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176 results on '"Young, K.H."'

4. Implementing an Integrated Critical Care Curriculum to Improve Resident Education in the Medical Intensive Care Unit: A Quality Improvement Project

Author

Asghar, A., primary, Allgaier, J.C., additional, Khan, S., additional, Primera, G., additional, Matta, J.G., additional, Eubank, L., additional, Young, K.H., additional, McFarland, D., additional, Quarles, R.H., additional, Garcia, C.G., additional, Tiru, B., additional, and Tidswell, M.A., additional

Published
2023
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6. A Phase II Trial of TGFβ Type I Receptor Inhibitor, Galunisertib, plus Neoadjuvant Chemoradiation in Patients with Locally Advanced Rectal Cancer

Author

Yamazaki, T., primary, Gunderson, A.J., additional, Gilchrist, M., additional, Whiteford, M., additional, Kiely, M.X., additional, Hayman, A., additional, O'Brien, D.P., additional, Ahmad, R., additional, Manchio, J.V., additional, Fox, N., additional, McCarty, K., additional, Phillips, M., additional, Brosnan, E., additional, Vaccaro, G., additional, Li, R., additional, Simon, M., additional, Bernstein, E., additional, McCormick, M., additional, Yamasaki, L., additional, Drokin, A., additional, Carnahan, T., additional, To, Y.Y., additional, Redmond, W.L., additional, Lee, B., additional, Louie, J., additional, Hansen, E.K., additional, Solhjem, M.C., additional, Cramer, J., additional, Urba, W.J., additional, Gough, M., additional, Crittenden, M.R., additional, and Young, K.H., additional

Published
2022
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9. IRF8 is a transcriptional activator of CD37 expression in diffuse large B-cell lymphoma

Author

Elfrink, S., Beest, M.B. ter, Janssen, Luuk, Baltissen, M.P.A., Jansen, P. W., Kenyon, A.N., Steen, R.M., Windt, D. de, Hagemann, P.M., Hess, C.J., Spronsen, D.J. van, Hoevenaars, B.M., Spek, E. van der, Xu-Monette, Z.Y., Young, K.H., Kaffa, C., Bervoets, S., Heek, J. van, Hesius, E.A.M., Winde, C.M. de, Vermeulen, M., Brand, M. van den, Scheijen, B., Spriel, A.B. van, Elfrink, S., Beest, M.B. ter, Janssen, Luuk, Baltissen, M.P.A., Jansen, P. W., Kenyon, A.N., Steen, R.M., Windt, D. de, Hagemann, P.M., Hess, C.J., Spronsen, D.J. van, Hoevenaars, B.M., Spek, E. van der, Xu-Monette, Z.Y., Young, K.H., Kaffa, C., Bervoets, S., Heek, J. van, Hesius, E.A.M., Winde, C.M. de, Vermeulen, M., Brand, M. van den, Scheijen, B., and Spriel, A.B. van

Abstract

Contains fulltext : 248786.pdf (Publisher’s version ) (Open Access), Diffuse large B-cell lymphoma (DLBCL) represents the most common form of non-Hodgkin lymphoma (NHL) that is still incurable in a large fraction of patients. Tetraspanin CD37 is highly expressed on mature B lymphocytes, and multiple CD37-targeting therapies are under clinical development for NHL. However, CD37 expression is nondetectable in ∼50% of DLBCL patients, which correlates with inferior treatment outcome, but the underlying mechanisms for differential CD37 expression in DLBCL are still unknown. Here, we investigated the regulation of the CD37 gene in human DLBCL at the (epi-)genetic and transcriptional level. No differences were observed in DNA methylation within the CD37 promoter region between CD37-positive and CD37-negative primary DLBCL patient samples. On the contrary, CD37-negative DLBCL cells specifically lacked CD37 promoter activity, suggesting differential regulation of CD37 gene expression. Using an unbiased quantitative proteomic approach, we identified transcription factor IRF8 to be significantly higher expressed in nuclear extracts of CD37-positive as compared with CD37-negative DLBCL. Direct binding of IRF8 to the CD37 promoter region was confirmed by DNA pulldown assay combined with mass spectrometry and targeted chromatin immunoprecipitation (ChIP). Functional analysis indicated that IRF8 overexpression enhanced CD37 protein expression, while CRISPR/Cas9 knockout of IRF8 decreased CD37 levels in DLBCL cell lines. Immunohistochemical analysis in a large cohort of primary DLBCL (n = 206) revealed a significant correlation of IRF8 expression with detectable CD37 levels. Together, this study provides new insight into the molecular mechanisms underlying differential CD37 expression in human DLBCL and reveals IRF8 as a transcriptional regulator of CD37 in B-cell lymphoma.

Published
2022

17. Immunoglobulin somatic hypermutation has clinical impact in DLBCL and potential implications for immune checkpoint blockade and neoantigen-based immunotherapies

Author

Xu-Monette, Z.Y., Li, Jianyong, Xia, Y., Crossley, Beryl, Bremel, Robert D., Miao, Yi, Krieken, J.H. van, Kirsch, Ilan, Young, K.H., Xu-Monette, Z.Y., Li, Jianyong, Xia, Y., Crossley, Beryl, Bremel, Robert D., Miao, Yi, Krieken, J.H. van, Kirsch, Ilan, and Young, K.H.

Abstract

Contains fulltext : 214157.pdf (publisher's version ) (Open Access)

Published
2019

18. PD-1/PD-L1 expression and interaction by automated quantitative immunofluorescent analysis show adverse prognostic impact in patients with diffuse large B-cell lymphoma having T-cell infiltration: a study from the International DLBCL Consortium Program

Author

Li, Ling, Sun, R., Miao, Yi, Tran, Thai, Adams, Lisa, Roscoe, Nathan, Krieken, J.H. van, Xu-Monette, Z.Y., Young, K.H., Li, Ling, Sun, R., Miao, Yi, Tran, Thai, Adams, Lisa, Roscoe, Nathan, Krieken, J.H. van, Xu-Monette, Z.Y., and Young, K.H.

Abstract

Item does not contain fulltext

Published
2019

21. HTS-based switched fiter banks and delay lines

Author

Martens, J.S., Hietala, V.M., Ginley, D.S., Tigges, C.P., Plut, T.A., Truman, J.K., Track, E.K., Young, K.H., and Young, R.T.

Subjects
Delay lines -- Research, High temperature superconductors -- Research, Filtering (Electronics) -- Research, Semiconductor switches -- Research, Microwave circuits -- Research, Business, Electronics, Electronics and electrical industries
Abstract

The utilization of thermal switches for the development of circuits for microwave signal control is discussed. Experiments were conducted to evaluate its performance regarding insertion loss, signal purity and bandwidth capacity. It was found that a trade-off in power handling and switching speed/control power requirements exists between the materials used for the circuits and their substrate dependencies.

Published
1993

23. Multiparametric MRI Measures Correlate with Treatment Response and CD8 T Cell Infiltrate in Phase II Study of Tgfβri Inhibitor with Chemoradiation in Locally Advanced Rectal Cancer

Author

Elhalawani, H., primary, He, R., additional, Yamazaki, T., additional, Gunderson, A.J., additional, Phillips, M., additional, McCarty, K., additional, McCormick, M., additional, Cochran, D., additional, Mohamed, A.S., additional, Fuller, C.D., additional, Gough, M., additional, Crittenden, M.R., additional, and Young, K.H., additional

Published
2019
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26. Concordant bone marrow involvement of diffuse large B-cell lymphoma represents a distinct clinical and biological entity in the era of immunotherapy

Author

Yao, Z., Deng, L., Xu-Monette, Z.Y., Manyam, G.C., Jain, P., Tzankov, A., Krieken, J.H.J.M. van, Cortes, J., Young, K.H., Yao, Z., Deng, L., Xu-Monette, Z.Y., Manyam, G.C., Jain, P., Tzankov, A., Krieken, J.H.J.M. van, Cortes, J., and Young, K.H.

Abstract

Contains fulltext : 189837.pdf (Publisher’s version ) (Open Access)

Published
2018

27. AKT Hyperactivation and the Potential of AKT-Targeted Therapy in Diffuse Large B-Cell Lymphoma.

Author

Wang, Jinfen, Xu-Monette, Z.Y., Jabbar, K.J., Manyam, G.C., Tzankov, A., Visco, C., Montes-Moreno, S., Dybkær, K., Bhagat, G., Hsi, E.D., Krieken, J.H. van, Ponzoni, M., Ferreri, A.J., Wang, S., Møller, M.B., Piris, M.A., Medeiros, L.J., Li, Y., Young, K.H., Wang, Jinfen, Xu-Monette, Z.Y., Jabbar, K.J., Manyam, G.C., Tzankov, A., Visco, C., Montes-Moreno, S., Dybkær, K., Bhagat, G., Hsi, E.D., Krieken, J.H. van, Ponzoni, M., Ferreri, A.J., Wang, S., Møller, M.B., Piris, M.A., Medeiros, L.J., Li, Y., and Young, K.H.

Abstract

Contains fulltext : 177844.pdf (Publisher’s version ) (Open Access)

Published
2017

28. Loss of PRDM1/BLIMP-1 function contributes to poor prognosis of activated B-cell-like diffuse large B-cell lymphoma

Author

Xia, Y., Xu-Monette, Z.Y., Tzankov, A., Li, X., Manyam, G.C., Murty, V., Bhagat, G., Zhang, S., Pasqualucci, L., Visco, C., Dybkaer, K., Chiu, A., Orazi, A., Zu, Y., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Moller, M.B., Parsons, B.M., Winter, J.N., Piris, M.A., Westin, J., Fowler, N., Miranda, R.N., Ok, C.Y., Li, Y., Li, J., Medeiros, L.J., Young, K.H., Xia, Y., Xu-Monette, Z.Y., Tzankov, A., Li, X., Manyam, G.C., Murty, V., Bhagat, G., Zhang, S., Pasqualucci, L., Visco, C., Dybkaer, K., Chiu, A., Orazi, A., Zu, Y., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Moller, M.B., Parsons, B.M., Winter, J.N., Piris, M.A., Westin, J., Fowler, N., Miranda, R.N., Ok, C.Y., Li, Y., Li, J., Medeiros, L.J., and Young, K.H.

Abstract

Contains fulltext : 173033.pdf (Publisher’s version ) (Open Access), PRDM1/BLIMP-1, a master regulator of plasma-cell differentiation, is frequently inactivated in activated B-cell-like (ABC) diffuse large B-cell lymphoma (DLBCL) patients. Little is known about its genetic aberrations and relevant clinical implications. A large series of patients with de novo DLBCL was effectively evaluated for PRDM1/BLIMP-1 deletion, mutation, and protein expression. BLIMP-1 expression was frequently associated with the ABC phenotype and plasmablastic morphologic subtype of DLBCL, yet 63% of the ABC-DLBCL patients were negative for BLIMP-1 protein expression. In these patients, loss of BLIMP-1 was associated with Myc overexpression and decreased expression of p53 pathway molecules. In addition, homozygous PRDM1 deletions and PRDM1 mutations within exons 1 and 2, which encode for domains crucial for transcriptional repression, were found to show a poor prognostic impact in patients with ABC-DLBCL but not in those with germinal center B-cell-like DLBCL (GCB-DLBCL). Gene expression profiling revealed that loss of PRDM1/BLIMP-1 expression correlated with a decreased plasma-cell differentiation signature and upregulation of genes involved in B-cell receptor signaling and tumor-cell proliferation. In conclusion, these results provide novel clinical and biological insight into the tumor-suppressive role of PRDM1/BLIMP-1 in ABC-DLBCL patients and suggest that loss of PRDM1/BLIMP-1 function contributes to the overall poor prognosis of ABC-DLBCL patients.

Published
2017

29. Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356

Author

Klionsky, D.J. Abdelmohsen, K. Abe, A. Abedin, M.J. Abeliovich, H. Arozena, A.A. Adachi, H. Adams, C.M. Adams, P.D. Adeli, K. Adhihetty, P.J. Adler, S.G. Agam, G. Agarwal, R. Aghi, M.K. Agnello, M. Agostinis, P. Aguilar, P.V. Aguirre-Ghiso, J. Airoldi, E.M. Ait-Si-Ali, S. Akematsu, T. Akporiaye, E.T. Al-Rubeai, M. Albaiceta, G.M. Albanese, C. Albani, D. Albert, M.L. Aldudo, J. Algül, H. Alirezaei, M. Alloza, I. Almasan, A. Almonte-Beceril, M. Alnemri, E.S. Alonso, C. Altan-Bonnet, N. Altieri, D.C. Alvarez, S. Alvarez-Erviti, L. Alves, S. Amadoro, G. Amano, A. Amantini, C. Ambrosio, S. Amelio, I. Amer, A.O. Amessou, M. Amon, A. An, Z. Anania, F.A. Andersen, S.U. Andley, U.P. Andreadi, C.K. Andrieu-Abadie, N. Anel, A. Ann, D.K. Anoopkumar-Dukie, S. Antonioli, M. Aoki, H. Apostolova, N. Aquila, S. Aquilano, K. Araki, K. Arama, E. Aranda, A. Araya, J. Arcaro, A. Arias, E. Arimoto, H. Ariosa, A.R. Armstrong, J.L. Arnould, T. Arsov, I. Asanuma, K. Askanas, V. Asselin, E. Atarashi, R. Atherton, S.S. Atkin, J.D. Attardi, L.D. Auberger, P. Auburger, G. Aurelian, L. Autelli, R. Avagliano, L. Avantaggiati, M.L. Avrahami, L. Azad, N. Awale, S. Bachetti, T. Backer, J.M. Bae, D.-H. Bae, J.-S. Bae, O.-N. Bae, S.H. Baehrecke, E.H. Baek, S.-H. Baghdiguian, S. Bagniewska-Zadworna, A. Bai, H. Bai, J. Bai, X.-Y. Bailly, Y. Balaji, K.N. Balduini, W. Ballabio, A. Balzan, R. Banerjee, R. Bánhegyi, G. Bao, H. Barbeau, B. Barrachina, M.D. Barreiro, E. Bartel, B. Bartolomé, A. Bassham, D.C. Bassi, M.T. Bast, R.C., Jr. Basu, A. Batista, M.T. Batoko, H. Battino, M. Bauckman, K. Baumgarner, B.L. Bayer, K.U. Beale, R. Beaulieu, J.-F. Beck, G.R., Jr. Becker, C. Beckham, J.D. Bédard, P.-A. Bednarski, P.J. Begley, T.J. Behl, C. Behrends, C. Behrens, G.M.N. Behrns, K.E. Bejarano, E. Belaid, A. Belleudi, F. Bénard, G. Berchem, G. Bergamaschi, D. Bergami, M. Berkhout, B. Berliocchi, L. Bernard, A. Bernard, M. Bernassola, F. Bertolotti, A. Bess, A.S. Besteiro, S. Bettuzzi, S. Bhalla, S. Bhattacharyya, S. Bhutia, S.K. Biagosch, C. Bianchi, M.W. Biard-Piechaczyk, M. Billes, V. Bincoletto, C. Bingol, B. Bird, S.W. Bitoun, M. Bjedov, I. Blackstone, C. Blanc, L. Blanco, G.A. Blomhoff, H.K. Boada-Romero, E. Böckler, S. Boes, M. Boesze-Battaglia, K. Boise, L.H. Bolino, A. Boman, A. Bonaldo, P. Bordi, M. Bosch, J. Botana, L.M. Botti, J. Bou, G. Bouché, M. Bouchecareilh, M. Boucher, M.-J. Boulton, M.E. Bouret, S.G. Boya, P. Boyer-Guittaut, M. Bozhkov, P.V. Brady, N. Braga, V.M.M. Brancolini, C. Braus, G.H. Bravo-San-Pedro, J.M. Brennan, L.A. Bresnick, E.H. Brest, P. Bridges, D. Bringer, M.-A. Brini, M. Brito, G.C. Brodin, B. Brookes, P.S. Brown, E.J. Brown, K. Broxmeyer, H.E. Bruhat, A. Brum, P.C. Brumell, J.H. Brunetti-Pierri, N. Bryson-Richardson, R.J. Buch, S. Buchan, A.M. Budak, H. Bulavin, D.V. Bultman, S.J. Bultynck, G. Bumbasirevic, V. Burelle, Y. Burke, R.E. Burmeister, M. Bütikofer, P. Caberlotto, L. Cadwell, K. Cahova, M. Cai, D. Cai, J. Cai, Q. Calatayud, S. Camougrand, N. Campanella, M. Campbell, G.R. Campbell, M. Campello, S. Candau, R. Caniggia, I. Cantoni, L. Cao, L. Caplan, A.B. Caraglia, M. Cardinali, C. Cardoso, S.M. Carew, J.S. Carleton, L.A. Carlin, C.R. Carloni, S. Carlsson, S.R. Carmona-Gutierrez, D. Carneiro, L.A.M. Carnevali, O. Carra, S. Carrier, A. Carroll, B. Casas, C. Casas, J. Cassinelli, G. Castets, P. Castro-Obregon, S. Cavallini, G. Ceccherini, I. Cecconi, F. Cederbaum, A.I. Ceña, V. Cenci, S. Cerella, C. Cervia, D. Cetrullo, S. Chaachouay, H. Chae, H.-J. Chagin, A.S. Chai, C.-Y. Chakrabarti, G. Chamilos, G. Chan, E.Y.W. Chan, M.T.V. Chandra, D. Chandra, P. Chang, C.-P. Chang, R.C.-C. Chang, T.Y. Chatham, J.C. Chatterjee, S. Chauhan, S. Che, Y. Cheetham, M.E. Cheluvappa, R. Chen, C.-J. Chen, G. Chen, G.-C. Chen, G. Chen, H. Chen, J.W. Chen, J.-K. Chen, M. Chen, M. Chen, P. Chen, Q. Chen, Q. Chen, S.-D. Chen, S. Chen, S.S.-L. Chen, W. Chen, W.-J. Chen, W.Q. Chen, W. Chen, X. Chen, Y.-H. Chen, Y.-G. Chen, Y. Chen, Y. Chen, Y. Chen, Y.-J. Chen, Y.-Q. Chen, Y. Chen, Z. Chen, Z. Cheng, A. Cheng, C.H.K. Cheng, H. Cheong, H. Cherry, S. Chesney, J. Cheung, C.H.A. Chevet, E. Chi, H.C. Chi, S.-G. Chiacchiera, F. Chiang, H.-L. Chiarelli, R. Chiariello, M. Chieppa, M. Chin, L.-S. Chiong, M. Chiu, G.N.C. Cho, D.-H. Cho, S.-G. Cho, W.C. Cho, Y.-Y. Cho, Y.-S. Choi, A.M.K. Choi, E.-J. Choi, E.-K. Choi, J. Choi, M.E. Choi, S.-I. Chou, T.-F. Chouaib, S. Choubey, D. Choubey, V. Chow, K.-C. Chowdhury, K. Chu, C.T. Chuang, T.-H. Chun, T. Chung, H. Chung, T. Chung, Y.-L. Chwae, Y.-J. Cianfanelli, V. Ciarcia, R. Ciechomska, I.A. Ciriolo, M.R. Cirone, M. Claerhout, S. Clague, M.J. Cl� ria, J. Clarke, P.G.H. Clarke, R. Clementi, E. Cleyrat, C. Cnop, M. Coccia, E.M. Cocco, T. Codogno, P. Coers, J. Cohen, E.E.W. Colecchia, D. Coletto, L. Coll, N.S. Colucci-Guyon, E. Comincini, S. Condello, M. Cook, K.L. Coombs, G.H. Cooper, C.D. Cooper, J.M. Coppens, I. Corasaniti, M.T. Corazzari, M. Corbalan, R. Corcelle-Termeau, E. Cordero, M.D. Corral-Ramos, C. Corti, O. Cossarizza, A. Costelli, P. Costes, S. Cotman, S.L. Coto-Montes, A. Cottet, S. Couve, E. Covey, L.R. Cowart, L.A. Cox, J.S. Coxon, F.P. Coyne, C.B. Cragg, M.S. Craven, R.J. Crepaldi, T. Crespo, J.L. Criollo, A. Crippa, V. Cruz, M.T. Cuervo, A.M. Cuezva, J.M. Cui, T. Cutillas, P.R. Czaja, M.J. Czyzyk-Krzeska, M.F. Dagda, R.K. Dahmen, U. Dai, C. Dai, W. Dai, Y. Dalby, K.N. Valle, L.D. Dalmasso, G. D'amelio, M. Damme, M. Darfeuille-Michaud, A. Dargemont, C. Darley-Usmar, V.M. Dasarathy, S. Dasgupta, B. Dash, S. Dass, C.R. Davey, H.M. Davids, L.M. Dávila, D. Davis, R.J. Dawson, T.M. Dawson, V.L. Daza, P. de Belleroche, J. de Figueiredo, P. de Figueiredo, R.C.B.Q. de la Fuente, J. De Martino, L. De Matteis, A. De Meyer, G.R.Y. De Milito, A. De Santi, M. de Souza, W. De Tata, V. De Zio, D. Debnath, J. Dechant, R. Decuypere, J.-P. Deegan, S. Dehay, B. Del Bello, B. Del Re, D.P. Delage-Mourroux, R. Delbridge, L.M.D. Deldicque, L. Delorme-Axford, E. Deng, Y. Dengjel, J. Denizot, M. Dent, P. Der, C.J. Deretic, V. Derrien, B. Deutsch, E. Devarenne, T.P. Devenish, R.J. Di Bartolomeo, S. Di Daniele, N. Di Domenico, F. Di Nardo, A. Di Paola, S. Di Pietro, A. Di Renzo, L. Di Antonio, A. Díaz-Araya, G. Díaz-Laviada, I. Diaz-Meco, M.T. Diaz-Nido, J. Dickey, C.A. Dickson, R.C. Diederich, M. Digard, P. Dikic, I. Dinesh-Kumar, S.P. Ding, C. Ding, W.-X. Ding, Z. Dini, L. Distler, J.H.W. Diwan, A. Djavaheri-Mergny, M. Dmytruk, K. Dobson, R.C.J. Doetsch, V. Dokladny, K. Dokudovskaya, S. Donadelli, M. Dong, X.C. Dong, X. Dong, Z. Donohue, T.M., Jr. Donohue-Jr, T.M. Doran, K.S. D'orazi, G. Dorn, G.W., II Dosenko, V. Dridi, S. Drucker, L. Du, J. Du, L.-L. Du, L. du Toit, A. Dua, P. Duan, L. Duann, P. Dubey, V.K. Duchen, M.R. Duchosal, M.A. Duez, H. Dugail, I. Dumit, V.I. Duncan, M.C. Dunlop, E.A. Dunn, W.A., Jr. Dupont, N. Dupuis, L. Durán, R.V. Durcan, T.M. Duvezin-Caubet, S. Duvvuri, U. Eapen, V. Ebrahimi-Fakhari, D. Echard, A. Eckhart, L. Edelstein, C.L. Edinger, A.L. Eichinger, L. Eisenberg, T. Eisenberg-Lerner, A. Eissa, N.T. El-Deiry, W.S. El-Khoury, V. Elazar, Z. Eldar-Finkelman, H. Elliott, C.J.H. Emanuele, E. Emmenegger, U. Engedal, N. Engelbrecht, A.-M. Engelender, S. Enserink, J.M. Erdmann, R. Erenpreisa, J. Eri, R. Eriksen, J.L. Erman, A. Escalante, R. Eskelinen, E.-L. Espert, L. Esteban-Martínez, L. Evans, T.J. Fabri, M. Fabrias, G. Fabrizi, C. Facchiano, A. Færgeman, N.J. Faggioni, A. Fairlie, W.D. Fan, C. Fan, D. Fan, J. Fang, S. Fanto, M. Fanzani, A. Farkas, T. Faure, M. Favier, F.B. Fearnhead, H. Federici, M. Fei, E. Felizardo, T.C. Feng, H. Feng, Y. Feng, Y. Ferguson, T.A. Fernández, Á.F. Fernandez-Barrena, M.G. Fernandez-Checa, J.C. Fernández-López, A. Fernandez-Zapico, M.E. Feron, O. Ferraro, E. Ferreira-Halder, C.V. Fesus, L. Feuer, R. Fiesel, F.C. Filippi-Chiela, E.C. Filomeni, G. Fimia, G.M. Fingert, J.H. Finkbeiner, S. Finkel, T. Fiorito, F. Fisher, P.B. Flajolet, M. Flamigni, F. Florey, O. Florio, S. Floto, R.A. Folini, M. Follo, C. Fon, E.A. Fornai, F. Fortunato, F. Fraldi, A. Franco, R. Francois, A. François, A. Frankel, L.B. Fraser, I.D.C. Frey, N. Freyssenet, D.G. Frezza, C. Friedman, S.L. Frigo, D.E. Fu, D. Fuentes, J.M. Fueyo, J. Fujitani, Y. Fujiwara, Y. Fujiya, M. Fukuda, M. Fulda, S. Fusco, C. Gabryel, B. Gaestel, M. Gailly, P. Gajewska, M. Galadari, S. Galili, G. Galindo, I. Galindo, M.F. Galliciotti, G. Galluzzi, L. Galluzzi, L. Galy, V. Gammoh, N. Gandy, S. Ganesan, A.K. Ganesan, S. Ganley, I.G. Gannagé, M. Gao, F.-B. Gao, F. Gao, J.-X. Nannig, L.G. Véscovi, E.G. Garcia-Macía, M. Garcia-Ruiz, C. Garg, A.D. Garg, P.K. Gargini, R. Gassen, N.C. Gatica, D. Gatti, E. Gavard, J. Gavathiotis, E. Ge, L. Ge, P. Ge, S. Gean, P.-W. Gelmetti, V. Genazzani, A.A. Geng, J. Genschik, P. Gerner, L. Gestwicki, J.E. Gewirtz, D.A. Ghavami, S. Ghigo, E. Ghosh, D. Giammarioli, A.M. Giampieri, F. Giampietri, C. Giatromanolaki, A. Gibbings, D.J. Gibellini, L. Gibson, S.B. Ginet, V. 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Published
2016

30. Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Author

Klionsky, D.J. Abdelmohsen, K. Abe, A. Abedin, M.J. Abeliovich, H. Arozena, A.A. Adachi, H. Adams, C.M. Adams, P.D. Adeli, K. Adhihetty, P.J. Adler, S.G. Agam, G. Agarwal, R. Aghi, M.K. Agnello, M. Agostinis, P. Aguilar, P.V. Aguirre-Ghiso, J. Airoldi, E.M. Ait-Si-Ali, S. Akematsu, T. Akporiaye, E.T. Al-Rubeai, M. Albaiceta, G.M. Albanese, C. Albani, D. Albert, M.L. Aldudo, J. Algül, H. Alirezaei, M. Alloza, I. Almasan, A. Almonte-Beceril, M. Alnemri, E.S. Alonso, C. Altan-Bonnet, N. Altieri, D.C. Alvarez, S. Alvarez-Erviti, L. Alves, S. Amadoro, G. Amano, A. Amantini, C. Ambrosio, S. Amelio, I. Amer, A.O. Amessou, M. Amon, A. An, Z. Anania, F.A. Andersen, S.U. Andley, U.P. Andreadi, C.K. Andrieu-Abadie, N. Anel, A. Ann, D.K. Anoopkumar-Dukie, S. Antonioli, M. Aoki, H. Apostolova, N. Aquila, S. Aquilano, K. Araki, K. Arama, E. Aranda, A. Araya, J. Arcaro, A. Arias, E. Arimoto, H. Ariosa, A.R. Armstrong, J.L. Arnould, T. Arsov, I. Asanuma, K. Askanas, V. Asselin, E. Atarashi, R. Atherton, S.S. Atkin, J.D. Attardi, L.D. Auberger, P. Auburger, G. Aurelian, L. Autelli, R. Avagliano, L. Avantaggiati, M.L. Avrahami, L. Azad, N. Awale, S. Bachetti, T. Backer, J.M. Bae, D.-H. Bae, J.-S. Bae, O.-N. Bae, S.H. Baehrecke, E.H. Baek, S.-H. Baghdiguian, S. Bagniewska-Zadworna, A. Bai, H. Bai, J. Bai, X.-Y. Bailly, Y. Balaji, K.N. Balduini, W. Ballabio, A. Balzan, R. Banerjee, R. Bánhegyi, G. Bao, H. Barbeau, B. Barrachina, M.D. Barreiro, E. Bartel, B. Bartolomé, A. Bassham, D.C. Bassi, M.T. Bast, R.C., Jr. Basu, A. Batista, M.T. Batoko, H. Battino, M. Bauckman, K. Baumgarner, B.L. Bayer, K.U. Beale, R. Beaulieu, J.-F. Beck, G.R., Jr. Becker, C. Beckham, J.D. Bédard, P.-A. Bednarski, P.J. Begley, T.J. Behl, C. Behrends, C. Behrens, G.M.N. Behrns, K.E. Bejarano, E. Belaid, A. Belleudi, F. Bénard, G. Berchem, G. Bergamaschi, D. Bergami, M. Berkhout, B. Berliocchi, L. Bernard, A. Bernard, M. Bernassola, F. Bertolotti, A. Bess, A.S. Besteiro, S. Bettuzzi, S. Bhalla, S. Bhattacharyya, S. Bhutia, S.K. Biagosch, C. Bianchi, M.W. Biard-Piechaczyk, M. Billes, V. Bincoletto, C. Bingol, B. Bird, S.W. Bitoun, M. Bjedov, I. Blackstone, C. Blanc, L. Blanco, G.A. Blomhoff, H.K. Boada-Romero, E. Böckler, S. Boes, M. Boesze-Battaglia, K. Boise, L.H. Bolino, A. Boman, A. Bonaldo, P. Bordi, M. Bosch, J. Botana, L.M. Botti, J. Bou, G. Bouché, M. Bouchecareilh, M. Boucher, M.-J. Boulton, M.E. Bouret, S.G. Boya, P. Boyer-Guittaut, M. Bozhkov, P.V. Brady, N. Braga, V.M.M. Brancolini, C. Braus, G.H. Bravo-San-Pedro, J.M. Brennan, L.A. Bresnick, E.H. Brest, P. Bridges, D. Bringer, M.-A. Brini, M. Brito, G.C. Brodin, B. Brookes, P.S. Brown, E.J. Brown, K. Broxmeyer, H.E. Bruhat, A. Brum, P.C. Brumell, J.H. Brunetti-Pierri, N. Bryson-Richardson, R.J. Buch, S. Buchan, A.M. Budak, H. Bulavin, D.V. Bultman, S.J. Bultynck, G. Bumbasirevic, V. Burelle, Y. Burke, R.E. Burmeister, M. Bütikofer, P. Caberlotto, L. Cadwell, K. Cahova, M. Cai, D. Cai, J. Cai, Q. Calatayud, S. Camougrand, N. Campanella, M. Campbell, G.R. Campbell, M. Campello, S. Candau, R. Caniggia, I. Cantoni, L. Cao, L. Caplan, A.B. Caraglia, M. Cardinali, C. Cardoso, S.M. Carew, J.S. Carleton, L.A. Carlin, C.R. Carloni, S. Carlsson, S.R. Carmona-Gutierrez, D. Carneiro, L.A.M. Carnevali, O. Carra, S. Carrier, A. Carroll, B. Casas, C. Casas, J. Cassinelli, G. Castets, P. Castro-Obregon, S. Cavallini, G. Ceccherini, I. Cecconi, F. Cederbaum, A.I. Ceña, V. Cenci, S. Cerella, C. Cervia, D. Cetrullo, S. Chaachouay, H. Chae, H.-J. Chagin, A.S. Chai, C.-Y. Chakrabarti, G. Chamilos, G. Chan, E.Y.W. Chan, M.T.V. Chandra, D. Chandra, P. Chang, C.-P. Chang, R.C.-C. Chang, T.Y. Chatham, J.C. Chatterjee, S. Chauhan, S. Che, Y. Cheetham, M.E. Cheluvappa, R. Chen, C.-J. Chen, G. Chen, G.-C. Chen, G. Chen, H. Chen, J.W. Chen, J.-K. Chen, M. Chen, M. Chen, P. Chen, Q. Chen, Q. Chen, S.-D. Chen, S. Chen, S.S.-L. Chen, W. Chen, W.-J. Chen, W.Q. Chen, W. Chen, X. Chen, Y.-H. Chen, Y.-G. Chen, Y. Chen, Y. 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Rogov, V.V. Rohn, T.T. Rohrer, B. Romanelli, D. Romani, L. Romano, P.S. Roncero, M.I.G. Rosa, J.L. Rosello, A. Rosen, K.V. Rosenstiel, P. Rost-Roszkowska, M. Roth, K.A. Roué, G. Rouis, M. Rouschop, K.M. Ruan, D.T. Ruano, D. Rubinsztein, D.C. Rucker, E.B., III Rudich, A. Rudolf, E. Rudolf, R. Ruegg, M.A. Ruiz-Roldan, C. Ruparelia, A.A. Rusmini, P. Russ, D.W. Russo, G.L. Russo, G. Russo, R. Rusten, T.E. Ryabovol, V. Ryan, K.M. Ryter, S.W. Sabatini, D.M. Sacher, M. Sachse, C. Sack, M.N. Sadoshima, J. Saftig, P. Sagi-Eisenberg, R. Sahni, S. Saikumar, P. Saito, T. Saitoh, T. Sakakura, K. Sakoh-Nakatogawa, M. Sakuraba, Y. Salazar-Roa, M. Salomoni, P. Saluja, A.K. Salvaterra, P.M. Salvioli, R. Samali, A. Sanchez, A.M.J. Sánchez-Alcázar, J.A. Sanchez-Prieto, R. Sandri, M. Sanjuan, M.A. Santaguida, S. Santambrogio, L. Santoni, G. Dos Santos, C.N. Saran, S. Sardiello, M. Sargent, G. Sarkar, P. Sarkar, S. Sarrias, M.R. Sarwal, M.M. Sasakawa, C. Sasaki, M. Sass, M. Sato, K. Sato, M. Satriano, J. Savaraj, N. Saveljeva, S. Schaefer, L. Schaible, U.E. Scharl, M. Schatzl, H.M. Schekman, R. Scheper, W. Schiavi, A. Schipper, H.M. Schmeisser, H. Schmidt, J. Schmitz, I. Schneider, B.E. Schneider, E.M. Schneider, J.L. Schon, E.A. Schönenberger, M.J. Schönthal, A.H. Schorderet, D.F. Schröder, B. Schuck, S. Schulze, R.J. Schwarten, M. Schwarz, T.L. Sciarretta, S. Scotto, K. Scovassi, A.I. Screaton, R.A. Screen, M. Seca, H. Sedej, S. Segatori, L. Segev, N. Seglen, P.O. Seguí-Simarro, J.M. Segura-Aguilar, J. Seiliez, I. Seki, E. Sell, C. Semenkovich, C.F. Semenza, G.L. Sen, U. Serra, A.L. Serrano-Puebla, A. Sesaki, H. Setoguchi, T. Settembre, C. Shacka, J.J. Shajahan-Haq, A.N. Shapiro, I.M. Sharma, S. She, H. Shen, C.-K.J. Shen, C.-C. Shen, H.-M. Shen, S. Shen, W. Sheng, R. Sheng, X. Sheng, Z.-H. Shepherd, T.G. Shi, J. Shi, Q. Shi, Q. Shi, Y. Shibutani, S. Shibuya, K. Shidoji, Y. Shieh, J.-J. Shih, C.-M. Shimada, Y. Shimizu, S. Shin, D.W. Shinohara, M.L. Shintani, M. Shintani, T. Shioi, T. Shirabe, K. Shiri-Sverdlov, R. Shirihai, O. Shore, G.C. Shu, C.-W. Shukla, D. Sibirny, A.A. Sica, V. Sigurdson, C.J. Sigurdsson, E.M. Sijwali, P.S. Sikorska, B. Silveira, W.A. Silvente-Poirot, S. Silverman, G.A. Simak, J. Simmet, T. Simon, A.K. Simon, H.-U. Simone, C. Simons, M. Simonsen, A. Singh, R. Singh, S.V. Singh, S.K. Sinha, D. Sinha, S. Sinicrope, F.A. Sirko, A. Sirohi, K. Sishi, B.J.N. Sittler, A. Siu, P.M. Sivridis, E. Skwarska, A. Slack, R. Slaninová, I. Slavov, N. Smaili, S.S. Smalley, K.S.M. Smith, D.R. Soenen, S.J. Soleimanpour, S.A. Solhaug, A. Somasundaram, K. Son, J.H. Sonawane, A. Song, C. Song, F. Song, H.K. Song, J.-X. Song, W. Soo, K.Y. Sood, A.K. Soong, T.W. Soontornniyomkij, V. Sorice, M. Sotgia, F. Soto-Pantoja, D.R. Sotthibundhu, A. Sousa, M.J. Spaink, H.P. Span, P.N. Spang, A. Sparks, J.D. Speck, P.G. Spector, S.A. Spies, C.D. Springer, W. Clair, D.S. Stacchiotti, A. Staels, B. Stang, M.T. Starczynowski, D.T. Starokadomskyy, P. Steegborn, C. Steele, J.W. Stefanis, L. Steffan, J. Stellrecht, C.M. Stenmark, H. Stepkowski, T.M. Stern, S.T. Stevens, C. Stockwell, B.R. Stoka, V. Storchova, Z. Stork, B. Stratoulias, V. Stravopodis, D.J. Strnad, P. Strohecker, A.M. Ström, A.-L. Stromhaug, P. Stulik, J. Su, Y.-X. Su, Z. Subauste, C.S. Subramaniam, S. Sue, C.M. Suh, S.W. Sui, X. Sukseree, S. Sulzer, D. Sun, F.-L. Sun, J. Sun, J. Sun, S.-Y. Sun, Y. Sun, Y. Sun, Y. Sundaramoorthy, V. Sung, J. Suzuki, H. Suzuki, K. Suzuki, N. Suzuki, T. Suzuki, Y.J. Swanson, M.S. Swanton, C. Swärd, K. Swarup, G. Sweeney, S.T. Sylvester, P.W. Szatmari, Z. Szegezdi, E. Szlosarek, P.W. Taegtmeyer, H. Tafani, M. Taillebourg, E. Tait, S.W.G. Takacs-Vellai, K. Takahashi, Y. Takáts, S. Takemura, G. Takigawa, N. Talbot, N.J. Tamagno, E. Tamburini, J. Tan, C.-P. Tan, L. Tan, M.L. Tan, M. Tan, Y.-J. Tanaka, K. Tanaka, M. Tang, D. Tang, D. Tang, G. Tanida, I. Tanji, K. Tannous, B.A. Tapia, J.A. Tasset-Cuevas, I. Tatar, M. Tavassoly, I. Tavernarakis, N. Taylor, A. Taylor, G.S. Taylor, G.A. Taylor, J.P. Taylor, M.J. Tchetina, E.V. Tee, A.R. Teixeira-Clerc, F. Telang, S. Tencomnao, T. Teng, B.-B. Teng, R.-J. Terro, F. Tettamanti, G. Theiss, A.L. Theron, A.E. Thomas, K.J. Thomé, M.P. Thomes, P.G. Thorburn, A. Thorner, J. Thum, T. Thumm, M. Thurston, T.L.M. Tian, L. Till, A. Ting, J.P.-Y. Ting, J.P.Y. Titorenko, V.I. Toker, L. Toldo, S. Tooze, S.A. Topisirovic, I. Torgersen, M.L. Torosantucci, L. Torriglia, A. Torrisi, M.R. Tournier, C. Towns, R. Trajkovic, V. Travassos, L.H. Triola, G. Tripathi, D.N. Trisciuoglio, D. Troncoso, R. Trougakos, I.P. Truttmann, A.C. Tsai, K.-J. Tschan, M.P. Tseng, Y.-H. Tsukuba, T. Tsung, A. Tsvetkov, A.S. Tu, S. Tuan, H.-Y. Tucci, M. Tumbarello, D.A. Turk, B. Turk, V. Turner, R.F.B. Tveita, A.A. Tyagi, S.C. Ubukata, M. Uchiyama, Y. Udelnow, A. Ueno, T. Umekawa, M. Umemiya-Shirafuji, R. Underwood, B.R. Ungermann, C. Ureshino, R.P. Ushioda, R. Uversky, V.N. Uzcátegui, N.L. Vaccari, T. Vaccaro, M.I. Váchová, L. Vakifahmetoglu-Norberg, H. Valdor, R. Valente, E.M. Vallette, F. Valverde, A.M. Van den Berghe, G. Van Den Bosch, L. van den Brink, G.R. van der Goot, F.G. van der Klei, I.J. van der Laan, L.J.W. van Doorn, W.G. van Egmond, M. van Golen, K.L. Van Kaer, L. Campagne, M.L. Vandenabeele, P. Vandenberghe, W. Vanhorebeek, I. Varela-Nieto, I. Vasconcelos, M.H. Vasko, R. Vavvas, D.G. Vega-Naredo, I. Velasco, G. Velentzas, A.D. Velentzas, P.D. Vellai, T. Vellenga, E. Vendelbo, M.H. Venkatachalam, K. Ventura, N. Ventura, S. Veras, P.S.T. Verdier, M. Vertessy, B.G. Viale, A. Vidal, M. Vieira, H.L.A. Vierstra, R.D. Vigneswaran, N. Vij, N. Vila, M. Villar, M. Villar, V.H. Villarroya, J. Vindis, C. Viola, G. Viscomi, M.T. Vitale, G. Vogl, D.T. Voitsekhovskaja, O.V. von Haefen, C. von Schwarzenberg, K. Voth, D.E. Vouret-Craviari, V. Vuori, K. Vyas, J.M. Waeber, C. Walker, C.L. Walker, M.J. Walter, J. Wan, L. Wan, X. Wang, B. Wang, C. Wang, C.-Y. Wang, C. Wang, C. Wang, C. Wang, D. 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Zhang, J. Zhang, J.-P. Zhang, L. Zhang, L. Zhang, L. Zhang, M.-Y. Zhang, X. Zhang, X.D. Zhang, Y. Zhang, Y. Zhang, Y. Zhang, Y. Zhang, Y. Zhao, M. Zhao, W.-L. Zhao, X. Zhao, Y.G. Zhao, Y. Zhao, Y. Zhao, Y.-X. Zhao, Z. Zhao, Z.J. Zheng, D. Zheng, X.-L. Zheng, X. Zhivotovsky, B. Zhong, Q. Zhou, G.-Z. Zhou, G. Zhou, H. Zhou, S.-F. Zhou, X.-J. Zhu, H. Zhu, H. Zhu, W.-G. Zhu, W. Zhu, X.-F. Zhu, Y. Zhuang, S.-M. Zhuang, X. Ziparo, E. Zois, C.E. Zoladek, T. Zong, W.-X. Zorzano, A. Zughaier, S.M.

Published
2016

31. Early safety, immune monitoring, and efficacy results from three patients enrolled in a Phase 2 trial of TGFÃŽÂ 2 RI inhibitor, LY2157299, with neoadjuvant 5-fluorouracil and radiation in patients with locally advanced rectal cancer

Author

Koguchi, Y., primary, Phillips, M., additional, McCarty, K., additional, To, Y.Y., additional, Devine, D., additional, Redmond, W.L., additional, Gough, M., additional, Crittenden, M.R., additional, and Young, K.H., additional

Published
2017
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33. ETS1 PHOSPHORYLATION AT THR38 (PETS1) IS ASSOCIATED WITH CELL OF ORIGIN (COO), CELL CYCLE ACTIVATION, AND INFERIOR OUTCOME IN DIFFUSE LARGE B CELL LYMPHOMA (DLBCL)

Author

Chung, E.Y., primary, Ponzoni, M., additional, Xu-Monette, Z.Y., additional, Cascione, L., additional, Priebe, V., additional, Gaudio, E., additional, Wang, J., additional, Zhang, J., additional, Visco, C., additional, Bhagat, G., additional, Zucca, E., additional, Rossi, D., additional, Young, K.H., additional, and Bertoni, F., additional

Published
2017
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34. RITUXIMAB, LENALIDOMIDE, AND IBRUTINIB ALONE AND COMBINED WITH CHEMOTHERAPY FOR PATIENTS WITH NEWLY DIAGNOSED DIFFUSE LARGE B-CELL LYMPHOMA

Author

Westin, J.R., primary, Fayad, L., additional, Oki, Y., additional, Nastoupil, L., additional, Hagemeister, F., additional, Turturro, F., additional, Lee, H.J., additional, Rodriguez, A., additional, Young, K.H., additional, McDonnell, T., additional, Ford, R., additional, Neelapu, S., additional, and Davis, R.E., additional

Published
2017
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35. p63 expression confers significantly better survival outcomes in high-risk diffuse large B-cell lymphoma and demonstrates p53-like and p53-independent tumor suppressor function

Author

Xu-Monette, Z.Y., Zhang, S., Li, X., Manyam, G.C., Wang, X.X., Xia, Y., Visco, C., Tzankov, A., Zhang, L., Montes-Moreno, S., Dybkaer, K., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H. van, Huh, J., Ponzoni, M., Ferreri, A.J., Zhao, X., Moller, M.B., Parsons, B.M., Winter, J.N., Piris, M.A., Medeiros, L.J., Young, K.H., Xu-Monette, Z.Y., Zhang, S., Li, X., Manyam, G.C., Wang, X.X., Xia, Y., Visco, C., Tzankov, A., Zhang, L., Montes-Moreno, S., Dybkaer, K., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H. van, Huh, J., Ponzoni, M., Ferreri, A.J., Zhao, X., Moller, M.B., Parsons, B.M., Winter, J.N., Piris, M.A., Medeiros, L.J., and Young, K.H.

Abstract

Contains fulltext : 171992.pdf (publisher's version ) (Open Access), The role of p53 family member p63 in oncogenesis is the subject of controversy. Limited research has been done on the clinical implications of p63 expression in diffuse large B-cell lymphoma (DLBCL). In this study, we assessed p63 expression in de novo DLBCL samples (n=795) by immunohistochemistry with a pan-p63-monoclonal antibody and correlated it with other clinicopathologic factors and clinical outcomes. p63 expression was observed in 42.5% of DLBCL, did not correlate with p53 levels, but correlated with p21, MDM2, p16INK4A, Ki-67, Bcl-6, IRF4/MUM-1 and CD30 expression, REL gains, and BCL6 translocation. p63 was an independent favorable prognostic factor in DLBCL, which was most significant in patients with International Prognostic Index (IPI) >2, and in activated-B-cell-like DLBCL patients with wide- type TP53. The prognostic impact in germinal-center-B-cell-like DLBCL was not apparent, which was likely due to the association of p63 expression with high-risk IPI, and potential presence of Np63 isoform in TP63 rearranged patients (a mere speculation). Gene expression profiling suggested that p63 has both overlapping and distinct functions compared with p53, and that p63 and mutated p53 antagonize each other. In summary, p63 has p53-like and p53-independent functions and favorable prognostic impact, however this protective effect can be abolished by TP53 mutations.

Published
2016

36. Assessment of CD37 B-cell antigen and cell of origin significantly improves risk prediction in diffuse large B-cell lymphoma

Author

Xu-Monette, Z.Y., Li, L, Byrd, J.C., Jabbar, K.J., Manyam, G.C., Winde, C. Maria de, Brand, M. van den, Tzankov, A., Visco, C., Wang, J, Dybkaer, K., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Huh, J., Ponzoni, M., Ferreri, A.J., Moller, M.B., Parsons, B.M., Winter, J.N., Wang, M., Hagemeister, F.B., Piris, M.A., Krieken, J.H. van, Medeiros, L.J., Li, Y., Spriel, A.B. van, Young, K.H., Xu-Monette, Z.Y., Li, L, Byrd, J.C., Jabbar, K.J., Manyam, G.C., Winde, C. Maria de, Brand, M. van den, Tzankov, A., Visco, C., Wang, J, Dybkaer, K., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Huh, J., Ponzoni, M., Ferreri, A.J., Moller, M.B., Parsons, B.M., Winter, J.N., Wang, M., Hagemeister, F.B., Piris, M.A., Krieken, J.H. van, Medeiros, L.J., Li, Y., Spriel, A.B. van, and Young, K.H.

Abstract

Contains fulltext : 171804.pdf (publisher's version ) (Closed access), CD37 (tetraspanin TSPAN26) is a B-cell surface antigen widely expressed on mature B cells. CD37 is involved in immune regulation and tumor suppression but its function has not been fully elucidated. We assessed CD37 expression in de novo diffuse large B-cell lymphoma (DLBCL), and investigated its clinical and biologic significance in 773 patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) and 231 patients treated with CHOP. We found that CD37 loss (CD37-) in approximately 60% of DLBCL patients showed significantly decreased survival after R-CHOP treatment, independent of the International Prognostic Index (IPI), germinal center B-cell-like (GCB)/activated B-cell-like (ABC) cell of origin, nodal/extranodal primary origin, and the prognostic factors associated with CD37-, including TP53 mutation, NF-kappaBhigh, Mychigh, phosphorylated STAT3high, survivinhigh, p63-, and BCL6 translocation. CD37 positivity predicted superior survival, abolishing the prognostic impact of high IPI and above biomarkers in GCB-DLBCL but not in ABC-DLBCL. Combining risk scores for CD37- status and ABC cell of origin with the IPI, defined as molecularly adjusted IPI for R-CHOP (M-IPI-R), or IPI plus immunohistochemistry (IHC; IPI+IHC) for CD37, Myc, and Bcl-2, significantly improved risk prediction over IPI alone. Gene expression profiling suggested that decreased CD20 and increased PD-1 levels in CD37- DLBCL, ICOSLG upregulation in CD37+ GCB-DLBCL, and CD37 functions during R-CHOP treatment underlie the pivotal role of CD37 status in clinical outcomes. In conclusion, CD37 is a critical determinant of R-CHOP outcome in DLBCL especially in GCB-DLBCL, representing its importance for optimal rituximab action and sustained immune responses. The combined molecular and clinical prognostic indices, M-IPI-R and IPI+IHC, have remarkable predictive values in R-CHOP-treated DLBCL.

Published
2016

37. Prognostic impact of concurrent MYC and BCL6 rearrangements and expression in de novo diffuse large B-cell lymphoma

Author

Ye, Q., Xu-Monette, Z.Y., Tzankov, A., Deng, L., Wang, X., Manyam, G.C., Visco, C., Montes-Moreno, S., Zhang, L., Dybkaer, K., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H. van, Huh, J., Ponzoni, M., Ferreri, A.J., Parsons, B.M., Moller, M.B., Piris, M.A., Winter, J.N., Medeiros, L.J., Hu, S., Young, K.H., Ye, Q., Xu-Monette, Z.Y., Tzankov, A., Deng, L., Wang, X., Manyam, G.C., Visco, C., Montes-Moreno, S., Zhang, L., Dybkaer, K., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H. van, Huh, J., Ponzoni, M., Ferreri, A.J., Parsons, B.M., Moller, M.B., Piris, M.A., Winter, J.N., Medeiros, L.J., Hu, S., and Young, K.H.

Abstract

Contains fulltext : 171272.pdf (publisher's version ) (Open Access), Double-hit B-cell lymphoma is a common designation for a group of tumors characterized by concurrent translocations of MYC and BCL2, BCL6, or other genes. The prognosis of concurrent MYC and BCL6 translocations is not well known. In this study, we assessed rearrangements and expression of MYC, BCL2 and BCL6 in 898 patients with de novo diffuse large B-cell lymphoma treated with standard chemotherapy (cyclophosphamide, doxorubicin, vincristine, and prednisone plus rituximab). Neither BCL6 translocation alone (more frequent in activated B-cell like diffuse large B-cell lymphoma) nor in combination with MYC translocation (observed in 2.0% of diffuse large B-cell lymphoma) predicted poorer survival in diffuse large B-cell lymphoma patients. Diffuse large B-cell lymphoma patients with MYC/BCL6 co-expression did have significantly poorer survival, however, MYC/BCL6 co-expression had no effect on prognosis in the absence of MYC/BCL2 co-expression, and had no additive impact in MYC+/BCL2+ cases. The isolated MYC+/BCL6+/BCL2- subset, more frequent in germinal center B-cell like diffuse large B-cell lymphoma, had significantly better survival compared with the isolated MYC+/BCL2+/BCL6- subset (more frequent in activated B-cell like diffuse large B-cell lymphoma). In summary, diffuse large B-cell lymphoma patients with either MYC/BCL6 rearrangements or MYC/BCL6 co-expression did not always have poorer prognosis; MYC expression levels should be evaluated simultaneously; and double-hit B-cell lymphoma needs to be refined based on the specific genetic abnormalities present in these tumors.

Published
2016

38. Clinical and Biologic Significance of MYC Genetic Mutations in De Novo Diffuse Large B-cell Lymphoma

Author

Xu-Monette, Z.Y., Deng, Q., Manyam, G.C., Tzankov, A., Li, L, Xia, Y., Wang, X.X., Zou, D., Visco, C., Dybkaer, K., Li, J., Zhang, L., Liang, H., Montes-Moreno, S., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Parsons, B.M., Moller, M.B., Wang, S.A., Miranda, R.N., Piris, M.A., Winter, J.N., Medeiros, L.J., Li, Y., Young, K.H., Xu-Monette, Z.Y., Deng, Q., Manyam, G.C., Tzankov, A., Li, L, Xia, Y., Wang, X.X., Zou, D., Visco, C., Dybkaer, K., Li, J., Zhang, L., Liang, H., Montes-Moreno, S., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Parsons, B.M., Moller, M.B., Wang, S.A., Miranda, R.N., Piris, M.A., Winter, J.N., Medeiros, L.J., Li, Y., and Young, K.H.

Abstract

Contains fulltext : 172126.pdf (publisher's version ) (Closed access), PURPOSE: MYC is a critical driver oncogene in many cancers, and its deregulation in the forms of translocation and overexpression has been implicated in lymphomagenesis and progression of diffuse large B-cell lymphoma (DLBCL). The MYC mutational profile and its roles in DLBCL are unknown. This study aims to determine the spectrum of MYC mutations in a large group of patients with DLBCL, and to evaluate the clinical significance of MYC mutations in patients with DLBCL treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) immunochemotherapy. EXPERIMENTAL DESIGN: We identified MYC mutations in 750 patients with DLBCL using Sanger sequencing and evaluated the prognostic significance in 602 R-CHOP-treated patients. RESULTS: The frequency of MYC mutations was 33.3% at the DNA level (mutations in either the coding sequence or the untranslated regions) and 16.1% at the protein level (nonsynonymous mutations). Most of the nonsynonymous mutations correlated with better survival outcomes; in contrast, T58 and F138 mutations (which were associated with MYC rearrangements), as well as several mutations occurred at the 3' untranslated region, correlated with significantly worse survival outcomes. However, these mutations occurred infrequently (only in approximately 2% of DLBCL). A germline SNP encoding the Myc-N11S variant (observed in 6.5% of the study cohort) was associated with significantly better patient survival, and resulted in reduced tumorigenecity in mouse xenografts. CONCLUSIONS: Various types of MYC gene mutations are present in DLBCL and show different impact on Myc function and clinical outcomes. Unlike MYC gene translocations and overexpression, most MYC gene mutations may not have a role in driving lymphomagenesis. Clin Cancer Res; 22(14); 3593-605. (c)2016 AACR.

Published
2016

39. Tetraspanin CD37 protects against the development of B cell lymphoma

Author

Winde, C.M. de, Veenbergen, S., Young, K.H., Xu-Monette, Z.Y., Wang, X.X., Xia, Y., Jabbar, K.J., Brand, M. van den, Schaaf, A. van der, Elfrink, S., Houdt, I.S. van, Gijbels, M.J., Loo, F.A. van de, Bennink, M.B., Hebeda, K.M., Groenen, P.J., Krieken, J.H. van, Figdor, C.G., Spriel, A.B. van, Winde, C.M. de, Veenbergen, S., Young, K.H., Xu-Monette, Z.Y., Wang, X.X., Xia, Y., Jabbar, K.J., Brand, M. van den, Schaaf, A. van der, Elfrink, S., Houdt, I.S. van, Gijbels, M.J., Loo, F.A. van de, Bennink, M.B., Hebeda, K.M., Groenen, P.J., Krieken, J.H. van, Figdor, C.G., and Spriel, A.B. van

Abstract

Contains fulltext : 165795.pdf (publisher's version ) (Closed access), Worldwide, B cell non-Hodgkin lymphoma is the most common hematological malignancy and represents a substantial clinical problem. The molecular events that lead to B cell lymphoma are only partially defined. Here, we have provided evidence that deficiency of tetraspanin superfamily member CD37, which is important for B cell function, induces the development of B cell lymphoma. Mice lacking CD37 developed germinal center-derived B cell lymphoma in lymph nodes and spleens with a higher incidence than Bcl2 transgenic mice. We discovered that CD37 interacts with suppressor of cytokine signaling 3 (SOCS3); therefore, absence of CD37 drives tumor development through constitutive activation of the IL-6 signaling pathway. Moreover, animals deficient for both Cd37 and Il6 were fully protected against lymphoma development, confirming the involvement of the IL-6 pathway in driving tumorigenesis. Loss of CD37 on neoplastic cells in patients with diffuse large B cell lymphoma (DLBCL) directly correlated with activation of the IL-6 signaling pathway and with worse progression-free and overall survival. Together, this study identifies CD37 as a tumor suppressor that directly protects against B cell lymphomagenesis and provides a strong rationale for blocking the IL-6 pathway in patients with CD37- B cell malignancies as a possible therapeutic intervention.

Published
2016

43. Clinical features, tumor biology, and prognosis associated with MYC rearrangement and Myc overexpression in diffuse large B-cell lymphoma patients treated with rituximab-CHOP

Author

Xu-Monette, Z.Y., Dabaja, B.S., Wang, X., Tu, M., Manyam, G.C., Tzankov, A., Xia, Y., Zhang, L., Sun, R., Visco, C., Dybkaer, K., Yin, L., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Moller, M.B., Parsons, B.M., Zhao, X., Winter, J.N., Piris, M.A., McDonnell, T.J., Miranda, R.N., Li, Y., Medeiros, L.J., Young, K.H., Xu-Monette, Z.Y., Dabaja, B.S., Wang, X., Tu, M., Manyam, G.C., Tzankov, A., Xia, Y., Zhang, L., Sun, R., Visco, C., Dybkaer, K., Yin, L., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Moller, M.B., Parsons, B.M., Zhao, X., Winter, J.N., Piris, M.A., McDonnell, T.J., Miranda, R.N., Li, Y., Medeiros, L.J., and Young, K.H.

Abstract

Contains fulltext : 152029.pdf (publisher's version ) (Closed access), MYC dysregulation, including MYC gene rearrangement and Myc protein overexpression, is of increasing clinical importance in diffuse large B-cell lymphoma (DLBCL). However, the roles of MYC and the relative importance of rearrangement vs overexpression remain to be refined. Gaining knowledge about the tumor biology associated with MYC dysregulation is important to understand the roles of MYC and MYC-associated biology in lymphomagenesis. In this study, we determined MYC rearrangement status (n=344) and Myc expression (n=535) in a well-characterized DLBCL cohort, individually assessed the clinical and pathobiological features of patients with MYC rearrangement and Myc protein overexpression, and analyzed the prognosis and gene expression profiling signatures associated with these MYC abnormalities in germinal center B-cell-like and activated B-cell-like DLBCL. Our results showed that the prognostic importance of MYC rearrangement vs Myc overexpression is significantly different in germinal center B-cell-like vs activated B-cell-like DLBCL. In germinal center B-cell-like DLBCL, MYC-rearranged germinal center B-cell-like DLBCL patients with Myc overexpression significantly contributed to the clinical, biological, and prognostic characteristics of the overall Myc-overexpressing germinal center B-cell-like DLBCL group. In contrast, in activated B-cell-like DLBCL, the occurrence, clinical and biological features, and prognosis of Myc overexpression were independent of MYC rearrangement. High Myc levels and Myc-independent mechanisms, either tumor cell intrinsic or related to tumor microenvironment, conferred significantly worse survival to MYC-rearranged germinal center B-cell-like DLBCL patients, even among Myc(high)Bcl-2(high) DLBCL patients. This study provides new insight into the tumor biology and prognostic effects associated with MYC dysregulation and suggest that detection of both MYC translocations and evaluation of Myc and Bcl-2 expression is necessary to predict

Published
2015

44. Age cutoff for Epstein-Barr virus-positive diffuse large B-cell lymphoma--is it necessary?

Author

Ok, C.Y., Ye, Q., Li, L, Manyam, G.C., Deng, L., Goswami, R.R., Wang, X., Montes-Moreno, S., Visco, C., Tzankov, A., Dybkaer, K., Zhang, L., Abramson, J., Sohani, A.R., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Zhang, S., Parsons, B.M., Xu, M., Moller, M.B., Winter, J.N., Piris, M.A., Xu-Monette, Z.Y., Medeiros, L.J., Young, K.H., Ok, C.Y., Ye, Q., Li, L, Manyam, G.C., Deng, L., Goswami, R.R., Wang, X., Montes-Moreno, S., Visco, C., Tzankov, A., Dybkaer, K., Zhang, L., Abramson, J., Sohani, A.R., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Zhang, S., Parsons, B.M., Xu, M., Moller, M.B., Winter, J.N., Piris, M.A., Xu-Monette, Z.Y., Medeiros, L.J., and Young, K.H.

Abstract

Contains fulltext : 153699.pdf (publisher's version ) (Open Access), Epstein-Barr virus-positive diffuse large B-cell lymphoma of the elderly (EBV+ DLBCL-e) is a molecularly distinct variant of DLBCL, characterized by a monoclonal B-cell proliferation that occurs in patients >50 years of age without a history or clinicopathologic evidence of immunodeficiency. However, patients with EBV+ DLBCL younger than 50-years-old also exist in Western countries. We evaluated the clinicopathologic, immunophenotypic and genetic features in Cacausian patients with EBV+ DLBCL who are 50 years. In patients who are 50 years, common expression of CD30, p50, pSTAT3 and less frequent expression of BCL6 were observed. Older patients also more commonly had a poor performance status (ECOG>/=2). Comparing EBV+ DLBCL patients in 50 years, both groups had similar clinicopathologic, immunophenotypic and genetic features. Gene expression profiling, microRNA profiling and treatment outcome of the younger patients with EBV+ DLBCL was not distinctive from tumors in older patients. Based on our data, we suggest that the arbitrary age cutoff for EBV+ DLBCL is unnecessary and should be eliminated in the WHO lymphoma classification scheme.

Published
2015

45. Clinical and biological significance of de novo CD5+ diffuse large B-cell lymphoma in Western countries

Author

Xu-Monette, Z.Y., Tu, M., Jabbar, K.J., Cao, X., Tzankov, A., Visco, C., Cai, Q., Montes-Moreno, S., An, Y., Dybkaer, K., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Zhao, X., Moller, M.B., Farnen, J.P., Winter, J.N., Piris, M.A., Miranda, R.N., Medeiros, L.J., Young, K.H., Xu-Monette, Z.Y., Tu, M., Jabbar, K.J., Cao, X., Tzankov, A., Visco, C., Cai, Q., Montes-Moreno, S., An, Y., Dybkaer, K., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Zhao, X., Moller, M.B., Farnen, J.P., Winter, J.N., Piris, M.A., Miranda, R.N., Medeiros, L.J., and Young, K.H.

Abstract

Contains fulltext : 154770.pdf (publisher's version ) (Open Access), CD5 is a pan-T-cell surface marker and is rarely expressed in diffuse large B-cell lymphoma (DLBCL). Large-scale studies of de novo CD5+ DLBCL are lacking in Western countries. In this study by the DLBCL Rituximab-CHOP Consortium, CD5 was expressed in 5.5% of 879 DLBCL patients from Western countries. CD5+ DLBCL was associated with higher frequencies of >1 ECOG performance status, bone marrow involvement, central nervous system relapse, activated B-cell-like subtype, Bcl-2 overexpression, and STAT3 and NF-kappaB activation, whereas rarely expressed single-stranded DNA-binding protein 2 (SSBP2), CD30 or had MYC mutations. With standard R-CHOP chemotherapy, CD5+ DLBCL patients had significantly worse overall survival (median, 25.3 months vs. not reached, P< .0001) and progression-free survival (median, 21.3 vs. 85.8 months, P< .0001) than CD5- DLBCL patients, which was independent of Bcl-2, STAT3, NF-kappaB and the International Prognostic Index. Interestingly, SSBP2 expression abolished the prognostic significance of CD5 expression, suggesting a tumor-suppressor role of SSBP2 for CD5 signaling. Gene-expression profiling demonstrated that B-cell receptor signaling dysfunction and microenvironment alterations are the important mechanisms underlying the clinical impact of CD5 expression. This study shows the distinctive clinical and biological features of CD5+ DLBCL patients in Western countries and underscores important pathways with therapeutic implications.

Published
2015

46. Evaluation of NF-kappaB subunit expression and signaling pathway activation demonstrates that p52 expression confers better outcome in germinal center B-cell-like diffuse large B-cell lymphoma in association with CD30 and BCL2 functions

Author

Ok, C.Y., Xu-Monette, Z.Y., Li, L, Manyam, G.C., Montes-Moreno, S., Tzankov, A., Visco, C., Dybkaer, K., Routbort, M.J., Zhang, L., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Parsons, B.M., Rao, H., Moller, M.B., Winter, J.N., Piris, M.A., Wang, S.A., Medeiros, L.J., Young, K.H., Ok, C.Y., Xu-Monette, Z.Y., Li, L, Manyam, G.C., Montes-Moreno, S., Tzankov, A., Visco, C., Dybkaer, K., Routbort, M.J., Zhang, L., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Parsons, B.M., Rao, H., Moller, M.B., Winter, J.N., Piris, M.A., Wang, S.A., Medeiros, L.J., and Young, K.H.

Abstract

Contains fulltext : 155215.pdf (publisher's version ) (Closed access), Nuclear factor-kappaB (NF-kappaB) is a transcription factor with a well-described oncogenic role. Study for each of five NF-kappaB pathway subunits was only reported on small cohorts in diffuse large B-cell lymphoma (DLBCL). In this large cohort (n=533) of patients with de novo DLBCL, we evaluated the protein expression frequency, gene expression signature, and clinical implication for each of these five NF-kappaB subunits. Expression of p50, p52, p65, RELB, and c-Rel was 34%, 12%, 20%, 14%, and 23%, whereas p50/p65, p50/c-Rel, and p52/RELB expression was 11%, 11%, and 3%, respectively. NF-kappaB subunits were expressed in both germinal center B-cell-like (GCB) and activated B-cell-like (ABC) DLBCL, but p50 and p50/c-Rel were associated with ABC-DLBCL. p52, RELB, and p52/RELB expressions were associated with CD30 expression. p52 expression was negatively associated with BCL2 (B-cell lymphoma 2) expression and BCL2 rearrangement. Although p52 expression was associated with better progression-free survival (PFS) (P=0.0170), singular expression of the remaining NF-kappaB subunits alone did not show significant prognostic impact in the overall DLBCL cohort. Expression of p52/RELB was associated with better overall survival (OS) and PFS (P=0.0307 and P=0.0247). When cases were stratified into GCB- and ABC-DLBCL, p52 or p52/RELB dimer expression status was associated with better OS and PFS (P=0.0134 and P=0.0124) only within the GCB subtype. However, multivariate analysis did not show p52 expression to be an independent prognostic factor. Beneficial effect of p52 in GCB-DLBC appears to be its positive correlation with CD30 and negative correlation with BCL2 expression. Gene expression profiling (GEP) showed that p52(+) GCB-DLBCL was distinct from p52(-) GCB-DLBCL. Collectively, our data suggest that DLBCL patients with p52 expression might not benefit from therapy targeting the NF-kappaB pathway.

Published
2015

47. Dysregulated CXCR4 expression promotes lymphoma cell survival and independently predicts disease progression in germinal center B-cell-like diffuse large B-cell lymphoma

Author

Chen, J., Xu-Monette, Z.Y., Deng, L., Shen, Q., Manyam, G.C., Martinez-Lopez, A., Zhang, L., Montes-Moreno, S., Visco, C., Tzankov, A., Yin, L., Dybkaer, K., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Zhao, X., Moller, M.B., Farnen, J.P., Winter, J.N., Piris, M.A., Pham, L., Young, K.H., Chen, J., Xu-Monette, Z.Y., Deng, L., Shen, Q., Manyam, G.C., Martinez-Lopez, A., Zhang, L., Montes-Moreno, S., Visco, C., Tzankov, A., Yin, L., Dybkaer, K., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Zhao, X., Moller, M.B., Farnen, J.P., Winter, J.N., Piris, M.A., Pham, L., and Young, K.H.

Abstract

Contains fulltext : 155086.pdf (publisher's version ) (Open Access), Abnormal expression of the chemokine receptor CXCR4 plays an essential role in tumor cell dissemination and disease progression. However, the significance of CXCR4 overexpression in de novo diffuse large B cell lymphoma (DLBCL) is unknown. In 743 patients with de novo diffuse large B cell lymphoma (DLBCL) who received standard Rituximab-CHOP immunochemotherapy, we assessed the expression of CXCR4 and dissected its prognostic significance in various DLBCL subsets. Our results showed that CXCR4+ patients was associated with male, bulky tumor, high Ki-67 index, activated B-cell-like (ABC) subtype, and Myc, Bcl-2 or p53 overexpression. Moreover, CXCR4+ was an independent factor predicting poorer progression-free survival in germinal-center B-cell-like (GCB)-DLBCL, but not in ABC-DLBCL; and in patients with an IPI of 2. The lack of prognostic significance of CXCR4 in ABC-DLBCL was likely due to the activation of p53 tumor suppressor attenuating CXCR4 signaling. Furthermore, concurrent CXCR4+ and BCL2 translocation showed dismal outcomes resembling but independent of MYC/BCL2 double-hit DLBCL. Gene expression profiling suggested that alterations in the tumor microenvironment and immune responses, increased tumor proliferation and survival, and the dissemination of CXCR4+ tumor cells to distant organs or tissues were underlying molecular mechanisms responsible for the CXCR4+ associated poor prognosis.

Published
2015

48. Resolved magnetic-field structure and variability near the event horizon of Sagittarius A(star)

Author

Johnson, M.D., Fish, V.L, Doeleman, S.S., Marrone, D.P., Plambeck, R.L., Wardle, J.F.C., Akiyama, K., Asada, K., Beaudoin, C., Blackburn, L., Blundell, R., Bower, G.C., Brinkerink, C., Broderick, A.E., Cappallo, R., Chael, A.A., Crew, G.B., Dexter, J., Dexter, M., Freund, R., Friberg, P., Gold, R., Gurwell, M.A., Ho, P.T.P., Honma, M., Inoue, M., Kosowsky, M., Krichbaum, T.P., Lamb, J., Loeb, A., Lu, R.S., MacMahon, D., McKinney, J.C., Moran, J.M., Narayan, R., Primiani, R.A., Psaltis, D., Rogers, A.E.E., Rosenfeld, K., SooHoo, J., Tilanus, R.P.J., Titus, M., Vertatschitsch, L., Weintroub, J., Wright, M., Young, K.H., Zensus, J.A., Ziurys, L.M., Johnson, M.D., Fish, V.L, Doeleman, S.S., Marrone, D.P., Plambeck, R.L., Wardle, J.F.C., Akiyama, K., Asada, K., Beaudoin, C., Blackburn, L., Blundell, R., Bower, G.C., Brinkerink, C., Broderick, A.E., Cappallo, R., Chael, A.A., Crew, G.B., Dexter, J., Dexter, M., Freund, R., Friberg, P., Gold, R., Gurwell, M.A., Ho, P.T.P., Honma, M., Inoue, M., Kosowsky, M., Krichbaum, T.P., Lamb, J., Loeb, A., Lu, R.S., MacMahon, D., McKinney, J.C., Moran, J.M., Narayan, R., Primiani, R.A., Psaltis, D., Rogers, A.E.E., Rosenfeld, K., SooHoo, J., Tilanus, R.P.J., Titus, M., Vertatschitsch, L., Weintroub, J., Wright, M., Young, K.H., Zensus, J.A., and Ziurys, L.M.

Abstract

Item does not contain fulltext

Published
2015

49. Prognostic impact of c-Rel nuclear expression and REL amplification and crosstalk between c-Rel and the p53 pathway in diffuse large B-cell lymphoma

Author

Li, L, Xu-Monette, Z.Y., Ok, C.Y., Tzankov, A., Manyam, G.C., Sun, R., Visco, C., Zhang, M., Montes-Moreno, S., Dybkaer, K., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Moller, M.B., Wang, J, Parsons, B.M., Winter, J.N., Piris, M.A., Pham, L.V., Medeiros, L.J., Young, K.H., Li, L, Xu-Monette, Z.Y., Ok, C.Y., Tzankov, A., Manyam, G.C., Sun, R., Visco, C., Zhang, M., Montes-Moreno, S., Dybkaer, K., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Moller, M.B., Wang, J, Parsons, B.M., Winter, J.N., Piris, M.A., Pham, L.V., Medeiros, L.J., and Young, K.H.

Abstract

Contains fulltext : 153743.pdf (publisher's version ) (Closed access), Dysregulated NF-kappaB signaling is critical for lymphomagenesis. The regulation, function, and clinical relevance of c-Rel/NF-kappaB activation in diffuse large B-cell lymphoma (DLBCL) have not been well studied. In this study we analyzed the prognostic significance and gene-expression signature of c-Rel nuclear expression as surrogate of c-Rel activation in 460 patients with de novo DLBCL. Nuclear c-Rel expression, observed in 137 (26.3%) DLBCL patients frequently associated with extranoal origin, did not show significantly prognostic impact in the overall- or germinal center B-like-DLBCL cohort, likely due to decreased pAKT and Myc levels, up-regulation of FOXP3, FOXO3, MEG3 and other tumor suppressors coincided with c-Rel nuclear expression, as well as the complicated relationships between NF-kappaB members and their overlapping function. However, c-Rel nuclear expression correlated with significantly poorer survival in p63+ and BCL-2- activated B-cell-like-DLBCL, and in DLBCL patients with TP53 mutations. Multivariate analysis indicated that after adjusting clinical parameters, c-Rel positivity was a significantly adverse prognostic factor in DLBCL patients with wild type TP53. Gene expression profiling suggested dysregulations of cell cycle, metabolism, adhesion, and migration associated with c-Rel activation. In contrast, REL amplification did not correlate with c-Rel nuclear expression and patient survival, likely due to co-amplification of genes that negatively regulate NF-kappaB activation. These insights into the expression, prognostic impact, regulation and function of c-Rel as well as its crosstalk with the p53 pathway underscore the importance of c-Rel and have significant therapeutic implications.

Published
2015

50. Prognostic and biological significance of survivin expression in patients with diffuse large B-cell lymphoma treated with rituximab-CHOP therapy

Author

Liu, Z., Xu-Monette, Z.Y., Cao, X., Manyam, G.C., Wang, X., Tzankov, A., Xia, Y., Li, X., Visco, C., Sun, R., Zhang, L., Montes-Moreno, S., Dybkaer, K., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Parsons, B.M., Moller, M.B., Piris, M.A., Winter, J.N., O'Malley, D.P., Medeiros, L.J., Young, K.H., Liu, Z., Xu-Monette, Z.Y., Cao, X., Manyam, G.C., Wang, X., Tzankov, A., Xia, Y., Li, X., Visco, C., Sun, R., Zhang, L., Montes-Moreno, S., Dybkaer, K., Chiu, A., Orazi, A., Zu, Y., Bhagat, G., Richards, K.L., Hsi, E.D., Choi, W.W., Krieken, J.H.J.M. van, Huh, J., Ponzoni, M., Ferreri, A.J., Parsons, B.M., Moller, M.B., Piris, M.A., Winter, J.N., O'Malley, D.P., Medeiros, L.J., and Young, K.H.

Abstract

Contains fulltext : 153740.pdf (publisher's version ) (Closed access), Survivin, a member of the inhibitor of apoptosis protein family, is overexpressed in a variety of human neoplasms. The prognostic significance of survivin expression in diffuse large B-cell lymphoma patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) is unclear. We used standard immunohistochemistry methods to quantify survivin expression in 463 patients with de novo diffuse large B-cell lymphoma who received the R-CHOP. Of the 463 patients, 269 (58%) had survivin overexpression with a cutoff of >25%, associated with an International Prognostic Index score of >2 (P=0.015), disease in >/=2 extranodal sites (P=0.011), and a high Ki-67 index (P<0.0001). Among patients with activated B cell-like disease, the overall survival rate of survivin-positive patients was significantly lower than that of survivin-negative patients (P=0.033); multivariate analysis confirmed that in these patients, survivin overexpression was an independent prognostic factor for survival. Among patients with wild-type p53 overexpression, the overall survival and progression-free survival rates of the survivin-positive group were significantly lower than those of the survivin-negative group (P=0.035 and P=0.04 respectively). In STAT3-positive patients, survivin overexpression was associated with significantly better survival. Among patients with activated B cell-like disease, survivin-positive compared with survivin-negative groups had significantly different gene expression signatures, including genes involved in mitosis or tumor cell proliferation. Our results indicate that survivin is an independent prognostic factor for poor outcome in patients with activated B cell-like disease treated with the R-CHOP regimen, and patients with survivin-positive activated B cell-like diffuse large B-cell lymphoma seem to benefit less from this treatment and may require additional novel agents.

Published
2015

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