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2. Proceedings of the Canadian Frailty Network Workshop: Identifying Biomarkers of Frailty to Support Frailty Risk Assessment, Diagnosis and Prognosis. Toronto, January 15, 2018

Author

Muscedere, John, Kim, P. M., Afilalo, J., Balion, C., Baracos, V. E., Bowdish, D., Cesari, M., Erusalimsky, J. D., Fülöp, T., Heckman, G., Howlett, S. E., Khadaroo, R. G., Kirkland, J. L., Rodriguez Mañas, L., Marzetti, E., Paré, G., Raina, P., Rockwood, K., Sinclair, A., Skappak, C., Verschoor, C., Walter, S., and Canadian Frailty Network

Published
2019
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6. Can prehabilitation during neoadjuvant treatment modulate body composition in patients with gastrointestinal cancers? An open label randomized controlled trial

Author

Velho, S., Branco, M., Capitão, C., Moço, S., Abreu, C., Alves, R., Pires, F., Borges, A., Sousa, P., Cruz, R., Agostinho, L., Costa, L., Rodrigues, S., Miranda, P., Clemente, S., Lopes, F., Godinho, J., Passos Coelho, J., Teixeira, J., Luz, G., Garrido, R., Maio, R., Baracos, V., and Cravo, M.

Published
2024
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7. The Effects of the Serious Illness Care Program (SICP) on Health Care Resource Utilization (HRU)

Author

Muscedere, John, Truelove, Amber Hastings, Stockley, Denise, Fowler, Jennifer, Barrie, Carol, Hafid, A., Guenter, D., Gallagher, E., Howard, M., You, J., Nidumolu, A., Lagrotteria, A., Motehayerarani, A., Virk, N., Sinnarajah, A., Human, T., Ying, I., Wong, H., Cummings, G., Pattullo, A., Wang, J., Lee, J., Moffat, D., Grinman, M., Montgomery, C. L., Rolfson, D. B., Stelfox, H. T., Zuege, D., Zygun, D. A., Hudson, D., Opgenorth, D., Bagshaw, S. M., Laur, C., Bell, J., Valaitis, R., Ray, S., Keller, H., Prevett, C., Fang, H., Shkredova, D., Xie, F., Zoratti, M., Gordon, C., Adachi, J., Phillips, S., Richardson, J., Tang, A., Ma, C., Riehm, L., Kendell, C., Urquhart, R., Burge, F., Kotecha, J., Martin, M., Jorgensen, M., Han, H., Dubé, D., Gutman, G., Sussman, T., DeVries, B., Gahagan, J., Brotman, S., Koo, E., Wegier, P., Embuldeniya, G., Ansari, S., Kobewka, D., O’Connor, E., Wu, P., Steinberg, L., Bell, C., Walton, T., Colstello, J., van Walraven, C., Downar, J., Wu, P. E., Costello, J., Wu, R., Frost, D., Kawaguchi, S., Mahtani, R., Toor, H., Goldman, R., Myers, J., Forster, A., Hladkowicz, E., Taljaard, M., Bryson, G., Beaulé, P. E., Gagné, S., Hamilton, G., Huang, A., Joanisse, J. A., Lavallée, L. T., MacDonald, D., Moloo, H., Thavorn, K., Yang, H., Forster, A. J., McIsaac, D. I., Sypes, E. E., de Grood, C., Parsons Leigh, J., Clement, F. M., Niven, D. J., Bitschy, A. M., Donald, E., Ewing, G., Grande, G., Sawatzky, R., Stajduhar, K. I., Parascandalo, F., Yu-Hin Siu, H., Delleman, B., Langevin, J., Mangin, D., Fang, Q., Price, D., Chan, D., Ting Wang, H., Nguyen, Q. D., Menard, C. A., Morinville, A., Hirdes, J. P., Hebert, P., Singh, J., Swinton, M., Morrison, J. M., Laur, C. V., Ebad, M., Dubin, J. A., Chen, H., Curtis, L.J., Bell, J. J., Gramlich, L. M., Keller, H. H., Dionne, J., Duan, E., Clarke, F., Hand, L., Millen, T., Sandu, G., Hodder, J., Santos, M., Shah, S., Trembley, M., Gomes, B., Leclair, L., Montroy, K., Watpool, I., Porteous, R., Acres, S., Foster, D., Auld, F., Williams, V., Marchand, J., Campisi, J., Alam, N., Lebrassier, M., Thompson, P., Hewer, T., Gilles, D., Hunt, M., Georgescu, I., Boyd, T., Lys, J., Marten, N., Campbell, E., Bentall, T., Kavikondala, K., Willems, S., Panchbhaya, Z., Booth, J., Ruddell, S., Richter, B., Tassy, D., Jesso, R., Marinoff, N., Perez, A., Kaur, N., Campbell, T., Lizotte, P., Lavoie, L., Dionne, M., Saunders, L., Zytaruk, N., Heels-Ansdell, D., Johnstone, J., Cook, D., Quinn, K. L., Campitelli, M. A., Diong, C., Daneman, N., Stall, N., Morris, A. M., Detsky, A. S., Jeffs, L., Maxwell, C. J., Bell, C. M., Bronskill, S. E., Alghamdi, M., Baracos, V., Karvellas, C., Churchill, T., Khadaroo, R. G., Moorhouse, P., Sampalli, T., Bedford, L., Edwards, L., Gibson, R., Mallery, L., Taylor, D., Warner, G., Harnish, A., Law, V., Lawson, B. J., Wood, S., Buckler, M., Fernandes, P., Elliott, J., Stolee, P., Ali, G., Dunichand-Hoedl, A., Salim, S. Y., Mazurak, V. C., Baracos, V. E., Heckman, G. A., Hebert, P. C., Costa, A. P., Arthur, S. A., Jones, A., Salam-White, L., Tanner, D., Negm, A. M., Kennedy, C. C., Ioannidis, G., Gajic-Veljanoski, O., Thabane, L., Adachi, J. D., Marr, S., Lau, A., Atkinson, S., Petruccelli, D., DeBeer, J., Winemaker, M., Avram, V., Williams, D., Armstrong, D., Lumb, B., Panju, A., Papaioannou, A., Boucher, A., Haesebaert, J., Freitas, A., Adekpedjou, R., Landry, M., Bourassa, H., Dawn, S., Croteau, J., Légaré, F., Takaoka, A. M., Clarke, F. J., Shears, M. S., Muscedere, J., Cook, D. J., Lee, A., Bouchard, D. R., Sénéchal, M., Mayo, A., Hrubeniuk, T. J., Keshavarz, M., Robertson, C., Read, E. A., Norris, C M., Meyer, S. R., Zibdawi, M., Marshall, H. D., Moody, E. M., Martin-Misener, R., Hawken, E. R., Boyd, J. G., Im, J., Mak, S., Upshur, R., Steinbreg, L., Kuluski, K., Van Damme, J., Delvin, M-E., Medves, J., Woddhouse, K., Sakamoto, M. L., Durepos, P., Ploeg, J., Akhtar-Danesh, N., Punia, H., Kaasalainen, S., Hewston, P., Kennedy, C., Merom, D., Patterson, C., Sztramko, R., Trainor, L., Grenier, A., Woolhouse, M., Petrella, A.F.M., Heath, M., Hyland, B., Fan, M., Hamilton, M., Reding, R., Trbovich, P., O’Reilly, D. M., O’Donnell, S., Bruning, P., Donovan, J., Anoveros-Barrera, A., Coletta, G., Jakubowski, J., Pritchard, J. M., Werner, G. E., Hoben, M., Estabrooks, C. A., Leaker, H. R., Holroyd-Leduc, J., Fox, L., Smallbone, J., Stinchcombe, A., Wilson, K., Kortes-Miller, K., Rees-Milton, K. J., Hulbert, M., Turner, M. E., Berger, C., Anastassiades, T. P., Hopman, W. M., Adams, M. A., Powley, W. L., Holden, R. M., Grewal, K., Sheets, D., Smith, A. P., Trites, M., Kennedy, M., MacDonald, S., Sivarajah, L., Lamarche, L., Giangregorio, A., Radcliffe, S., Ioannidi, G., Negm, A., Connolly, M. S., Klein, J. M., Huber, J. S., Safaraz, S., Foster, A. J., Simpson, J. A., Brunt, K.R., Elfassy, M. D., Munshi, L., Mehta, N., Martinez Guasch, F., Kamen, C., Burry, L., Soong, C., Mehta, S., McKay, S., Yetman, L., Slayter, J., McCollum, A., McGibbon, C. A., Jarrett, P., Robinson, B., Kolyvas, A., McCloskey, R., Gionet, S., Scheme, E., Harris, B., D’Aoust, T. R., Shao, T., Egan, R., Muscedere, J. G., Milne, B., Fitzpatrick, M., Yingwei Peng, P., Parlow, J., and Johnson, A. P.

Subjects
Abstracts
Published
2019

14. Validation of the Consensus-Definition for Cancer Cachexia and evaluation of a classification model—a study based on data from an international multicentre project (EPCRC-CSA)

Author

Blum, D., Stene, G. B., Solheim, T. S., Fayers, P., Hjermstad, M. J., Baracos, V. E., Fearon, K., Strasser, F., Kaasa, S., Block Lieve, Van den, Koen, Meeussen, Sarah, Brearley, Augusto, Caraceni, Joachim, Cohen, Massimo, Costantini, Anneke, Francke, Richard, Harding, Higginson Irene, J, Stein, Kaasa, Karen, Linden, Guido, Miccinesi, Bregje, Onwuteaka-Philipsen, Koen, Pardon, Roeline, Pasman, Sophie, Pautex, Sheila, Payne, and Luc, Deliens

Published
2014
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22. INTRODUCTION

Author

Muscedere, John, Bebenek, Sarah Grace, Stockley, Denise, Kinderman, Laura, Barrie, Carol, Salim, S., Warkentin, L., Gallivan, A., Churchill, T., Baracos, V., Khadaroo, R., McCullough, J., Keller, H., Vesnaver, E., Marcus, H., Lister, T., Nasser, R., Belley, L., Laur, C., Gainer, R., Moorhouse, P., Mallery, L., Hirsch, G., Hamilton, G., Wheeler, K., Di Michelle, J., Lalu, M.M, McIsaac, D. I, Mallery, K., Theou, O., Goldstein, J., Armstrong, J., Webb, J., Greene, J., Doyle, E., Douglas, B., Lee, J., Rockwood, K., Whitty, R., Koo, E., Porter, S., Battu, K., Kalocsai, C., Reid, J., Kho, M., Molloy, A., Herridge, M. S, Karachi, T., Fox-Robichaud, A., Koo, K. KY, Lo, V., Mathur, S., McCaughan, M., Pellizzari, J., Rudkowski, J., Figueiredo, S., Morais, J., Mayo, N., Meffen, K., Penner, C., Meyyappan, R., Sandoval, R., Broderick, J., Hoffer, A., Chambers, S., Ball, I., Martin, C., Awan, S., Rajji, T., Uranis, C., Kim, D., Burhan, A., Ting, R., Ito, H., Graff, A., Gerretsen, P., Woo, V., Mulsant, B., Davies, S., Paul, L. Read, Spice, R., Sinnarajah, A., Ho, G., Webb, M., Uniacke, J., Linsey, J., Kettle, J., Salmon, C., Mohammed, R., Whitby, C., Cowie, B., Wang, S., Sawatzky, R., Chan, E., Wolfs, D., Harding, W., Laforest, E., Schick-Makaroff, K., King, G., Cohen, S. R., Neufeld, C., Lett, J., Voth, J., Durepos, P., Wickson-Griffiths, A., Hazzan, A. Abiola, Kaasalainen, S., Vastis, V., Battistella, L., Papaioannou, A., Asselin, G., Klein, D., Tan, A., Kendell, C., Burge, F., Kotecha, J., Marshall, E., Cash, C., Tschupruk, C., Urquhart, R., Cottrell, L., Erbacker, L., Pesut, B., Duggleby, W., Bui, M., Te, A., Brazil, E., Sussman, T., Team, SPA-LTC, Delicaet, K., MacDonald, J., Hartwick, M., des Ordons, A. Roze, Myers, J., Pereira, J., Simon, J., Abdul-Razzak, A., Sharma, A., Ogilvie, L., Downar, J., Choukou, M.A., Holroyd-Leduc, J. M., Kazanjian, A., Durand, P. J, Straus, S. E, Légaré, F., Turgeon, A. F., Tourigny, A., Dumont, S., Mc Giguere, A., Lounsbury, K., Friesen, D., Bitschy, A., Donald, E. E, Stajduhar, K., Knapp, A., Klinger, C., Wentlandt, K., Urowitz, S., Walton, T., Chahal, M., Zwicker, V., Cohen, T., Morales, M. López, Miller, K., Duggan, K., Barnett-Cowan, M., Kortes-Miller, K., Kelley, M. Lou, Nayfeh, A., Marcoux, I., Jutai, J., Virag, O., Khakoo, A., Incardona, N., Workentin, K., Maxwell, C., Stock, K., Hogan, D. B., Tyas, S. L., Bronskill, S. E., Morris, A. M., Bell, C. M., Jeffs, L., Gandhi, S., Blain, J., Toubasi, S., Andrew, M., Ashe, M., Atkinson, E., Ayala, A. P., Bergman, H., Ploeg, J., McGilton, K., Patten, S. B., Maxwell, C. J., Delleman, B., Chan, D., Siu, H., Howard, M., Mangin, D., Akioyamen, L., Hoben, M., Estabrooks, C., McArthur, C., Gibbs, J. C., Patel, R., Neves, P., Killingbeck, J., Hirdes, J., Milligan, J., Berg, K., Giangreogrio, L., Adekpedjou, R., Stacey, D., Brière, N., Freitas, A., Marjolein, M., Garvelink, Turcotte, S., Heyer, M., Boscart, V., Heckman, G., Zahradnik, M., Jeffs, L. P., Mainville, C., Maione, M., Morris, A., Bell, C., Bronskill, S., Tscheng, D., Sever, L., Hyland, S., Emond, J., Garvelink, M., Menear, M., MacLeod, T., LeBlanc, C., Allen, M., McLean-Veysey, P., Rodney-Cail, N., Steeves, B., Bezanson, E., Van Ooteghem, K., Trinh, A., Cowan, D., Kwok, L., Fels, D., Meza, M., Fels-Leung, S., Ouellette-Kuntz, H., McKenzie, K., Martin, L., Bark, D., Hanafi, S., Gibson, W., Wagg, A., Tanel, M., Laing, A., Weaver, T., Lupo, J., Giangregorio, L., Payne, A., Sheets, D., Beach, C., Elliott, J., Stolee, P., Stinchcombe, A., Bédard, M., Enright, J., Wilson, K., Ozen, L., Silman, J., Gibbons, C., McKinnon, T., Timble, J., Willison, K., Boland, L., Perez, M. Margarita Becerra, McIsaac, D., Edmond, J., Brown, K., Leigh, J. Parsons, Buchner, D., Stelfox, H. T., Aziz, J., Crake, D., Ren, Z., Grant, T., Goubran, R., Knoefel, F., Sveistrup, H., Bilodeau, M., Oliver, J., Chidwick, P., Booi, L., Magyar, T., Martin, M., Ko, J. Hyun, Shannon, J., Wilson-Pease, E., Kephart, G., Babin, N., Malik, H., Maximos, M., Seng, S., Vandenberg, G., Dal Bello-Haas, V., Lagrotteria, A., Sullivan, K., Mihaylova, A., Lu, C., Koh, J., Hamielec, C., Steer, M., Jimenez, C., Woo, K., Julian, P., Martin, L. Schindel, McLelland, V., Ryan, D., Wilding, L., Chang, C. E., van Schooten, K. S, Wong, F., Robinovitch, S. N, Balasubramanaiam, B., Chenkin, J., Snider, T. G., Melady, D., Lee, J. S., Petrella, A., Heath, M., Shellington, E., Laguë, A., Voyer, P., Ouellet, M., Boucher, V., Pelletier, M., Gouin, É., Daoust, R., Berthelot, S., Giroux, M., Sirois, M., Émond, M., Bergstrom, V., Tate, K., Lee, S., Reid, C., Rowe, B., Cummings, G., Holroyd-Leduc, J., El-Bialy, R., Zhao, B., Baumbusch, J., Busson, C., Kohr, R., Donovan, J., Philpott, K., Kingston, J., Rickards, T., Weiler, C., Lanovaz, J., Arnold, C., Chiu, K., Cuperfain, A., Zhu, K., Zhao, X., Zhao, S., Iaboni, A., Perrella, A., Chau, V., Hu, C. Dong, Farooqi, M., Patel, S., Bauer, J., Lee, L., Schill, C., Patel, T., Mroz, L., Kryworuchko, J., Carter, R., Spencer, L., Barwich, D., Roy, N., Després, C., Leyenaar, M., McLeod, B., Poss, J., Costa, A., Blums, J., Costa, I. Geraldina, Tregunno, D., Kirkham, J., Seitz, D., Velkers, C., Krawczyk, M., Garland, E., Michaud, M., Pakzad, S., Bourque, P. E., Eamer, G., Gibson, J. A, Gillis, C., Hsu, A. T, MacDonald, E., Whitlock, R., Khadaroo, R. G, Brisebois, R., Clement, F., Hathaway, J., Bagheri, Z. S., Costa, I. G., Schinkel-Ivy, A., Rodney, P. (Paddy), Varcoe, C., Jiwani, B., Fenton, T., Gramlich, L., Tangri, N., Eng, F., Bohm, C., Komenda, P., Rigatto, C., Brar, R., McCloskey, R., Keeping-Burke, L., Donovan, C., Verma, A., Razak, F., Kwan, J., Lapointe-Shaw, L., Rawal, S., Tang, T., Weinerman, A., Guo, Y., Mamdani, M., McNicholl, T., Valaitis, R., Tarraf, R., Boakye, O., Suter, E., Boulanger, P., Birney, A., Sadowski, C. A, Gill, G., Mrklas, K., Plaisance, A., Noiseux, F., Francois, R., LeBlanc, A., McGinn, C. A., Tapp, D., Archambault, P. M., Begum, J., Wikjord, N., Roy, P., Reimer-Kirkham, S., Doane, G., Hilliard, N., Giesbrech, M., Dujela, C., Harerimana, B., Forchuk, C., Booth, R., Vasudev, A., Isaranuwatchai, W., Seth, P., Ramsey, D., Rudnick, A., Heisel, M., Reiss, J., Lee, E., Mate, K., Aubertin-Leheude, M., Fiore, J., Auais, M., Moriello, C., Scott, S., Wilson, M., McDonald, E., Lee, T., Arora, N., Hanvey, L., Elston, D., Heyland, R., Heyland, D., Langevin, J., Fang, Q., Price, D., Nowak, C., Fang, H., Richardson, J., Phillips, S., Gordon, C., Xie, F., Adachi, J., Tang, A., Swinton, M., Winhall, M., Clark, B., Sinuff, T., Abelson, J., You, J., Shears, M., Takaoka, A., Tina, M., Amanda, H., Surenthar, T., Li, G., Rochwerg, B., Woo, T., Bagshaw, S., Johnstone, J., Cook, D., Beaton, D., Drance, E., Leblanc, M.E., O’Connor, D., Ono, E., Phinney, A., Reid, R. C., Rodney, P. A., Tait, J., Ward-Griffin, C., Millen, T., Clarke, F., Thabane, L., Dogba, M. J., Rivest, L.l, Durand, P. J., Fraser, K., Bourassa, H., Embuldeniya, G., Farmanova, E., Auguste, D., Witteman, H. O, Kröger, E., Beaulieu, É., MC Giguere, A., Paragg, J., Swindle, J., Webber, T., Porterfield, P., Husband, A., Kryworucko, J., Trenaman, L., Bryan, S., Cuthbertson, L., Bansback, N., de Grood, C., Dodek, P., Fowler, R., Forster, A., Boyd, J., Stelfox, H., Kruger, S., Steinberg, M., Quinn, K., Yarnell, C., Fu, L., Manuel, D., Tanuseputro, P., Stukel, T., Pinto, R., Scales, D., Laupacis, A., Varughese, R., Huang, A., Famure, O., Chowdhury, N., Renner, E., Kim, J., MacIver, J., Singer, L., Gali, B., Brewster, P., Asche, C., Mitz, A., Hundza, S., MacDonald, S., Kaechele, N., Donald, E., Kaur, S., Fernandes, P., Pauloff, K., Gordon, A., Kallan, L., Grinman, M., Human, T., Ying, I., Pattullo, A., Wong, H., Feldman, S., Moffat, D., Zjadewicz, K., McIntosh, C. J., Alghamdi, M., McComb, A., Ferrone, A., Geng, W., Weeks-Levy, C., and Menon, C.

Subjects
Abstracts, Canadian Frailty Network Abstracts from the Meeting in Toronto, September 27–29, 2015, Canadian Frailty Network Abstracts from the Meeting Held in Toronto, April 23–24, 2017
Published
2017

26. 1-03 Role of Activin A in human cancer cachexia (ACTICA study)

Author

Baracos, Vickie, Muscaritoli, Maurizio, Aversa, Zaira, Rossi Fanelli, Filippo, Loumaye, A, de Barsy, M, Nachit, M, Frateur, L, Lause, P, Van Maanen, A, Thissen, JP, Awasthi, R, Gillis, C, Liberman, S, Stein, B, Charlebois, P, Carli, F, Ahmad, Sultan, Chiche, Dan, Reza Kazemi-Bajestani, Seyyed Mohammad, Becher, Harald, Venner, Peter, North, Scott, Vickie, Baracos, Li, Yi-Ping, Zhang, Guohua, Ma, Jennifer, Hall, Derek, Patel, Devang, Robinson, Samantha, Di Marco, Sergio, Gallouzi, Imed-Eddine, Sartori, Roberta, Penna, Fabio, Costelli, Paola, Sandri, Marco, Gregorevic, Paul, Toth, Michael J, Miller, Mark S, Callahan, Damien M, Couch, Marion E, Dittus, Kim, Sharma, Mridula, Argilés, Josep M, Bedard, N, Wiles, B, Jammoul, S, Miao, M, Wykes, L, Coyne, E, Hallauer, PL, Hastings, KEM, Stretch, C, Baracos, VE, Chevalier, S, Wing, SS, Marchildon, François, Lala, Neena, St-Louis, Catherine, Wiper-Bergeron, Nadine, Santos Silva, Kleiton Augusto, Dong, Jiangling, Tweardy, David J, Mitch, William E, Zhang, Liping, Hall, Derek T, Ma, Jennifer F, Griss, Takla, Jones, Russell G, Marco, Sergio Di, Marks, Daniel L, Rudnicki, Michael A, Laine, Aaron, Narayanan, Sriram, Choy, Hak, Girard, Luc, Gazdar, Adi, Minna, John, Infante, Rodney, Iyengar, Puneeth, Petruzzelli, Michele, Schweiger, Martina, Rincon, Mercedes, Robertson, Graham, Zechner, Rudolf, Wagner, Erwin F, Pin, Fabrizio, Costamagna, Domiziana, Camperi, Andrea, Sampaolesi, Maurilio, He, Wei, Talbert, Erin, Londhe, Priya, Bloomston, Mark, Croce, Carlo, Guttridge, Denis, Breit, Samuel N, Tsai, Vicky WW, Manandhar, Rakesh, Lin, Shu, Sainsbury, Amanda, Brown, David A, Ferrara, Michele, Reano, Simone, Angelino, Elia, Sabry, Omar, Filigheddu, Nicoletta, Graziani, Andrea, Tsoli, Maria, Allen, John, Taylor, Ryland, Scwheiger, Martina, Swarbrick, Michael M, Ehteda, Anahid, Miekle, Peter, Molloy, Mark, Waning, David L, Mohammad, Khalid S, Reiken, Steven, Xie, Wenjun, Marks, Andrew R, Guise, Theresa A, Moya, Rosita, Zhao, Chunfang, Davies, Joanna D, Carson, James, Everett Couch, Marion, Stecher, Michael, El Mouelhi, Mohamed, Tseng, Yu-Chou, Kulp, Samuel K, Lai, I-Lu, Hsu, En-Chi, He, Wei A, Frankhouser, David E, Yan, Pearlly S, Mo, Xiaokui, Lesinski, Gregory B, Marcucci, Guido, Guttridge, Denis C, Bekaii-Saab, Tanios, Chen, Ching-Shih, Haddad, AHI Al, Al-Azwani, EK, Mahamoud, Y, Safi, F, Salhat, H El, Malek, JA, Adrian, TE, Fearon, K, Temel, J, Currow, D, Gleich, L, Friend, J, Abernethy, A, Garcia, Jose M, Dubé, A, Patoine, D, Lemire, BB, Thériault, M-E, Ribeiro, F, Debigaré, R, Maltais, F, Smuder, Ashley J, Min, Kisuk, Kwon, Oh-Sung, Wiggs, Michael P, Sollanenk, Kurt J, Christou, Demetra D, Yoo, Jeung-Ki, Hwang, Moon-Hyon, Szeto, Hazel H, Kavazis, Andreas N, Powers, Scott K, Kroenke, Candyce H, Meyerhardt, Jeffrey A, Kwan, Marilyn L, Prado, Carla, Xiao, Jingjie, Weltzien, Erin, Castillo, Adrienne, Caan, Bette J, Guan, Chen, Giles, Kaitlin, Wing, Simon, Mazurak, Vera, Jagoe, R Thomas, Wiles, Benjamin, Miao, Miao, Coyne, Erin, Larose, Louise, Cybulsky, Andrey V, Wing, Simon S, Marino, Francesco Elia, Risbridger, Gail, Gold, Elspeth, Segatto, Marco, Fittipaldi, Raffaella, Caretti, Giuseppina, Lee, Hwabin, Fu, Dechen, Dwarkasing, JT, Boekschoten, MV, Argilès, JM, van Dijk, M, Busquets, S, Penna, F, Toledo, M, Laviano, A, Witkamp, RF, van Norren, K, Bédard, Nathalie, Plourde, Marie, Chevalier, Stéphanie, Lala-Tabbert, Neena, Marchildon, Francois, Torabi, S, Glare, P, Plodkowski, A, Margaron, Yoran, Fernandes, Mathieu, Morales, Delphine, Poydenot, Pauline, Menager, Pauline, Fuchs, Alexandra, Degot, Sébastien, Calore, Federica, Canella, Alessandro, Croce, Carlo M, Srinivasan, Kalayarasan, Pulliparracharuvil, Suprabha, Meyer, Jeffrey, Scherer, Philipp E, Kambadur, Ravi, Martinelli, Giulia B, Talamini, Laura, Previdi, Sara, Piccirillo, Rosanna, Jafri, Syed H, Previgliano, Carlos, Khandelwal, Keerti, Shi, Runhua, Mills, Glenn, Amato, Robert, Coats, Valérie, Ribeiro, Fernanda, Tremblay, Lise, Lacasse, Yves, Maltais, François, Saey, Didier, AL Vigano, Antonio, Ciutto, Lorella, Tomasso, Jonathan Di, Kilgour, Robert D, Morais, José A, Borod, Manuel, Almasud, A, Giles, K, Baracos, V, Guan, L, Mazurak, V, Khanuja, Jasleen, Gresham, Gillian, Osipov, Arsen, Tan, Carlyn-Rose, Tuli, Richard, Hendifar, Andrew, Narasimhan, Ashok, Greiner, Russell, Yasui, Yutaka, Bathe, Oliver, Fearon, Kenneth, Damaraju, Sambasivarao, Banh, Taylor, Kliewer, Kara, Hsiao, Yung-Hsuan, Belury, Martha A, Caan, Bette, Quesenberry, Charles, Kwan, Marilyn, Prado, Carla MM, Baracos, Vickie E, Birdsell, Laura, Stuyckens, Kim, Park, Youn Choi, Parekh, Trilok, Sawyer, Michael B, Wu, C, Fernandez, SA, Criswell, T, Chidiac, T, Guttridge, D, Villalona-Calero, M, Bekaii-Saab, T, Khan, Sarah, ALVigano, Antonio, Matos-Neto, EM, Figuerêdo, RG, Camargo, RG, Lima, JDCC, Alves, MJ, Riccardi, D, Alcantara, PS, Pinhata, J, Maximiano, L, Seelaender, M, Lamarche, Émilie, Au, Ernie D, Desai, Aditya P, Koniaris, Leonidas G, Zimmers, Teresa A, Manring, Heather, Weisleder, Noah, Okamura, Heidi, Frankhouser, David, Yan, Pearlly, Tomasso, Jonathan di, Fabbro, Egidio G Del, Davis, Mellar P, Fearon, Kenneth CH, Jatoi, Aminah A, Vigano, Antonio, Putman, Ted, Kezhuo, Zhang, Sladek, Robert, Enjiu, LM, Gomes, SP, Matos-Neto, E, Rossi-Fanneli, F, Seelaender, MC, Ebadi, Maryam, Mazurak, Vera C, Bhatia, Nikita, Padliya, Neerav D, Stadler, Volker, Dariani, Maghsoud, Hariri, Robert J, Parker, Valorie A, Matthews, Ryan R, Bonetto, Andrea, Puppa, Melissa, Kang, Kyung Shin, Mohammed, Khalid S, Robling, Alexander G, Toledo, Míriam, Oliva, Francesc, Luque, Melania, Betancourt, Angelica, Marmonti, Enrica, López-Soriano, Francisco J, Busquets, Sílvia, Theal, Rebecca, Jiang, Heng, Sanchez, Anthony, Hussain, Sabah N, Serpe, R, Madeddu, C, Gudiño, V, Gabba, S, Antoni, G, Macciò, A, and Banni, S

Subjects
Abstracts
Published
2015

27. Rates of ubiquitin conjugation increase when muscles atrophy, largely through activation of the N-end rule pathway

Author

Solomon, V, Baracos, V, Sarraf, P, and Goldberg, A. L

Subjects
Life Sciences (General)
Abstract

The rapid loss of muscle mass that accompanies many disease states, such as cancer or sepsis, is primarily a result of increased protein breakdown in muscle, and several observations have suggested an activation of the ubiquitin-proteasome system. Accordingly, in extracts of atrophying muscles from tumor-bearing or septic rats, rates of 125I-ubiquitin conjugation to endogenous proteins were found to be higher than in control extracts. On the other hand, in extracts of muscles from hypothyroid rats, where overall proteolysis is reduced below normal, the conjugation of 125I-ubiquitin to soluble proteins decreased by 50%, and treatment with triiodothyronine (T3) restored ubiquitination to control levels. Surprisingly, the N-end rule pathway, which selectively degrades proteins with basic or large hydrophobic N-terminal residues, was found to be responsible for most of these changes in ubiquitin conjugation. Competitive inhibitors of this pathway that specifically block the ubiquitin ligase, E3alpha, suppressed most of the increased ubiquitin conjugation in the muscle extracts from tumor-bearing and septic rats. These inhibitors also suppressed ubiquitination in normal extracts toward levels in hypothyroid extracts, which showed little E3alpha-dependent ubiquitination. Thus, the inhibitors eliminated most of the differences in ubiquitination under these different pathological conditions. Moreover, 125I-lysozyme, a model N-end rule substrate, was ubiquitinated more rapidly in extracts from tumor-bearing and septic rats, and more slowly in those from hypothyroid rats, than in controls. Thus, the rate of ubiquitin conjugation increases in atrophying muscles, and these hormone- and cytokine-dependent responses are in large part due to activation of the N-end rule pathway.

Published
1998
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28. Activation of the ATP-ubiquitin-proteasome pathway in skeletal muscle of cachectic rats bearing a hepatoma

Author

Baracos, V. E, DeVivo, C, Hoyle, D. H, and Goldberg, A. L

Subjects
Life Sciences (General)
Abstract

Rats implanted with Yoshida ascites hepatoma (YAH) show a rapid and selective loss of muscle protein due mainly to a marked increase (63-95%) in the rate of protein degradation (compared with rates in muscles of pair-fed controls). To define which proteolytic pathways contribute to this increase, epitrochlearis muscles from YAH-bearing and control rats were incubated under conditions that modify different proteolytic systems. Overall proteolysis in either group of rats was not affected by removal of Ca2+ or by blocking the Ca(2+)-dependent proteolytic system. Inhibition of lysosomal function with methylamine reduced proteolysis (-12%) in muscles from YAH-bearing rats, but not in muscles of pair-fed rats. When ATP production was also inhibited, the remaining accelerated proteolysis in muscles of tumor-bearing rats fell to control levels. Muscles of YAH-bearing rats showed increased levels of ubiquitin-conjugated proteins and a 27-kDa proteasome subunit in Western blot analysis. Levels of mRNA encoding components of proteolytic systems were quantitated using Northern hybridization analysis. Although their total RNA content decreased 20-38%, pale muscles of YAH-bearing rats showed increased levels of ubiquitin mRNA (590-880%) and mRNA for multiple subunits of the proteasome (100-215%). Liver, kidney, heart, and brain showed no weight loss and no change in these mRNA species. Muscles of YAH-bearing rats also showed small increases (30-40%) in mRNA for cathepsins B and D, but not for calpain I or heat shock protein 70. Our findings suggest that accelerated muscle proteolysis and muscle wasting in tumor-bearing rats result primarily from activation of the ATP-dependent pathway involving ubiquitin and the proteasome.

Published
1995

29. Validation of the Consensus-Definition for Cancer Cachexia and evaluation of a classification model—a study based on data from an international multicentre project (EPCRC-CSA)

Author

Blum, D., Stene, G. B., Solheim, T. S., Fayers, P., Hjermstad, M. J., Baracos, V. E., Fearon, K., Strasser, F., Kaasa, S., Block Lieve, Van den, Koen, Meeussen, Sarah, Brearley, Augusto, Caraceni, Joachim, Cohen, Massimo, Costantini, Anneke, Francke, Richard, Harding, Higginson Irene, J., Stein, Kaasa, Karen, Linden, Guido, Miccinesi, Bregje, Onwuteaka-Philipsen, Koen, Pardon, Roeline, Pasman, Sophie, Pautex, Sheila, Payne, and Luc, Deliens

Abstract

A cancer cachexia classification into stages is warranted in order to guide treatment decisions and clinical trial inclusion. Weight loss and BMI clearly discriminate between non-cachectic and cachectic patients both with regards to all the domains (Intake, Catabolism and Function) and survival. The precachexia stage might be better defined by additional factors in order to be discriminative

Published
2017

32. Functional Body Composition and Related Aspects in Research on Obesity and Cachexia

Author

Müller, M.J., Baracos, V., Bosy-Westphal, A., Dulloo, A., Eckel, J., Fearon, K.C.H., Hall, K.D., Pietrobelli, A., Sørensen, T.I.A., Speakman, J., Trayhurn, P., Visser, M., and Heymsfield, S.B.

Subjects
Cachexia, Body Weight, Congresses as Topic, Article, Disease Models, Animal, Adipokines, Adipose Tissue, Germany, Body Composition, Animals, Humans, Obesity, Energy Metabolism, Muscle, Skeletal
Abstract

The 12th Stock Conference addressed body composition and related functions in two extreme situations, obesity and cancer cachexia. The concept of 'functional body composition' integrates body components into regulatory systems relating the mass of organs and tissues to corresponding in vivo functions and metabolic processes. This concept adds to an understanding of organ/tissue mass and function in the context of metabolic adaptations to weight change and disease. During weight gain and loss, there are associated changes in individual body components while the relationships between organ and tissue mass are fixed. Thus an understanding of body weight regulation involves an examination of the relationships between organs and tissues rather than individual organ and tissue masses only. The between organ/tissue mass relationships are associated with and explained by crosstalks between organs and tissues mediated by cytokines, hormones and metabolites that are coupled with changes in body weight, composition and function as observed in obesity and cancer cachexia. In addition to established roles in intermediary metabolism, cell function and inflammation, organ-tissue crosstalk mediators are determinants of body composition and its change with weight gain and loss. The 12th Stock Conference supported Michael Stocks' concept of gaining new insights by integrating research ideas from obesity and cancer cachexia. The conference presentations provide an in-depth understanding of body composition and metabolism.

Published
2014

36. The association of nutritional assessment criteria with health-related quality of life in patients with advanced colorectal carcinoma

Author

Thoresen, L, Frykholm, G, Lydersen, S, Ulveland, H, Baracos, V, Birdsell, L, and Falkmer, Ursula

Subjects
humanities
Abstract

THORESEN L., FRYKHOLM G., LYDERSEN S., ULVELAND H., BARACOS V., BIRDSELL L. & FALKMER U. (2012) European Journal of Cancer Care. The association of nutritional assessment criteria with health-related quality of life in patients with advanced colorectal carcinoma Health-related quality of life (QoL) is a goal in nutritional oncology but the association between nutritional status and QoL is rarely explored. The aim of the study was to investigate the association of nutritional assessment criteria with QoL in 50 patients with advanced colorectal carcinoma. A second aim was to investigate changes in body weight and QoL during a 3-month follow-up. Muscle mass, nutritional risk, malnutrition and cachexia according to three different criteria were assessed, as well as health-related QoL. At inclusion, 36 patients experienced weight loss, 10 patients sarcopenia, 25 were at nutritional risk, 16 were malnourished and 11, 14 and 31 patients had cachexia according to different criteria. All nutritional assessment criteria discriminated between groups of patients with worse or better QoL to varying degrees. Malnutrition and cachexia defined by the European Palliative Care Research Collaborative and adjusted for recent gain or stabilisation of body weight discriminated on most QoL scores. Weight loss at follow-up was associated with a decrease in several QoL scores. Recognition of weight loss as well as diagnosing malnutrition and cachexia should be the first steps in an interventional pathway to enhance nutritional status and QoL in patients with advanced colorectal carcinoma.

Published
2012
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40. Sarcopenic obesity: hidden muscle wasting and its impact for survival and complications of cancer therapy.

Author

Baracos, V E and Arribas, L

Subjects
*SARCOPENIA, *OVERWEIGHT persons, *ADIPOSE tissue diseases, *CANCER treatment complications, *BODY composition, *BODY mass index
Abstract

Body composition, defined as the proportions and distribution of lean and fat tissues in the human body, is an emergent theme in clinical oncology. Severe muscle depletion (sarcopenia) is most easily overlooked in obese patients; the advent of secondary analysis of oncologic images provides a precise and specific assessment of sarcopenia. Here, we review the definitions, prevalence and clinical implications of sarcopenic obesity (SO) in medical and surgical oncology. Reported prevalence of SO varies due to the heterogeneity in the definitions and the variability in the cut points used to define low muscle mass and high fat mass. Prevalence of SO in advanced solid tumor patient populations average 9% (range 2.3%-14.6%) overall, and one in four (24.7%, range 5.9%-39.2%) patients with body mass index ≥30 kg/m2 are sarcopenic. SO is independently associated with higher mortality and higher rate of complications in systemic and surgical cancer treatment, across multiple cancer sites and treatment plans. These associations remain unexplained, however, it has been hypothesized that patients with sarcopenia are generally unfit and unable to tolerate stress. Another proposed mechanism relates to increased exposure to antineoplastic therapy, i.e. a large fat mass would be expected to inflate drug dose in BSA-based treatments, causing an increased rate of dose-limiting toxicity. Pharmacokinetic data are needed to confirm or refute this hypothesis. Old age, deconditioning, cancer progression, acute or chronic nonmalignant disease and drug side-effects are suggested causes of muscle loss, and it is unknown the degree to which this can be reversed. Sarcopenia can be readily detected before start of cancer treatment, however, clinical management protocols for SO patients require development. Studies of cancer treatment dose-modulation are in progress. [ABSTRACT FROM AUTHOR]

Published
2018
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46. Regulation and importance of the ubiquitin-proteasome pathway in skeletal muscle

Author

Goldberg, Alfred, Attaix, Didier, Baracos, V., Wing, Simon, Medina, R., Estrela, J., Sawada, H., Tawa, N., Mitch, W., Unité de nutrition et métabolisme protéique, Institut National de la Recherche Agronomique (INRA), and ProdInra, Migration

Subjects
[SDV] Life Sciences [q-bio], ATP, [SDV]Life Sciences [q-bio], ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
1992

48. Sarcopenia is associated with postoperative infection and delayed recovery from colorectal cancer resection surgery.

Author

Lieffers, J R, Bathe, O F, Fassbender, K, Winget, M, and Baracos, V E

Subjects
COLON cancer treatment, SARCOPENIA, POSTOPERATIVE period, SURGICAL excision, LENGTH of stay in hospitals, CONFIDENCE intervals, HEALTH outcome assessment
Abstract

Background:Skeletal muscle depletion (sarcopenia) predicts morbidity and mortality in the elderly and cancer patients.Methods:We tested whether sarcopenia predicts primary colorectal cancer resection outcomes in stage II-IV patients (n=234). Sarcopenia was assessed using preoperative computed tomography images. Administrative hospitalisation data encompassing the index surgical admission, direct transfers for inpatient rehabilitation care and hospital re-admissions within 30 days was searched for International Classification of Disease (ICD)-10 codes for postoperative infections and inpatient rehabilitation care and used to calculate length of stay (LOS).Results:Overall, 38.9% were sarcopenic; 16.7% had an infection and 9.0% had inpatient rehabilitation care. Length of stay was longer for sarcopenic patients overall (15.9±14.2 days vs 12.3±9.8 days, P=0.038) and especially in those 65 years (20.2±16.9 days vs 13.1±8.3 days, P=0.008). Infection risk was greater for sarcopenic patients overall (23.7% vs 12.5%; P=0.025), and especially those 65 years (29.6% vs 8.8%, P=0.005). Most (90%) inpatient rehabilitation care was in patients 65 years. Inpatient rehabilitation was more common in sarcopenic patients overall (14.3% vs 5.6%; P=0.024) and those 65 years (24.1% vs 10.7%, P=0.06). In a multivariate model in patients 65 years, sarcopenia was an independent predictor of both infection (odds ratio (OR) 4.6, (95% confidence interval (CI) 1.5, 13.9) P<0.01) and rehabilitation care (OR 3.1 (95% CI 1.04, 9.4) P<0.04).Conclusion:Sarcopenia predicts postoperative infections, inpatient rehabilitation care and consequently a longer LOS. [ABSTRACT FROM AUTHOR]

Published
2012
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49. Skeletal muscle anabolism is a side effect of therapy with the MEK inhibitor: selumetinib in patients with cholangiocarcinoma.

Author

Prado, C M M, Bekaii-Saab, T, Doyle, L A, Shrestha, S, Ghosh, S, Baracos, V E, and Sawyer, M B

Subjects
SKELETAL muscle, METABOLISM, DRUG side effects, CHOLANGIOCARCINOMA, CACHEXIA, INTERLEUKIN-6
Abstract

Background:Cancer cachexia is characterised by skeletal muscle wasting; however, potential for muscle anabolism in patients with advanced cancer is unproven.Methods:Quantitative analysis of computed tomography images for loss/gain of muscle in cholangiocarcinoma patients receiving selumetinib (AZD6244; ARRY-142886) in a Phase II study, compared with a separate standard therapy group. Selumetinib is an inhibitor of mitogen-activated protein/extracellular signal-regulated kinase and of interleukin-6 secretion, a putative mediator of muscle wasting.Results:Overall, 84.2% of patients gained muscle after initiating selumetinib; mean overall gain of total lumbar muscle cross-sectional area was 13.6 cm2/100 days (∼2.3 kg on a whole-body basis). Cholangiocarcinoma patients who began standard treatment were markedly catabolic, with overall muscle loss of −7.3 cm2/100 days (∼1.2 kg) and by contrast only 16.7% of these patients gained muscle.Conclusion:Our findings suggest that selumetinib promotes muscle gain in patients with cholangiocarcinoma. Specific mechanisms and relevance for cachexia therapy remain to be investigated. [ABSTRACT FROM AUTHOR]

Published
2012
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50. Is there a genetic cause for cancer cachexia? - a clinical validation study in 1797 patients.

Author

Solheim, T S, Fayers, P M, Fladvad, T, Tan, B, Skorpen, F, Fearon, K, Baracos, V E, Klepstad, P, Strasser, F, and Kaasa, S

Subjects
CACHEXIA, CANCER patients, GENETIC polymorphisms, BODY mass index, HARDY-Weinberg formula, DISEASES
Abstract

Background: Cachexia has major impact on cancer patients' morbidity and mortality. Future development of cachexia treatment needs methods for early identification of patients at risk. The aim of the study was to validate nine single-nucleotide polymorphisms (SNPs) previously associated with cachexia, and to explore 182 other candidate SNPs with the potential to be involved in the pathophysiology.Method: A total of 1797 cancer patients, classified as either having severe cachexia, mild cachexia or no cachexia, were genotyped.Results: After allowing for multiple testing, there was no statistically significant association between any of the SNPs analysed and the cachexia groups. However, consistent with prior reports, two SNPs from the acylpeptide hydrolase (APEH) gene showed suggestive statistical significance (P=0.02; OR, 0.78).Conclusion: This study failed to detect any significant association between any of the SNPs analysed and cachexia; although two SNPs from the APEH gene had a trend towards significance. The APEH gene encodes the enzyme APEH, postulated to be important in the endpoint of the ubiquitin system and thus the breakdown of proteins into free amino acids. In cachexia, there is an extensive breakdown of muscle proteins and an increase in the production of acute phase proteins in the liver. [ABSTRACT FROM AUTHOR]

Published
2011
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