, B, Roelli, P, Romano, V, Rossier, G, Roth, A, Rougemont, J, Roux, J, Royo, H, Ruch, P, Ruinelli, M, Rustom, M, Sates, A, Roehrig, UF, Rueeger, S, Salamin, N, Sankar, M, Sarkar, N, Saxenhofer, M, Schaeffer, M, Schaerli, Y, Schaper, E, Schmid, A, Schmid, E, Schmid, C, Schmid, M, Schmidt, S, Schmocker, D, Schneider, M, Schuepbach, T, Schwede, T, Schuetz, F, Sengstag, T, Serrano, M, Sethi, A, Shahmirzadi, O, Sigrist, C, Silvestro, D, Simao Neto, FA, Simillion, C, Simonovic, M, Skunca, N, Sluzek, K, Soneson, C, Sprouffske, K, Stadler, M, Staehli, S, Stevenson, B, Stockinger, H, Straszewski, J, Stricker, T, Studer, G, Stutz, A, Suffiotti, M, Sundaram, S, Szklarczyk, D, Szovenyi, P, Tegenfeldt, F, Teixeira, D, Tellenbach, S, Smith, AAT, Tognolli, M, Topolsky, I, Thuong, VDT, Tsantoulis, P, Tzika, AC, Agote, AU, van Nimwegen, E, von Mering, C, Varadarajan, A, Veranneman, M, Verbregue, L, Veuthey, A-L, Vishnyakova, D, Vyas, R, Wagner, A, Walther, D, Wan, HW, Wang, M, Waterhouse, R, Waterhouse, A, Wicki, A, Wigger, L, Wirapati, P, Witschi, U, Wyder, S, Wyler, K, Wuethrich, D, Xenarios, I, Yamada, K, Yan, Z, Yasrebi, H, Zahn, M, Zangger, N, Zdobnov, E, Zerzion, D, Zoete, V, Zoller, S, Bultet, LA, Aguilar-Rodriguez, J, Ahrens, CH, Ahrne, EL, Ai, N, Aimo, L, Akalin, A, Aleksiev, T, Alocci, D, Altenhoff, A, Alves, I, Ambrosini, G, Pedone, PA, Angelina, P, Anisimova, M, Appel, R, Argoud-Puy, G, Arnold, K, Arpat, B, Artimo, P, Ascencao, K, Auchincloss, A, Axelsen, K, Gerritsen, VB, Bairoch, A, Barisal, P, Baratin, D, Barbato, A, Barbie, V, Barras, D, Barreiro, M, Barret, S, Bastian, F, Batista Neto, TM, Baudis, M, Beaudoing, E, Beckmann, JS, Bekkar, AK, Cammoun, LBH, Benmohammed, S, Bernard, M, Bertelli, C, Bertoni, M, Bienert, S, Bignucolo, O, Bilbao, A, Bilican, A, Blank, D, Blatter, M-C, Blum, L, Bocquet, J, Boeckmann, B, Bolleman, JT, Bordoli, L, Bosshard, L, Boucher, G, Bougueleret, L, Boutet, E, Bovigny, C, Bratulic, S, Breuza, L, Bridge, AJ, Britan, A, Brito, F, Frazao, JB, Bruggmann, R, Bucher, P, Burdet, F, Burger, L, Cabello, EM, Gomez, RMC, Calderon, S, Cannarozzi, G, Carl, S, Casas, CC, Catherinet, S, Perier, RC, Charpilloz, C, Chaskar, PD, Chen, W, Pepe, AC, Chopard, B, Chu, HY, Civic, N, Claassen, M, Clottu, S, Colombo, M, Cosandier, I, Coudert, E, Crespo, I, Creus, M, Cuche, B, Cuendet, MA, Cusin, I, Daga, N, Daina, A, Dauvillier, J, David, F, Davydov, I, Ferreira, MDSRM, de Beer, T, de Castro, E, de Santana, C, Delafontaine, J, Delorenzi, M, Delucinge-Vivier, C, Demirel, O, Derham, R, Dermitzakis, EM, Dib, L, Diene, S, Dilek, N, Dilmi, J, Domagalski, MJ, Dorier, J, Dornevil, D, Dousse, A, Dreos, R, Duchen, P, Roggli, PD, Duperret, ID, Durinx, C, Duvaud, S, Engler, R, Frkek, S, Lopez, PE, Fstreicher, A, Excoffier, L, Fabbretti, R, Falcone, J-L, Falquet, L, Famiglietti, ML, Ferreira, A-M, Feuermann, M, Filliettaz, M, Hegel, V, Foucal, A, Franceschini, A, Fucile, G, Gaidatzis, D, Garcia, V, Gasteiger, E, Gateau, A, Gatti, L, Gaudet, P, Gaudinat, A, Gehant, S, Gfeller, D, Gharib, WH, Ghraichy, M, Gidoin, C, Gil, M, Gleizes, A, Gobeill, J, Gonnet, G, Gos, A, Gotz, L, Gouy, A, Grbic, D, Groux, R, Gruaz-Gumowski, N, Grun, D, Gschwind, A, Guex, N, Gupta, S, Getaz, M, Haake, D, Haas, J, Hatzimanikatis, V, Heckel, G, Gardiol, DFH, Hinard, V, Hinz, U, Homicsko, K, Horlacher, O, Hosseini, S-R, Hotz, H-R, Hulo, C, Hundsrucker, C, Ibberson, M, Ilmjarv, S, Ioannidis, V, Ioannidis, P, Iseli, C, Ivanek, R, Iwaszkiewicz, J, Jacquet, P, Jacquot, M, Jagannathan, V, Jan, M, Jensen, J, Johansson, MU, Johner, N, Jungo, F, Junier, T, Kahraman, A, Katsantoni, M, Keller, G, Kerhornou, A, Khalid, F, Klingbiel, D, Kimljenovic, A, Kriventseva, E, Kryuchkova, N, Kumar, S, Kutalik, Z, Kuznetsov, D, Kuzyakiv, R, Lane, L, Lara, V, Ledesma, L, Leleu, M, Lemercier, P, Lew, D, Lieberherr, D, Liechti, R, Lisacek, F, Fischer, H, Litsios, G, Liu, J, Lombardot, T, Mace, A, Maffioletti, S, Mahi, M-A, Maiolo, M, Majjigapu, SR, Malmstrom, L, Mangold, V, Marek, D, Mariethoz, J, Marin, R, Martin, O, Martin, X, Martin-Campos, T, Mary, C, Masclaux, F, Masson, P, Meier, C, Messina, A, Lenoir, MM, Meyer, X, Michel, P-A, Michielin, O, Milanese, A, Missiaglia, E, Perez, JM, Caria, VM, Moret, P, Moretti, S, Morgat, A, Mottaz, A, Mottin, L, Mouscaz, Y, Mueller, M, Murri, R, Mylonas, R, Neuenschwander, S, Nikitin, F, Niknejad, A, Nouspikel, N, Nso, LN, Okoniewski, M, Omasits, U, Paccaud, B, Pachkov, M, Paesano, SG, Pagni, M, Palagi, PM, Pasche, E, Payne, JL, Pedruzzi, I, Peischl, S, Peitsch, M, Perlini, S, Pilbout, S, Podvinec, M, Pohlmann, R, Polizzi, D, Potter, D, Poux, S, Pozzato, M, Pradervand, S, Praz, V, Pruess, M, Pujadas, E, Racle, J, Raschi, M, Ratib, O, Rausell, A, de Laval, VR, Redaschi, N, Rempfer, C, Ren, G, Vandati, RAR, Rib, L, Grognuz, OR, Altimiras, ER, Rivoire, C, Robin, T, Robinson-Rechavi, M, Rodrigues, J, Roechert, B, Roelli, P, Romano, V, Rossier, G, Roth, A, Rougemont, J, Roux, J, Royo, H, Ruch, P, Ruinelli, M, Rustom, M, Sates, A, Roehrig, UF, Rueeger, S, Salamin, N, Sankar, M, Sarkar, N, Saxenhofer, M, Schaeffer, M, Schaerli, Y, Schaper, E, Schmid, A, Schmid, E, Schmid, C, Schmid, M, Schmidt, S, Schmocker, D, Schneider, M, Schuepbach, T, Schwede, T, Schuetz, F, Sengstag, T, Serrano, M, Sethi, A, Shahmirzadi, O, Sigrist, C, Silvestro, D, Simao Neto, FA, Simillion, C, Simonovic, M, Skunca, N, Sluzek, K, Soneson, C, Sprouffske, K, Stadler, M, Staehli, S, Stevenson, B, Stockinger, H, Straszewski, J, Stricker, T, Studer, G, Stutz, A, Suffiotti, M, Sundaram, S, Szklarczyk, D, Szovenyi, P, Tegenfeldt, F, Teixeira, D, Tellenbach, S, Smith, AAT, Tognolli, M, Topolsky, I, Thuong, VDT, Tsantoulis, P, Tzika, AC, Agote, AU, van Nimwegen, E, von Mering, C, Varadarajan, A, Veranneman, M, Verbregue, L, Veuthey, A-L, Vishnyakova, D, Vyas, R, Wagner, A, Walther, D, Wan, HW, Wang, M, Waterhouse, R, Waterhouse, A, Wicki, A, Wigger, L, Wirapati, P, Witschi, U, Wyder, S, Wyler, K, Wuethrich, D, Xenarios, I, Yamada, K, Yan, Z, Yasrebi, H, Zahn, M, Zangger, N, Zdobnov, E, Zerzion, D, Zoete, V, and Zoller, S

Abstract

The SIB Swiss Institute of Bioinformatics (www.isb-sib.ch) provides world-class bioinformatics databases, software tools, services and training to the international life science community in academia and industry. These solutions allow life scientists to turn the exponentially growing amount of data into knowledge. Here, we provide an overview of SIB's resources and competence areas, with a strong focus on curated databases and SIB's most popular and widely used resources. In particular, SIB's Bioinformatics resource portal ExPASy features over 150 resources, including UniProtKB/Swiss-Prot, ENZYME, PROSITE, neXtProt, STRING, UniCarbKB, SugarBindDB, SwissRegulon, EPD, arrayMap, Bgee, SWISS-MODEL Repository, OMA, OrthoDB and other databases, which are briefly described in this article.

Published
2016

13. High antigen levels induce an exhausted phenotype in a chronic infection without impairing T cell expansion and survival

Author

Utzschneider, DT, Alfei, F, Roelli, P, Barras, D, Chennupati, V, Darbre, S, Delorenzi, M, Pinschewer, DD, Zehn, D, Utzschneider, DT, Alfei, F, Roelli, P, Barras, D, Chennupati, V, Darbre, S, Delorenzi, M, Pinschewer, DD, and Zehn, D

Abstract

Chronic infections induce T cells showing impaired cytokine secretion and up-regulated expression of inhibitory receptors such as PD-1. What determines the acquisition of this chronic phenotype and how it impacts T cell function remain vaguely understood. Using newly generated recombinant antigen variant-expressing chronic lymphocytic choriomeningitis virus (LCMV) strains, we uncovered that T cell differentiation and acquisition of a chronic or exhausted phenotype depend critically on the frequency of T cell receptor (TCR) engagement and less significantly on the strength of TCR stimulation. In fact, we noted that low-level antigen exposure promotes the formation of T cells with an acute phenotype in chronic infections. Unexpectedly, we found that T cell populations with an acute or chronic phenotype are maintained equally well in chronic infections and undergo comparable primary and secondary expansion. Thus, our observations contrast with the view that T cells with a typical chronic infection phenotype are severely functionally impaired and rapidly transition into a terminal stage of differentiation. Instead, our data unravel that T cells primarily undergo a form of phenotypic and functional differentiation in the early phase of a chronic LCMV infection without inheriting a net survival or expansion deficit, and we demonstrate that the acquired chronic phenotype transitions into the memory T cell compartment.

Published
2016

16. Inhibition of cell migration and invasion mediated by the TAT-RasGAP317–326 peptide requires the DLC1 tumor

Author

Barras, D, Lorusso, Girieca, Rüegg, Curzio, and Widmann, Christian

Abstract

TAT-RasGAP317–326, a peptide corresponding to the 317–326 sequence of p120 RasGAP coupled with a cell-permeable TAT-derived peptide, sensitizes the death response of various tumor cells to several anticancer treatments. We now report that this peptide is also able to increase cell adherence, prevent cell migration and inhibit matrix invasion. This is accompanied by a marked modification of the actin cytoskeleton and focal adhesion redistribution. Interestingly, integrins and the small Rho GTP-binding protein, which are well-characterized proteins modulating actin fibers, adhesion and migration, do not appear to be required for the pro-adhesive properties of TAT-RasGAP317–326. In contrast, deleted in liver cancer-1, a tumor suppressor protein, the expression of which is often deregulated in cancer cells, was found to be required for TAT-RasGAP317–326 to promote cell adherence and inhibit migration. These results show that TAT-RasGAP317–326, besides its ability to favor tumor cell death, hampers cell migration and invasion.

Published
2014

17. GAP-independent functions of DLC1 in metastasis

Author

Barras, D. and Widmann, C.

Abstract

Metastases are responsible for most cancer-related deaths. One of the hallmarks of metastatic cells is increased motility and migration through extracellular matrixes. These processes rely on specific small GTPases, in particular those of the Rho family. Deleted in liver cancer-1 (DLC1) is a tumor suppressor that bears a RhoGAP activity. This protein is lost in most cancers, allowing malignant cells to proliferate and disseminate in a Rho-dependent manner. However, DLC1 is also a scaffold protein involved in alternative pathways leading to tumor and metastasis suppressor activities. Recently, substantial information has been gathered on these mechanisms and this review is aiming at describing the potential and known alternative GAP-independent mechanisms allowing DLC1 to impair migration, invasion, and metastasis formation.

Published
2014

35. Inhibition of cell migration and invasion mediated by the TAT-RasGAP317-326 peptide requires the DLC1 tumor suppressor.

Author

Barras, D, Lorusso, G, Rüegg, C, and Widmann, C

Subjects
*CANCER cell migration, *TUMOR suppressor proteins, *TAT protein, *PEPTIDES, *ANTINEOPLASTIC agents, *CYTOSKELETON
Abstract

TAT-RasGAP317-326, a peptide corresponding to the 317-326 sequence of p120 RasGAP coupled with a cell-permeable TAT-derived peptide, sensitizes the death response of various tumor cells to several anticancer treatments. We now report that this peptide is also able to increase cell adherence, prevent cell migration and inhibit matrix invasion. This is accompanied by a marked modification of the actin cytoskeleton and focal adhesion redistribution. Interestingly, integrins and the small Rho GTP-binding protein, which are well-characterized proteins modulating actin fibers, adhesion and migration, do not appear to be required for the pro-adhesive properties of TAT-RasGAP317-326. In contrast, deleted in liver cancer-1, a tumor suppressor protein, the expression of which is often deregulated in cancer cells, was found to be required for TAT-RasGAP317-326 to promote cell adherence and inhibit migration. These results show that TAT-RasGAP317-326, besides its ability to favor tumor cell death, hampers cell migration and invasion. [ABSTRACT FROM AUTHOR]

Published
2014
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38. A Beta-Glucan Endo-Hydrolase from Schizosaccharomyces Pombe and Its Role in Cell Wall Growth

Author

NATIONAL RESEARCH COUNCIL OF CANADA OTTAWA (ONTARIO) BIOCHEMISTRY LAB, Barras,D. R., NATIONAL RESEARCH COUNCIL OF CANADA OTTAWA (ONTARIO) BIOCHEMISTRY LAB, and Barras,D. R.

Abstract

A beta-glucan hydrolases showing a marked specificity for beta-1,3-glucosidic linkages was found to be closely associated with the cell wall of the fission yeast Schizosaccharomyces pombe. Intact log-phase cells showed 40% of the enzyme activity measured in the cell homogenate. Cellular enzyme activity reached a maximum during the logarithmic growth phase and decreased sharply in the stationary. The possible role of the enzyme in cell wall extension in discussed. (Author)

Published
1971

39. Inhibition of cell migration and invasion mediated by the TAT-RasGAP317–326 peptide requires the DLC1 tumor

Author

Barras, D, Lorusso, Girieca, Rüegg, Curzio, Widmann, Christian, Barras, D, Lorusso, Girieca, Rüegg, Curzio, and Widmann, Christian

Abstract

TAT-RasGAP317–326, a peptide corresponding to the 317–326 sequence of p120 RasGAP coupled with a cell-permeable TAT-derived peptide, sensitizes the death response of various tumor cells to several anticancer treatments. We now report that this peptide is also able to increase cell adherence, prevent cell migration and inhibit matrix invasion. This is accompanied by a marked modification of the actin cytoskeleton and focal adhesion redistribution. Interestingly, integrins and the small Rho GTP-binding protein, which are well-characterized proteins modulating actin fibers, adhesion and migration, do not appear to be required for the pro-adhesive properties of TAT-RasGAP317–326. In contrast, deleted in liver cancer-1, a tumor suppressor protein, the expression of which is often deregulated in cancer cells, was found to be required for TAT-RasGAP317–326 to promote cell adherence and inhibit migration. These results show that TAT-RasGAP317–326, besides its ability to favor tumor cell death, hampers cell migration and invasion.

46. Tumor-reactive T cell clonotype dynamics underlying clinical response to TIL therapy in melanoma.

Author

Chiffelle J, Barras D, Pétremand R, Orcurto A, Bobisse S, Arnaud M, Auger A, Rodrigo BN, Ghisoni E, Sauvage C, Saugy D, Michel A, Murgues B, Fahr N, Imbimbo M, Ochoa de Olza M, Latifyan S, Crespo I, Benedetti F, Genolet R, Queiroz L, Schmidt J, Homicsko K, Zimmermann S, Michielin O, Bassani-Sternberg M, Kandalaft LE, Dafni U, Corria-Osorio J, Trueb L, Dangaj Laniti D, Harari A, and Coukos G

Subjects
Humans, Clone Cells, Animals, Treatment Outcome, Lymphocytes, Tumor-Infiltrating immunology, Melanoma immunology, Melanoma therapy, Immunotherapy, Adoptive methods, CD8-Positive T-Lymphocytes immunology, Receptors, Antigen, T-Cell immunology, Receptors, Antigen, T-Cell metabolism, Receptors, Antigen, T-Cell genetics
Abstract

Adoptive cell therapy (ACT) using in vitro expanded tumor-infiltrating lymphocytes (TILs) has inconsistent clinical responses. To better understand determinants of therapeutic success, we tracked TIL clonotypes from baseline tumors to ACT products and post-ACT blood and tumor samples in melanoma patients using single-cell RNA and T cell receptor (TCR) sequencing. Patients with clinical responses had baseline tumors enriched in tumor-reactive TILs, and these were more effectively mobilized upon in vitro expansion, yielding products enriched in tumor-specific CD8 + cells that preferentially infiltrated tumors post-ACT. Conversely, lack of clinical responses was associated with tumors devoid of tumor-reactive resident clonotypes and with cell products mostly composed of blood-borne clonotypes that persisted in blood but not in tumors post-ACT. Upon expansion, tumor-specific TILs lost tumor-associated transcriptional signatures, including exhaustion, and responders exhibited an intermediate exhausted effector state after TIL engraftment in the tumor, suggesting functional reinvigoration. Our findings provide insight into the nature and dynamics of tumor-specific clonotypes associated with clinical response to TIL-ACT, with implications for treatment optimization., Competing Interests: Declaration of interests G.C. has received grants, research support, or has been coinvestigator in clinical trials by Bristol-Myers Squibb, Tigen Pharma, Iovance, F. Hoffmann-La Roche AG, and Boehringer Ingelheim. The Lausanne University Hospital (CHUV) has received honoraria for advisory services G.C. has provided to Genentech, AstraZeneca AG, and EVIR. G.C. has previously received royalties from the University of Pennsylvania for CAR-T cell therapy licensed to Novartis and Tmunity Therapeutics. D.D.L., S.B., A.H., and G.C. are inventors on patent applications filed by the Ludwig Institute for Cancer Research Ltd. on behalf of the University of Lausanne and the CHUV pertaining to the subject matter disclosed herein, and such patent applications have been licensed to Tigen Pharma SA. S.Z. is currently an employee of F. Hoffmann-La Roche. O.M. has consulting/advisory roles for Bristol Myers Squibb, MSD, Roche, Novartis, Amgen, Pierre Fabre, and Neracare; research grants from Bristol Myers Squibb, MSD, Amgen, and PCL; was a consultant advisor or paid speaker for Bristol Myers Squibb, MSD, Novartis, Pierre Fabre, Amgen, and Nektar; and has received research funding from Bristol Myers Squibb and Pierre Fabre and is the cofounder of a cell therapy company called Cellula., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Published
2024
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47. Predicting Antigen-Specificities of Orphan T Cell Receptors from Cancer Patients with TCRpcDist.

Author

Perez MAS, Chiffelle J, Bobisse S, Mayol-Rullan F, Bugnon M, Bragina ME, Arnaud M, Sauvage C, Barras D, Laniti DD, Huber F, Bassani-Sternberg M, Coukos G, Harari A, and Zoete V

Subjects
Humans, Antigens, Neoplasm immunology, Lymphocytes, Tumor-Infiltrating immunology, Lymphocytes, Tumor-Infiltrating metabolism, Receptors, Antigen, T-Cell immunology, Receptors, Antigen, T-Cell metabolism, Neoplasms immunology, Neoplasms therapy
Abstract

Approaches to analyze and cluster T-cell receptor (TCR) repertoires to reflect antigen specificity are critical for the diagnosis and prognosis of immune-related diseases and the development of personalized therapies. Sequence-based approaches showed success but remain restrictive, especially when the amount of experimental data used for the training is scarce. Structure-based approaches which represent powerful alternatives, notably to optimize TCRs affinity toward specific epitopes, show limitations for large-scale predictions. To handle these challenges, TCRpcDist is presented, a 3D-based approach that calculates similarities between TCRs using a metric related to the physico-chemical properties of the loop residues predicted to interact with the epitope. By exploiting private and public datasets and comparing TCRpcDist with competing approaches, it is demonstrated that TCRpcDist can accurately identify groups of TCRs that are likely to bind the same epitopes. Importantly, the ability of TCRpcDist is experimentally validated to determine antigen specificities (neoantigens and tumor-associated antigens) of orphan tumor-infiltrating lymphocytes (TILs) in cancer patients. TCRpcDist is thus a promising approach to support TCR repertoire analysis and TCR deorphanization for individualized treatments including cancer immunotherapies., (© 2024 The Author(s). Advanced Science published by Wiley‐VCH GmbH.)

Published
2024
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48. Author Correction: Identification of clinically relevant T cell receptors for personalized T cell therapy using combinatorial algorithms.

Author

Pétremand R, Chiffelle J, Bobisse S, Perez MAS, Schmidt J, Arnaud M, Barras D, Lozano-Rabella M, Genolet R, Sauvage C, Saugy D, Michel A, Huguenin-Bergenat AL, Capt C, Moore JS, De Vito C, Labidi-Galy SI, Kandalaft LE, Dangaj Laniti D, Bassani-Sternberg M, Oliveira G, Wu CJ, Coukos G, Zoete V, and Harari A

Published
2024
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49. Identification of clinically relevant T cell receptors for personalized T cell therapy using combinatorial algorithms.

Author

Pétremand R, Chiffelle J, Bobisse S, Perez MAS, Schmidt J, Arnaud M, Barras D, Lozano-Rabella M, Genolet R, Sauvage C, Saugy D, Michel A, Huguenin-Bergenat AL, Capt C, Moore JS, De Vito C, Labidi-Galy SI, Kandalaft LE, Dangaj Laniti D, Bassani-Sternberg M, Oliveira G, Wu CJ, Coukos G, Zoete V, and Harari A

Abstract

A central challenge in developing personalized cancer cell immunotherapy is the identification of tumor-reactive T cell receptors (TCRs). By exploiting the distinct transcriptomic profile of tumor-reactive T cells relative to bystander cells, we build and benchmark TRTpred, an antigen-agnostic in silico predictor of tumor-reactive TCRs. We integrate TRTpred with an avidity predictor to derive a combinatorial algorithm of clinically relevant TCRs for personalized T cell therapy and benchmark it in patient-derived xenografts., (© 2024. The Author(s).)

Published
2024
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50. PGE 2 inhibits TIL expansion by disrupting IL-2 signalling and mitochondrial function.

Author

Morotti M, Grimm AJ, Hope HC, Arnaud M, Desbuisson M, Rayroux N, Barras D, Masid M, Murgues B, Chap BS, Ongaro M, Rota IA, Ronet C, Minasyan A, Chiffelle J, Lacher SB, Bobisse S, Murgues C, Ghisoni E, Ouchen K, Bou Mjahed R, Benedetti F, Abdellaoui N, Turrini R, Gannon PO, Zaman K, Mathevet P, Lelievre L, Crespo I, Conrad M, Verdeil G, Kandalaft LE, Dagher J, Corria-Osorio J, Doucey MA, Ho PC, Harari A, Vannini N, Böttcher JP, Dangaj Laniti D, and Coukos G

Subjects
Animals, Humans, Mice, Down-Regulation, Ferroptosis, Interleukin Receptor Common gamma Subunit biosynthesis, Interleukin Receptor Common gamma Subunit deficiency, Interleukin Receptor Common gamma Subunit metabolism, Interleukin-2 Receptor beta Subunit metabolism, Oxidative Stress, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha metabolism, Receptors, Prostaglandin E, EP2 Subtype metabolism, Receptors, Prostaglandin E, EP2 Subtype antagonists & inhibitors, Receptors, Prostaglandin E, EP4 Subtype metabolism, Receptors, Prostaglandin E, EP4 Subtype antagonists & inhibitors, TOR Serine-Threonine Kinases metabolism, Tumor Microenvironment immunology, CD8-Positive T-Lymphocytes cytology, CD8-Positive T-Lymphocytes immunology, CD8-Positive T-Lymphocytes metabolism, Cell Proliferation, Dinoprostone metabolism, Interleukin-2 antagonists & inhibitors, Interleukin-2 immunology, Interleukin-2 metabolism, Lymphocytes, Tumor-Infiltrating cytology, Lymphocytes, Tumor-Infiltrating immunology, Lymphocytes, Tumor-Infiltrating metabolism, Mitochondria metabolism, Signal Transduction
Abstract

Expansion of antigen-experienced CD8 + T cells is critical for the success of tumour-infiltrating lymphocyte (TIL)-adoptive cell therapy (ACT) in patients with cancer 1 . Interleukin-2 (IL-2) acts as a key regulator of CD8 + cytotoxic T lymphocyte functions by promoting expansion and cytotoxic capability 2,3 . Therefore, it is essential to comprehend mechanistic barriers to IL-2 sensing in the tumour microenvironment to implement strategies to reinvigorate IL-2 responsiveness and T cell antitumour responses. Here we report that prostaglandin E2 (PGE 2 ), a known negative regulator of immune response in the tumour microenvironment 4,5 , is present at high concentrations in tumour tissue from patients and leads to impaired IL-2 sensing in human CD8 + TILs via the PGE 2 receptors EP2 and EP4. Mechanistically, PGE 2 inhibits IL-2 sensing in TILs by downregulating the IL-2Rγ c chain, resulting in defective assembly of IL-2Rβ-IL2Rγ c membrane dimers. This results in impaired IL-2-mTOR adaptation and PGC1α transcriptional repression, causing oxidative stress and ferroptotic cell death in tumour-reactive TILs. Inhibition of PGE 2  signalling to EP2 and EP4 during TIL expansion for ACT resulted in increased IL-2 sensing, leading to enhanced proliferation of tumour-reactive TILs and enhanced tumour control once the cells were transferred in vivo. Our study reveals fundamental features that underlie impairment of human TILs mediated by PGE 2 in the tumour microenvironment. These findings have therapeutic implications for cancer immunotherapy and cell therapy, and enable the development of targeted strategies to enhance IL-2 sensing and amplify the IL-2 response in TILs, thereby promoting the expansion of effector T cells with enhanced therapeutic potential., (© 2024. The Author(s).)

Published
2024
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