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159 results on '"Tassaneeyakul W"'

7. Identification of drug-specific public TCR driving severe cutaneous adverse reactions

Author

Pan, R-Y, Chu, M-T, Wang, C-W, Lee, Y-S, Lemonnier, F, Michels, A.W., Schutte, R., Ostrov, D.A., Chen, C-B, Phillips, E.J., Mallal, S.A., Mockenhaupt, M., Bellón, T., Tassaneeyakul, W., White, K.D., Roujeau, J-C, Chung, W-H, Hung, S-L, Pan, R-Y, Chu, M-T, Wang, C-W, Lee, Y-S, Lemonnier, F, Michels, A.W., Schutte, R., Ostrov, D.A., Chen, C-B, Phillips, E.J., Mallal, S.A., Mockenhaupt, M., Bellón, T., Tassaneeyakul, W., White, K.D., Roujeau, J-C, Chung, W-H, and Hung, S-L

Abstract

Drug hypersensitivity such as severe cutaneous adverse reactions (SCAR), including Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), could be life-threatening. Here, we enroll SCAR patients to investigate the T cell receptor (TCR) repertoire by next-generation sequencing. A public αβTCR is identified from the cytotoxic T lymphocytes of patients with carbamazepine-SJS/TEN, with its expression showing drug/phenotype-specificity and an bias for HLA-B*15:02. This public αβTCR has binding affinity for carbamazepine and its structural analogs, thereby mediating the immune response. Adoptive transfer of T cell expressing this public αβTCR to HLA-B*15:02 transgenic mice receiving oral administration of carbamazepine induces multi-organ injuries and symptoms mimicking SCAR, including hair loss, erythema, increase of inflammatory lymphocytes in the skin and blood, and liver and kidney dysfunction. Our results not only demonstrate an essential role of TCR in the immune synapse mediating SCAR, but also implicate potential clinical applications and development of therapeutics.

Published
2019

8. 7th Drug hypersensitivity meeting: part two

Author

Elera, J.D., Boteanu, C., Blanco, M.A.J., Gonzalez-Mendiola, R., García, I.C., Alvarez, A., Martinez, J.J.L., Garrido, J.M., Barona, C.T., Chorda, C.P., Salgueiro, R.L., Palacios, M.D., De Rojas, D.H.F., Acar, E.A., Aktas, A., Ermertcan, A.T., Temiz, C., Lin, C-Y, Hui, C-Y.R., Chang, Y-C, Yang, C-H, Chung, W-H, Carolino, F., Silva, D., De Castro, E.D., Cernadas, J.R., Ensina, L.F., Aranda, C., Nunes, I.C., Lacerda, A., Martins, A.M., Goudouris, E., Ribeiro, M., Da Silva Franco, J.F., Queiroz, L., Solé, D., Dalgiç, C.T., Sin, A.Z., Günsen, F.D., Bulut, G., Ardeniz, F.Ö., Gülbahar, O., Gökmen, E.N.M., Kokuludag, A., De Francisco, A.M.M., De Vicente Jiménez, T.M., Mendoza Parra, A.M., Burgos Pimentel, A.M., Luque, A.G., Amaral, L., Leão, L.C., Pinto, N., Belo, J., Marques, J., Carreiro-Martins, P., Leiria-Pinto, P., Chaabane, A., Romdhane, H.B., Fredj, N.B., Chadly, Z., Boughattas, N.A., Aouam, K., Uyttebroek, A.P., Bridts, C.H., Romano, A., Ebo, D.G., Sabato, V., Lopes, A., Cosme, J., Aguiar, R., Lourenço, T., Paes, M-J, Spínola-Santos, A., Pereira-Barbosa, M., Cruz, C.R., Dos Reis, R.P., Tomaz, E., Pires, A.P., Inácio, F., Benito-Garcia, F., Mota, I., Correia, M., Gaspar, Â., Chambel, M., Piedade, S., Morais-Almeida, M., Nakonechna, A., Antipkin, Y., Umanets, T., Pineda, F., Arribas, F., Lapshyn, V., Miranda, P.A., De La Cruz Hoyos, B., Blanco, A.J., Del Pozo, M., Vultaggio, A., Nencini, F., Pratesi, S., Matucci, A., Maggi, E., Cegec, I., Nahal, D.J., Turk, V.E., Aumiler, M.R., Ausperger, K.M., Kraljickovic, I., Simic, I., Yamaguchi, Y., Watanabe, T., Satoh, M., Tanegashima, T., Oda, K., Wada, H., Aihara, M., Lee, J.J., Choi, J.C., Lee, H.Y., Fernandes, R-A.R., Faria, E., Pita, J., Sousa, N., Ribeiro, C., Carrapatoso, I., Bom, A.T., Rodolfo, A., Dias-Castro, E., Voronova, M., Valle, D.K., Coronel, V.P., Chordá, C.P., Madamba, R.C.Y., Ferrer, M., Goikoetxea, M.J., D’Amelio, C., Bernad, A., Vega, O., Gastaminza, G., Bibián, B.L., Salazar, M.L., Vilà-Nadal, G., Roman, A.M.F., Ortega, J.D., Muñoz, M.G., Gancedo, S.Q., Moreno, M.R.C., Hofmeier, K.S., Barzylovych, V., Pola, B., Lluncor, M., Fiandor, A., Bellón, T., Domínguez, J., Quirce, S., Yang, M-S, Kim, S-S, Kim, S-H, Kang, H-R, Park, H-W, Cho, S-H, Min, K-U, Chang, Y-S, Delahaye, C., Flabbee, J., Waton, J., Bauvin, O., Barbaud, A., Fadhel, N.B., Gulin, S.J., Chiriac, A., Cardoso, B.K., Viseu, R., Moreira, A., Cadinha, S., Neves, A.C., Barreira, P., Malheiro, D., Da Silva, J.P., Jurakic-Toncic, R., Ljubojevic, S., Turcic, P., Gilissen, L., Huygens, S., Goossens, A., Andreu, I., Romero, A.M., Cabezas, P.G., Parejo, P.A., Del Carmen Plaza-Serón, M., Doña, I., Blanca-López, N., Flores, C., Galindo, M.L., Molina, A., Perkins, J.R., Cornejo-García, J.A., García-Agúndez, J.A., García-Martín, E., Campo, P., Canto, M.G., Blanca, M., Guéant-Rodríguez, R.M., Jurado-Escobar, R., Barrionuevo, E., Salas, M., Canto, G., Guéant, J-L, Usui, T., Tailor, A., Faulkner, L., Farrell, J., Alfirevic, A., Kevin Park, B., Naisbitt, D.J., Trelles, O., Guerrero, M.A., Upton, A., Ueta, M., Sawai, H., Sotozono, C., Tokunaga, K., Kinoshita, S., Sukasem, C., Satapornpong, P., Tempark, T., Rerknimitr, P., Pairayayutakul, K., Klaewsongkram, J., Koomdee, N., Jantararoungtong, T., Santon, S., Puangpetch, A., Intusoma, U., Tassaneeyakul, W., Theeramoke, V., Ramirez, E., Borobia, A.M., Tong, H., Castañer, J.L., De Abajo, F.J., Galvao, V.R., Pavlos, R., McKinnon, E., Williams, K., Beeghly-Fadiel, A., Phillips, E., Castells, M., Boni, E., Russello, M., Mauro, M., Ue, K.L., Rutkowski, K., Gomis, V.S., Ferre, J.F., Rodriguez, A.E., Reig, V.C., Sanchez, J.F., Breynaert, C., Van Hoeyveld, E., Schrijvers, R., Irigoyen, R.F., Collado, D., Vida, Y., Najera, F., Perez-Inestrosa, E., Mesa-Antunez, P., Mayorga, C., Torres, M.J., Tannert, L.K., Mortz, C.G., Skov, P.S., Bindslev-Jensen, C., Pfützner, W., Dörnbach, H., Visse, J., Rauber, M., Möbs, C., Elzagallaai, A.A., Chow, L., Abuzgaia, A.M., Rieder, M.J., Trubiano, J., Woolnough, E., Cheng, C., Kato, K., Azukizawa, H., Hanafusa, T., Katayama, I., Fujiyama, T., Hashizume, H., Umayahara, T., Ito, T., Tokura, Y., Silar, M., Zidarn, M., Rupnik, H., Korosec, P., Redwood, A.J., Strautins, K., White, K., Chopra, A., Konvinse, K., Leary, S., Mallal, S., Cabañas, R., Fiandor, A.M., Sullivan, A., Whitaker, P., Peckham, D., Haw, W.Y., Polak, M.E., Mcguire, C., Ardern-Jones, M.R., Aoyama, Y., Shiohara, T., Correia, S., Gelincik, A., Demir, S., Sen, F., Bozbey, H.U., Olgac, M., Unal, D., Coskun, R., Colakoglu, B., Buyuozturk, S., Çatin-Aktas, E., Deniz, G., Laguna, J.J., Dionicio, J., Fernandez, T., Olazabal, I., Ruiz, M.D., Lafuente, A., Núñez, J., Fernández, T.D., Palomares, F., Fernández, R., Sanchez, M.I., Ruiz, A., Ariza, A., Alonso, A.B., Garófalo, C.D., Matute, O.V., Puga, M.F., Lapresa, M.J.G., Lasarte, G.G., Thinnes, A., Merk, H.F., Baron, J.M., Leverkus, M., Balakirski, G., Gibson, A., Ogese, M., Al-Attar, Z., Yaseen, F., Meng, X., Jenkins, R., Farrel, J., Alhilali, K., Xue, Y., Illing, P., Mifsud, N., Fettke, H., Lai, J., Ho, R., Kwan, P., Purcell, A., Ogese, M.O., Betts, C., Thomson, P., Alhaidari, M., Berry, N., O’Neill, P.M., Alzahrani, A., Azoury, M.E., Fili, L., Bechara, R., Scornet, N., Nhim, C., Weaver, R., Claude, N., Joseph, D., Maillere, B., Parronchi, P., Pallardy, M., Villani, A.P., Rozières, A., Bensaïd, B., Tardieu, M., Albert, F., Mutez, V., Baysal, T., Maryanski, J., Nicolas, J-F, Kanagawa, O., Vocanson, M., Hung, S-L, Harrison, C.J., Jenkins, R.E., French, N.S., Montañez, M.I., Fernandez, T.D., Martin-Serrano, A., Molina, N., Wood, S., Pirmohamed, M., Martín-Serrano, Á., Pérez-Inestrosa, E., Pérez-Sala, D., Guzmán, A.E., Ko, T-M, Chen, Y-T, Wu, J-Y, Sánchez-Gómez, F.J., González-Morena, J.M., Arreola, A.M., Corona, J.A.B., Flores, S.M., Cherit, J.D., Figueroa, N.V.D., Flores, J.L.C., Perkins, J., Pérez-Alzate, D., Bogas, G., Marti, L.M.T., De La Losa, F.P., Poves, F.A., Lopez, J.T., Santiago, T.L., Elera, J.D., Boteanu, C., Blanco, M.A.J., Gonzalez-Mendiola, R., García, I.C., Alvarez, A., Martinez, J.J.L., Garrido, J.M., Barona, C.T., Chorda, C.P., Salgueiro, R.L., Palacios, M.D., De Rojas, D.H.F., Acar, E.A., Aktas, A., Ermertcan, A.T., Temiz, C., Lin, C-Y, Hui, C-Y.R., Chang, Y-C, Yang, C-H, Chung, W-H, Carolino, F., Silva, D., De Castro, E.D., Cernadas, J.R., Ensina, L.F., Aranda, C., Nunes, I.C., Lacerda, A., Martins, A.M., Goudouris, E., Ribeiro, M., Da Silva Franco, J.F., Queiroz, L., Solé, D., Dalgiç, C.T., Sin, A.Z., Günsen, F.D., Bulut, G., Ardeniz, F.Ö., Gülbahar, O., Gökmen, E.N.M., Kokuludag, A., De Francisco, A.M.M., De Vicente Jiménez, T.M., Mendoza Parra, A.M., Burgos Pimentel, A.M., Luque, A.G., Amaral, L., Leão, L.C., Pinto, N., Belo, J., Marques, J., Carreiro-Martins, P., Leiria-Pinto, P., Chaabane, A., Romdhane, H.B., Fredj, N.B., Chadly, Z., Boughattas, N.A., Aouam, K., Uyttebroek, A.P., Bridts, C.H., Romano, A., Ebo, D.G., Sabato, V., Lopes, A., Cosme, J., Aguiar, R., Lourenço, T., Paes, M-J, Spínola-Santos, A., Pereira-Barbosa, M., Cruz, C.R., Dos Reis, R.P., Tomaz, E., Pires, A.P., Inácio, F., Benito-Garcia, F., Mota, I., Correia, M., Gaspar, Â., Chambel, M., Piedade, S., Morais-Almeida, M., Nakonechna, A., Antipkin, Y., Umanets, T., Pineda, F., Arribas, F., Lapshyn, V., Miranda, P.A., De La Cruz Hoyos, B., Blanco, A.J., Del Pozo, M., Vultaggio, A., Nencini, F., Pratesi, S., Matucci, A., Maggi, E., Cegec, I., Nahal, D.J., Turk, V.E., Aumiler, M.R., Ausperger, K.M., Kraljickovic, I., Simic, I., Yamaguchi, Y., Watanabe, T., Satoh, M., Tanegashima, T., Oda, K., Wada, H., Aihara, M., Lee, J.J., Choi, J.C., Lee, H.Y., Fernandes, R-A.R., Faria, E., Pita, J., Sousa, N., Ribeiro, C., Carrapatoso, I., Bom, A.T., Rodolfo, A., Dias-Castro, E., Voronova, M., Valle, D.K., Coronel, V.P., Chordá, C.P., Madamba, R.C.Y., Ferrer, M., Goikoetxea, M.J., D’Amelio, C., Bernad, A., Vega, O., Gastaminza, G., Bibián, B.L., Salazar, M.L., Vilà-Nadal, G., Roman, A.M.F., Ortega, J.D., Muñoz, M.G., Gancedo, S.Q., Moreno, M.R.C., Hofmeier, K.S., Barzylovych, V., Pola, B., Lluncor, M., Fiandor, A., Bellón, T., Domínguez, J., Quirce, S., Yang, M-S, Kim, S-S, Kim, S-H, Kang, H-R, Park, H-W, Cho, S-H, Min, K-U, Chang, Y-S, Delahaye, C., Flabbee, J., Waton, J., Bauvin, O., Barbaud, A., Fadhel, N.B., Gulin, S.J., Chiriac, A., Cardoso, B.K., Viseu, R., Moreira, A., Cadinha, S., Neves, A.C., Barreira, P., Malheiro, D., Da Silva, J.P., Jurakic-Toncic, R., Ljubojevic, S., Turcic, P., Gilissen, L., Huygens, S., Goossens, A., Andreu, I., Romero, A.M., Cabezas, P.G., Parejo, P.A., Del Carmen Plaza-Serón, M., Doña, I., Blanca-López, N., Flores, C., Galindo, M.L., Molina, A., Perkins, J.R., Cornejo-García, J.A., García-Agúndez, J.A., García-Martín, E., Campo, P., Canto, M.G., Blanca, M., Guéant-Rodríguez, R.M., Jurado-Escobar, R., Barrionuevo, E., Salas, M., Canto, G., Guéant, J-L, Usui, T., Tailor, A., Faulkner, L., Farrell, J., Alfirevic, A., Kevin Park, B., Naisbitt, D.J., Trelles, O., Guerrero, M.A., Upton, A., Ueta, M., Sawai, H., Sotozono, C., Tokunaga, K., Kinoshita, S., Sukasem, C., Satapornpong, P., Tempark, T., Rerknimitr, P., Pairayayutakul, K., Klaewsongkram, J., Koomdee, N., Jantararoungtong, T., Santon, S., Puangpetch, A., Intusoma, U., Tassaneeyakul, W., Theeramoke, V., Ramirez, E., Borobia, A.M., Tong, H., Castañer, J.L., De Abajo, F.J., Galvao, V.R., Pavlos, R., McKinnon, E., Williams, K., Beeghly-Fadiel, A., Phillips, E., Castells, M., Boni, E., Russello, M., Mauro, M., Ue, K.L., Rutkowski, K., Gomis, V.S., Ferre, J.F., Rodriguez, A.E., Reig, V.C., Sanchez, J.F., Breynaert, C., Van Hoeyveld, E., Schrijvers, R., Irigoyen, R.F., Collado, D., Vida, Y., Najera, F., Perez-Inestrosa, E., Mesa-Antunez, P., Mayorga, C., Torres, M.J., Tannert, L.K., Mortz, C.G., Skov, P.S., Bindslev-Jensen, C., Pfützner, W., Dörnbach, H., Visse, J., Rauber, M., Möbs, C., Elzagallaai, A.A., Chow, L., Abuzgaia, A.M., Rieder, M.J., Trubiano, J., Woolnough, E., Cheng, C., Kato, K., Azukizawa, H., Hanafusa, T., Katayama, I., Fujiyama, T., Hashizume, H., Umayahara, T., Ito, T., Tokura, Y., Silar, M., Zidarn, M., Rupnik, H., Korosec, P., Redwood, A.J., Strautins, K., White, K., Chopra, A., Konvinse, K., Leary, S., Mallal, S., Cabañas, R., Fiandor, A.M., Sullivan, A., Whitaker, P., Peckham, D., Haw, W.Y., Polak, M.E., Mcguire, C., Ardern-Jones, M.R., Aoyama, Y., Shiohara, T., Correia, S., Gelincik, A., Demir, S., Sen, F., Bozbey, H.U., Olgac, M., Unal, D., Coskun, R., Colakoglu, B., Buyuozturk, S., Çatin-Aktas, E., Deniz, G., Laguna, J.J., Dionicio, J., Fernandez, T., Olazabal, I., Ruiz, M.D., Lafuente, A., Núñez, J., Fernández, T.D., Palomares, F., Fernández, R., Sanchez, M.I., Ruiz, A., Ariza, A., Alonso, A.B., Garófalo, C.D., Matute, O.V., Puga, M.F., Lapresa, M.J.G., Lasarte, G.G., Thinnes, A., Merk, H.F., Baron, J.M., Leverkus, M., Balakirski, G., Gibson, A., Ogese, M., Al-Attar, Z., Yaseen, F., Meng, X., Jenkins, R., Farrel, J., Alhilali, K., Xue, Y., Illing, P., Mifsud, N., Fettke, H., Lai, J., Ho, R., Kwan, P., Purcell, A., Ogese, M.O., Betts, C., Thomson, P., Alhaidari, M., Berry, N., O’Neill, P.M., Alzahrani, A., Azoury, M.E., Fili, L., Bechara, R., Scornet, N., Nhim, C., Weaver, R., Claude, N., Joseph, D., Maillere, B., Parronchi, P., Pallardy, M., Villani, A.P., Rozières, A., Bensaïd, B., Tardieu, M., Albert, F., Mutez, V., Baysal, T., Maryanski, J., Nicolas, J-F, Kanagawa, O., Vocanson, M., Hung, S-L, Harrison, C.J., Jenkins, R.E., French, N.S., Montañez, M.I., Fernandez, T.D., Martin-Serrano, A., Molina, N., Wood, S., Pirmohamed, M., Martín-Serrano, Á., Pérez-Inestrosa, E., Pérez-Sala, D., Guzmán, A.E., Ko, T-M, Chen, Y-T, Wu, J-Y, Sánchez-Gómez, F.J., González-Morena, J.M., Arreola, A.M., Corona, J.A.B., Flores, S.M., Cherit, J.D., Figueroa, N.V.D., Flores, J.L.C., Perkins, J., Pérez-Alzate, D., Bogas, G., Marti, L.M.T., De La Losa, F.P., Poves, F.A., Lopez, J.T., and Santiago, T.L.

Abstract

No abstract available

Published
2016

9. 7th Drug hypersensitivity meeting: part two

Author

Elera, Javier Dionicio, primary, Boteanu, Cosmin, additional, Blanco, Maria Aranzazu Jimenez, additional, Gonzalez-Mendiola, Rosario, additional, García, Irene Carrasco, additional, Alvarez, Antonio, additional, Martinez, Jose Julio Laguna, additional, Garrido, Jaume Martí, additional, Barona, Carla Torán, additional, Chorda, Carolina Perales, additional, Salgueiro, Ramón López, additional, Palacios, Miguel Díaz, additional, De Rojas, Dolores Hernández Fernández, additional, Acar, Emre Ali, additional, Aktas, Ayse, additional, Ermertcan, Aylin Türel, additional, Temiz, Peyker, additional, Lin, Chien-Yio, additional, Hui, Chung-Yee Rosaline, additional, Chang, Ya-Ching, additional, Yang, Chih-Hsun, additional, Chung, Wen-Hung, additional, Carolino, Fabrícia, additional, Silva, Diana, additional, De Castro, Eunice Dias, additional, Cernadas, Josefina R., additional, Ensina, Luis Felipe, additional, Aranda, Carolina, additional, Nunes, Ines Camelo, additional, Lacerda, Alex, additional, Martins, Ana Maria, additional, Goudouris, Ekaterini, additional, Ribeiro, Marcia, additional, Da Silva Franco, José Francisco, additional, Queiroz, Leandra, additional, Solé, Dirceu, additional, Dalgiç, Ceyda Tunakan, additional, Sin, Aytül Zerrin, additional, Günsen, Fatma Düsünür, additional, Bulut, Gökten, additional, Ardeniz, Fatma Ömür, additional, Gülbahar, Okan, additional, Gökmen, Emine Nihal Mete, additional, Kokuludag, Ali, additional, De Francisco, Ana M. Montoro, additional, De Vicente Jiménez, Talía Mª, additional, Mendoza Parra, Adriana M., additional, Burgos Pimentel, Angella M., additional, Luque, Amelia García, additional, Amaral, Luis, additional, Leão, Leonor Carneiro, additional, Pinto, Nicole, additional, Belo, Joana, additional, Marques, João, additional, Carreiro-Martins, Pedro, additional, Leiria-Pinto, Paula, additional, Chaabane, Amel, additional, Romdhane, Haifa Ben, additional, Fredj, Nadia Ben, additional, Chadly, Zohra, additional, Boughattas, Naceur A., additional, Aouam, Karim, additional, Uyttebroek, Astrid P., additional, Bridts, Chris H., additional, Romano, Antonino, additional, Ebo, Didier G., additional, Sabato, Vito, additional, Lopes, Anabela, additional, Cosme, Joana, additional, Aguiar, Rita, additional, Lourenço, Tatiana, additional, Paes, Maria-João, additional, Spínola-Santos, Amélia, additional, Pereira-Barbosa, Manuel, additional, Cruz, Cíntia Rito, additional, Dos Reis, Rute Pereira, additional, Tomaz, Elza, additional, Pires, Ana Paula, additional, Inácio, Filipe, additional, Benito-Garcia, Filipe, additional, Mota, Inês, additional, Correia, Magna, additional, Gaspar, Ângela, additional, Chambel, Marta, additional, Piedade, Susana, additional, Morais-Almeida, Mário, additional, Nakonechna, Alla, additional, Antipkin, Yurij, additional, Umanets, Tetiana, additional, Pineda, Fernando, additional, Arribas, Francisca, additional, Lapshyn, Volodymyr, additional, Miranda, Pablo Andrés, additional, De La Cruz Hoyos, Bautista, additional, Blanco, Aranzazu Jimenez, additional, Del Pozo, Marta, additional, Vultaggio, Alessandra, additional, Nencini, Francesca, additional, Pratesi, Sara, additional, Matucci, Andrea, additional, Maggi, Enrico, additional, Cegec, Ivana, additional, Nahal, Danica Juricic, additional, Turk, Viktorija Erdeljic, additional, Aumiler, Matea Radacic, additional, Ausperger, Ksenija Makar, additional, Kraljickovic, Iva, additional, Simic, Iveta, additional, Yamaguchi, Yukie, additional, Watanabe, Tomoya, additional, Satoh, Megumi, additional, Tanegashima, Tomohiko, additional, Oda, Kayoko, additional, Wada, Hidefumi, additional, Aihara, Michiko, additional, Lee, Jaechun Jason, additional, Choi, Jay Chol, additional, Lee, Hwa Young, additional, Fernandes, Rosa-Anita Rodrigues, additional, Faria, Emília, additional, Pita, Joana, additional, Sousa, Nuno, additional, Ribeiro, Carmelita, additional, Carrapatoso, Isabel, additional, Bom, Ana Todo, additional, Rodolfo, Ana, additional, Dias-Castro, Eunice, additional, Voronova, Marina, additional, Valle, Diana Kury, additional, Coronel, Verónica Pacheco, additional, Chordá, Carolina Perales, additional, Madamba, Roselle Catherine Yu, additional, Ferrer, Marta, additional, Goikoetxea, Maria Jose, additional, D’Amelio, Carmen, additional, Bernad, Amalia, additional, Vega, Olga, additional, Gastaminza, Gabriel, additional, Bibián, Beatriz Pola, additional, Salazar, Marina Lluncor, additional, Vilà-Nadal, Gemma, additional, Roman, Ana María Fiandor, additional, Ortega, Javier Dominguez, additional, Muñoz, Miguel Gonzalez, additional, Gancedo, Santiago Quirce, additional, Moreno, Maria Rosario Cabañas, additional, Hofmeier, Kathrin Scherer, additional, Barzylovych, Vladyslava, additional, Pola, Beatriz, additional, Lluncor, Marina, additional, Fiandor, Ana, additional, Bellón, Teresa, additional, Domínguez, Javier, additional, Quirce, Santiago, additional, Yang, Min-Suk, additional, Kim, Sun-Sin, additional, Kim, Sae-Hoon, additional, Kang, Hye-Ryun, additional, Park, Heung-Woo, additional, Cho, Sang-Heon, additional, Min, Kyung-Up, additional, Chang, Yoon-Seok, additional, Delahaye, Clémence, additional, Flabbee, Jenny, additional, Waton, Julie, additional, Bauvin, Olivia, additional, Barbaud, Annick, additional, Fadhel, Najah Ben, additional, Gulin, Sandra Jerkovic, additional, Chiriac, Anca, additional, Cardoso, Bárbara Kong, additional, Viseu, Regina, additional, Moreira, Ana, additional, Cadinha, Susana, additional, Neves, Ana Castro, additional, Barreira, Patrícia, additional, Malheiro, Daniela, additional, Da Silva, J. P. Moreira, additional, Jurakic-Toncic, Ružica, additional, Ljubojevic, Suzana, additional, Turcic, Petra, additional, Gilissen, Liesbeth, additional, Huygens, Sara, additional, Goossens, An, additional, Andreu, Inmaculada, additional, Romero, Alicia Martinez, additional, Cabezas, Pau Gomez, additional, Parejo, Pedro Ayuso, additional, Del Carmen Plaza-Serón, Maria, additional, Doña, Inmaculada, additional, Blanca-López, Natalia, additional, Flores, Carlos, additional, Galindo, María Luisa, additional, Molina, Ana, additional, Perkins, James Richard, additional, Cornejo-García, José Antonio, additional, García-Agúndez, José Augusto, additional, García-Martín, Elena, additional, Campo, Paloma, additional, Canto, María Gabriela, additional, Blanca, Miguel, additional, Guéant-Rodríguez, Rosa María, additional, Jurado-Escobar, Raquel, additional, Barrionuevo, Esther, additional, Salas, María, additional, Canto, Gabriela, additional, Guéant, Jean-Louis, additional, Usui, Toru, additional, Tailor, Arun, additional, Faulkner, Lee, additional, Farrell, John, additional, Alfirevic, Ana, additional, Kevin Park, B., additional, Naisbitt, Dean J., additional, Trelles, Oswaldo, additional, Guerrero, María Auxiliadora, additional, Upton, Alex, additional, Ueta, Mayumi, additional, Sawai, Hiromi, additional, Sotozono, Chie, additional, Tokunaga, Katushi, additional, Kinoshita, Shigeru, additional, Sukasem, Chonlaphat, additional, Satapornpong, Patompong, additional, Tempark, Therdpong, additional, Rerknimitr, Pawinee, additional, Pairayayutakul, Kulprapat, additional, Klaewsongkram, Jettanong, additional, Koomdee, N., additional, Jantararoungtong, T., additional, Santon, S., additional, Puangpetch, A., additional, Intusoma, U., additional, Tassaneeyakul, W., additional, Theeramoke, V., additional, Ramirez, Elena, additional, Borobia, Alberto Manuel, additional, Tong, Hoi, additional, Castañer, Jose Luis, additional, De Abajo, Francisco José, additional, Galvao, Violeta Régnier, additional, Pavlos, Rebecca, additional, Mckinnon, Elizabeth, additional, Williams, Kristina, additional, Beeghly-Fadiel, Alicia, additional, Redwood, Alec, additional, Phillips, Elizabeth, additional, Castells, Mariana, additional, Boni, Elisa, additional, Russello, Marina, additional, Mauro, Marina, additional, Ue, Kok Loong, additional, Rutkowski, Krzysztof, additional, Gomis, Victor Soriano, additional, Ferre, Jorge Frances, additional, Rodriguez, Angel Esteban, additional, Reig, Vicente Cantó, additional, Sanchez, Javier Fernandez, additional, Breynaert, Christine, additional, Van Hoeyveld, Erna, additional, Schrijvers, Rik, additional, Irigoyen, Raquel Fuentes, additional, Collado, Daniel, additional, Vida, Yolanda, additional, Najera, Francisco, additional, Perez-Inestrosa, Ezequiel, additional, Mesa-Antunez, Pablo, additional, Mayorga, Cristobalina, additional, Torres, María José, additional, Tannert, Line K., additional, Mortz, Charlotte G., additional, Skov, Per Stahl, additional, Bindslev-Jensen, Carsten, additional, Pfützner, Wolfgang, additional, Dörnbach, Hannah, additional, Visse, Johanna, additional, Rauber, Michele, additional, Möbs, Christian, additional, Elzagallaai, Abdelbaset A., additional, Chow, Lindsey, additional, Abuzgaia, Awatif M., additional, Rieder, Michael J., additional, Trubiano, Jason, additional, Woolnough, Emily, additional, Stautins, Kaija, additional, Cheng, Christina, additional, Kato, Kenichi, additional, Azukizawa, Hiroaki, additional, Hanafusa, Takaaki, additional, Katayama, Ichiro, additional, Fujiyama, Toshiharu, additional, Hashizume, Hideo, additional, Umayahara, Takatsune, additional, Ito, Taisuke, additional, Tokura, Yoshiki, additional, Silar, Mira, additional, Zidarn, Mihaela, additional, Rupnik, Helena, additional, Korosec, Peter, additional, Redwood, Alec James, additional, Strautins, Kaija, additional, White, Katie, additional, Chopra, Abha, additional, Konvinse, Katherine, additional, Leary, Shay, additional, Mallal, Simon, additional, Cabañas, Rosario, additional, Fiandor, Ana María, additional, Sullivan, Andrew, additional, Whitaker, Paul, additional, Peckham, Daniel, additional, Haw, Wei Yann, additional, Polak, Marta E., additional, Mcguire, Carolann, additional, Ardern-Jones, Michael R., additional, Aoyama, Yumi, additional, Shiohara, Tetsuo, additional, Correia, Sara, additional, Gelincik, Asli, additional, Demir, Semra, additional, Sen, Fatma, additional, Bozbey, Hamza Ugur, additional, Olgac, Muge, additional, Unal, Derya, additional, Coskun, Raif, additional, Colakoglu, Bahauddin, additional, Buyuozturk, Suna, additional, Çatin-Aktas, Esin, additional, Deniz, Gunnur, additional, Laguna, Jose Julio, additional, Dionicio, J., additional, Fernandez, Tahia, additional, Olazabal, I., additional, Ruiz, Maria Dolores, additional, Torres, Maria José, additional, Lafuente, Alberto, additional, Núñez, Jorge, additional, Fernández, Tahia Diana, additional, Palomares, Francisca, additional, Fernández, Rubén, additional, Sanchez, Maria Isabel, additional, Fernandez, Tahía, additional, Ruiz, Arturo, additional, Ariza, Adriana, additional, Alonso, Amalia Bernad, additional, Garófalo, Carmen D’Amelio, additional, Matute, Olga Vega, additional, Puga, Marta Ferrer, additional, Lapresa, María José Goikoetxea, additional, Lasarte, Gabriel Gastaminza, additional, Thinnes, Antonia, additional, Merk, Hans F., additional, Baron, Jens Malte, additional, Leverkus, Martin, additional, Balakirski, Galina, additional, Gibson, Andrew, additional, Ogese, Monday, additional, Al-Attar, Zaid, additional, Yaseen, Fiazia, additional, Meng, Xiaoli, additional, Jenkins, Rozalind, additional, Farrel, John, additional, Alhilali, Khetam, additional, Xue, Yanni, additional, Illing, Patricia, additional, Mifsud, Nicole, additional, Fettke, Heidi, additional, Lai, Jeffrey, additional, Ho, Rebecca, additional, Kwan, Patrick, additional, Purcell, Anthony, additional, Ogese, Monday O., additional, Betts, Catherine, additional, Thomson, Paul, additional, Alhaidari, Mohammad, additional, Berry, Neill, additional, O’Neill, Paul M., additional, Alzahrani, Abdulaziz, additional, Azoury, Marie Eliane, additional, Fili, Lucia, additional, Bechara, Rami, additional, Scornet, Noémie, additional, Nhim, Cathy, additional, Weaver, Richard, additional, Claude, Nancy, additional, Joseph, Delphine, additional, Maillere, Bernard, additional, Parronchi, Paola, additional, Pallardy, Marc, additional, Villani, Axel Patrice, additional, Rozières, Aurore, additional, Bensaïd, Benoît, additional, Tardieu, Mathilde, additional, Albert, Floriane, additional, Mutez, Virginie, additional, Baysal, Tugba, additional, Maryanski, Janet, additional, Nicolas, Jean-François, additional, Kanagawa, Osami, additional, Vocanson, Marc, additional, Hung, Shuen-Iu, additional, Harrison, Caroline J., additional, Jenkins, Rosalind E., additional, French, Neil S., additional, Montañez, Maria Isabel, additional, Fernandez, Tahia D., additional, Martin-Serrano, Angela, additional, Torres, Maria Jose, additional, Molina, Noemi, additional, Wood, Sally, additional, Pirmohamed, Munir, additional, Montañez, María Isabel, additional, Martín-Serrano, Ángela, additional, Pérez-Inestrosa, Ezequiel, additional, Pérez-Sala, Dolores, additional, Guzmán, Antonio E., additional, Ko, Tai-Ming, additional, Chen, Yuan-Tsong, additional, Wu, Jer-Yuarn, additional, Sánchez-Gómez, Francisco J., additional, González-Morena, Juan M., additional, Torres, María J., additional, Arreola, Alejandra Monroy, additional, Corona, Jesus Agustin Badillo, additional, Flores, Silvia Mendez, additional, Cherit, Judith Dominguez, additional, Figueroa, Noe Valentin Duran, additional, Flores, Jose Luis Castrejon, additional, Perkins, James, additional, Pérez-Alzate, Diana, additional, Bogas, Gador, additional, Torres, María J, additional, Marti, Luis Mario Tubella, additional, De La Losa, Fernando Pineda, additional, Poves, Francisca Arribas, additional, Lopez, Jaime Tubella, additional, and Santiago, Teodora Lopez, additional

Published
2016
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10. Clinical pharmacogenetics implementation consortium (CPIC) guidelines for human leukocyte antigen B (HLA-B) genotype and allopurinol dosing: 2015 update

Author

Saito, Y., Stamp, L.K., Caudle, K.E., Hershfield, M.S., McDonagh, E.M., Callaghan, J.T., Tassaneeyakul, W., Mushiroda, T., Kamatani, N., Goldspiel, B.R., Phillips, E.J., Klein, T.E., Lee, M.T.M., Saito, Y., Stamp, L.K., Caudle, K.E., Hershfield, M.S., McDonagh, E.M., Callaghan, J.T., Tassaneeyakul, W., Mushiroda, T., Kamatani, N., Goldspiel, B.R., Phillips, E.J., Klein, T.E., and Lee, M.T.M.

Abstract

The Clinical Pharmacogenetics Implementation Consortium (CPIC) Guidelines for HLA-B*58:01 Genotype and Allopurinol Dosing was originally published in February 2013. We reviewed the recent literature and concluded that none of the evidence would change the therapeutic recommendations in the original guideline; therefore, the original publication remains clinically current. However, we have updated the Supplemental Material and included additional resources for applying CPIC guidelines into the electronic health record. Up-to-date information can be found at PharmGKB (http://www.pharmgkb.org).

Published
2015

11. Clinical Pharmacogenetics Implementation Consortium (CPIC) guidelines for human leukocyte antigen B (HLA-B) genotype and allopurinol dosing: 2015 update

Author

Saito, Y, primary, Stamp, LK, additional, Caudle, KE, additional, Hershfield, MS, additional, McDonagh, EM, additional, Callaghan, JT, additional, Tassaneeyakul, W, additional, Mushiroda, T, additional, Kamatani, N, additional, Goldspiel, BR, additional, Phillips, EJ, additional, Klein, TE, additional, and Lee, MTM, additional

Published
2015
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17. Downregulation of reversion-inducing-cysteine-rich protein with Kazal motifs (RECK) is associated with enhanced expression of matrix metalloproteinases and cholangiocarcinoma metastases

Author

Namwat, N., primary, Puetkasichonpasutha, J., additional, Loilome, W., additional, Yongvanit, P., additional, Techasen, A., additional, Puapairoj, A., additional, Sripa, B., additional, Tassaneeyakul, W., additional, Khuntikeo, N., additional, and Wongkham, S., additional

Published
2010
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19. Comparative bioavailability of two risperidone orodispersible tablet products after single dose administration

Author

Tassaneeyakul, W., primary, Kumar, S., additional, Gaysonsiri, D., additional, Kaewkamson, T., additional, Khuroo, A., additional, Tangsucharit, P., additional, Phunikhom, K., additional, Vannaprasaht, S., additional, Kanjanawart, S., additional, Thudi, N. Rao, additional, Jain, R., additional, Reyar, S., additional, and Monif, T., additional

Published
2010
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25. Human cytochrome P450 isoform specificity in the regioselective metabolism of toluene and o-, m- and p-xylene.

Author

Tassaneeyakul, W, Birkett, D J, Edwards, J W, Veronese, M E, Tassaneeyakul, W, Tukey, R H, and Miners, J O

Abstract

The conversion of toluene and o-, m- and p-xylene to their respective side-chain and ring monohydroxylated metabolites by human liver microsomes was investigated. Methyl hydroxylation, to form a benzylalcohol, was the major metabolic pathway for all four methylbenzenes. With the exception of 2,4-dimethylphenol formation from m-xylene, ring hydroxylation accounted for < 5% of total metabolite formation. However, regioselectivity of ring hydroxylation was apparent, with hydroxylation occurring only at positions ortho and/or para to a methyl substituent. Toluene and each xylene isomer exhibited biphasic methylhydroxylation kinetics in human liver microsomes. The high-affinity component of each methylhydroxylation was selectively inhibited by diethyldithiocarbamate and correlated significantly with cytochrome P-4502E1 (CYP2E1) content and activities in a panel of human liver microsomes. cDNA-expressed CYP2E1 was shown to catalyze the formation of each benzylalcohol, with apparent Km values similar to those of the high affinity microsomal reactions. In contrast, the conversion of m-xylene to 2,4-dimethylphenol followed single enzyme Michaelis-Menten kinetics, was inhibited selectively by furafylline, and correlated significantly with known CYP1A2 catalyzed reactions. cDNA-expressed CYP1A2 converted m-xylene to 2,4-dimethylphenol, with an apparent Km similar to that of the microsomal reaction. Although CYP1A2 appears to be responsible for the formation of the minor (phenolic) metabolites of toluene and the xylene isomers, CYP2E1 catalyzed methylhydroxylation will be the major determinant of the clearance of these compounds in humans.

Published
1996

26. Inhibitory effects of polyphenolic compounds on human arylamine N-acetyltransferase 1 and 2.

Author

Kukongviriyapan, V., Phromsopha, N., Tassaneeyakul, W., Kukongviriyapan, U., Sripa, B., Hahnvajanawong, V., and Bhudhisawasdi, V.

Subjects
POLYPHENOLS, CHEMICAL inhibitors, ACETYLTRANSFERASES, ACYLTRANSFERASES, RESPONSE inhibition, CATALYSTS, ENZYMES, CATALYSIS, PHENOLS
Abstract

Arylamine N -acetyltransferases (NAT) are important enzymes involved in the metabolic activation of aromatic and heterocyclic amines and inhibitors of NAT enzymes may be valuable as chemopreventive agents. Phytochemicals including cinnamic acid derivatives, various classes of flavonoids and coumarins were tested for the inhibitory activity on NAT1 and NAT2 from human liver and the human cholangiocarcinoma cell line: KMBC cells. Assays were performed using p -aminobenzoic acid and sulfamethazine as selective substrates for NAT1 and NAT2, respectively. NAT1 and NAT2 activities were present in liver cytosol. However, the KMBC cells showed only NAT1 activity. There was a marked difference in the ability of the test chemicals to inhibit NAT1 and NAT2. Caffeic acid, ferulic acid, gallic acid and EGCG inhibited NAT1 but not NAT2, whereas scopuletin and curcumin inhibited NAT2 but not NAT1. Quercetin, kaemferol and other flavonoids, except epicatechin and silymarin, inhibited both enzymes. The kinetics of inhibition of NAT1 by caffeic acid, EGCG and quercetin were of the non-competitive type, whereas that of NAT2 by quercetin, curcumin and kaemferol was also of the non-competitive type. The most potent inhibitor was quercetin, which has the inhibitory constants for NAT1 and NAT2 of 48.6?±?17.3 and 10.0?±?1.8?µM, respectively. [ABSTRACT FROM AUTHOR]

Published
2006
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28. Specificity of substrate and inhibitor probes for human cytochromes P450 1A1 and 1A2.

Author

Tassaneeyakul, W, Birkett, D J, Veronese, M E, McManus, M E, Tukey, R H, Quattrochi, L C, Gelboin, H V, and Miners, J O

Abstract

Kinetic and inhibitor studies using cDNA-expressed enzymes and human liver microsomes have characterized the specificity of a range of cytochrome P450 (CYP) 1A substrate and inhibitor probes towards the two isoforms comprising this subfamily. Expressed CYP1A1 and CYP1A2 both catalyzed the O-deethylation of phenacetin, although the apparent Km was about 4-fold lower for CYP1A2 (25 vs. 108 microM). Phenacetin O-deethylation exhibited biphasic kinetics in human liver microsomes, and the apparent Km for the high-affinity component (9 +/- 6 microM) was consistent with the involvement of CYP1A2 in this reaction. The prototypic CYP1A xenobiotic inhibitor and substrate probes alpha-naphthoflavone, ellipticine, 7-ethoxycoumarin and 7-ethoxyresorufin all inhibited CYP1A1- and CYP1A2-mediated phenacetin O-deethylation as well as the high-affinity component of human liver phenacetin O-deethylase activity. alpha-Naphthoflavone and 7-ethoxycoumarin were, however, approximately 10-fold more potent as inhibitors of CYP1A2 than CYP1A1. Other putative human CYP1A xenobiotic substrates and inhibitors, including caffeine, 5- and 8-methoxypsoralen, nifedipine, paraxanthine, propranolol and theophylline similarly inhibited CYP1A1- and 1A2-catalyzed phenacetin O-deethylation and the high-affinity human liver phenacetin O-deethylase. In contrast, the monoclonal antibody MAb 1-7-1, raised against 3-methylcholanthrene-inducible rat cytochromes 450, almost abolished CYP1A1-mediated phenacetin O-deethylation, but had no effect on human liver microsomal- or CYP1A2-catalyzed phenacetin dealkylation. Together with previous data, the results indicate that the majority of human CYP1A xenobiotic inhibitor and substrate probes are nonspecific in their recognition of CYP1A1 and CYP1A2, although selectivity is apparent for some compounds.

Published
1993

32. In vitro-in vivo extrapolation of CYP2C8-catalyzed paclitaxel 6a-hydroxylation : effects of albumin on in vitro kinetic parameters and assessment of interindividual variability in predicted clearance

Author

Verawan Uchaipichat, Thomas M. Polasek, Nitsupa Wattanachai, Wichittra Tassaneeyakul, Tahlia M. Heath, Wongwiwat Tassaneeyakul, John O. Miners, Wattanachai, N, Polasek, T.M, Heath, Tahlia Marie, Uchaipichat, V, Tassaneeyakul, W, and Miners, J

Subjects
Adult, Male, Paclitaxel, Metabolic Clearance Rate, Population, Tissue Banks, Pharmacology, Hydroxylation, Models, Biological, predicted paclitaxel hepatic, Cytochrome P-450 CYP2C8, chemistry.chemical_compound, Pharmacokinetics, In vivo, Fatty Acids, Omega-6, Humans, Computer Simulation, Pharmacology (medical), Bovine serum albumin, education, Aged, ADME, Aged, 80 and over, education.field_of_study, biology, Chemistry, Albumin, Reproducibility of Results, BSA supplementation, Serum Albumin, Bovine, General Medicine, Middle Aged, Antineoplastic Agents, Phytogenic, Recombinant Proteins, Kinetics, bovine serum albumin (BSA), Microsomes, Liver, biology.protein, Microsome, Female, Indicators and Reagents, Aryl Hydrocarbon Hydroxylases, Software
Abstract

Objectives This study aimed to characterize the effects of bovine serum albumin (BSA) on the kinetics of CYP2C8- catalyzed paclitaxel 6a-hydroxylation in vitro; determine whether the addition of BSA to incubations improves the prediction of paclitaxel hepatic clearance via this pathway in vivo; and assess interindividual variability in predicted clearance. Methods The kinetics of paclitaxel 6a-hydroxlation by human liver microsomes (HLM) and recombinant CYP2C8 were characterized in incubations performed with and without BSA (2% w/v) supplementation, and the in vitro kinetic data were extrapolated to provide estimates of in vivo clearances. The Simcyp population-based ADME simulator was used to determine interindividual variability in the predicted clearances. Results Supplementation of incubations of HLM with BSA resulted in a 3.6-fold increase in the microsomal intrinsic clearance for paclitaxel 6a-hydroxylation, due mainly to a reduction in Km (7.08+- 2.50 to 2.26 +- 0.39 uM), while addition of BSA to incubations of recombinant CYP2C8 resulted in an approximate doubling of intrinsic clearance. Mean values of predicted in vivo hepatic clearance were in good agreement with clinical data when in vitro data obtained in the presence of BSA were used for IV-IVE. Simcyp predicted 20- to 30-fold interindividual variability in in vivo paclitaxel hepatic clearance via the 6a-hydroxylation pathway. Conclusions Human liver microsomal Km and intrinsic clearance values are over- and underpredicted, respectively, when incubations of the CYP2C8 substrate paclitaxel are performed without BSA supplementation. IV-IVE based on kinetic parameters generated in the presence of BSA improves the accuracy of predicted paclitaxel hepatic clearance. Refereed/Peer-reviewed

Published
2011

33. Dual approaches in pharmacogenetics: Developing PCR-SSP and RT-PCR methods for HLA-B*13:01 screening to prevent dapsone and Co-trimoxazole SCARs.

Author

Attapong J, Kaset C, Nakkam N, Tassaneeyakul W, Wichukchinda N, and Chomean S

Abstract

Dapsone and co-trimoxazole are potent antibiotics for treating various infections and inflammations. However, several studies reported the strongly association between severe cutaneous adverse drug reactions (SCARs) to both drugs and the HLA-B*13:01 allele. Rapid and reliable screening for the HLA-B*13:01 allele can mitigate the risk of dapsone-induced SCARs. We developed two methods, multiplex sequence-specific primer PCR (PCR-SSP) and real-time PCR (RT-PCR), tailored for different clinical settings. These methods were optimized to minimize false positives among the Thai population. Clinical validation demonstrated excellent reproducibility, with both methods showing 100 % concordance in repeated tests. PCR-SSP achieved a limit of detection as low as 100 pg of genomic DNA, while RT-PCR reached 1 pg. Overall statistical accuracy was 100.00 % (95 % CI: 98.18 %-100.00 %). Screening for drug-related HLA alleles is crucial for reducing mortality from severe cutaneous adverse drug reactions, especially dapsone hypersensitivity syndrome (DHS) and dapsone-induced hypersensitivity reactions (DIHRs). Our screening approach for dapsone can also be extended to co-trimoxazole, representing a significant advancement in personalized medicine and preemptive pharmacogenetic testing for tailored patient care and safety, albeit further validation in diverse ethnic populations is warranted to ensure universal applicability., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2024 The Authors.)

Published
2024
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34. Complete mitochondrial genomes of patients from Thailand with cardiovascular diseases.

Author

Woravatin W, Wongkomonched R, Tassaneeyakul W, Stoneking M, Makarawate P, and Kutanan W

Subjects
Humans, Thailand epidemiology, Male, Female, Middle Aged, Adult, Cardiovascular Diseases genetics, Haplotypes, Aged, Mutation, Cardiomyopathy, Hypertrophic genetics, Young Adult, Genome, Mitochondrial, DNA, Mitochondrial genetics
Abstract

Several previous studies have reported that both variation and haplogroups of mitochondrial (mt) DNA were associated with various kinds of diseases, including cardiovascular diseases, in different populations, but such studies have not been carried out in Thailand. Here, we sequenced complete mtDNA genomes from 82 patients diagnosed with three types of cardiovascular disease, i.e., Hypertrophic Cardiomyopathy (HCM) (n = 26), Long Q-T Syndrome (LQTS) (n = 7) and Brugada Syndrome (BrS) (n = 49) and compared these with 750 previously published mitogenome sequences from interviewed normal individuals as a control group. Both patient and control groups are from the same geographic region of northeastern Thailand. We found 9, 2, and 5 novel mutations that were not both damaging and deleterious in HCM, LQTS, and BrS patients, respectively. Haplogroup R9c was significantly associated with HCM (P = 0.0032; OR = 62.42; 95%CI = 6.892-903.4) while haplogroup M12b was significantly associated with LQTS (P = 0.0039; OR = 32.93; 95% CI = 5.784-199.6). None of the haplogroups was found to be significantly associated with BrS. A significantly higher density of mtDNA variants in the rRNA genes was found in patients with HCM and BrS (P < 0.001) than in those with LQTS or the control group. Effects of detected SNPs in either protein coding or tRNA genes of all the mitogenome sequences were also predicted. Interestingly, three SNPs in two tRNA genes (MT-TA m.5618T>C and m.5631G>A heteroplasmic variants in two BrS patients and MT-TQ m.4392C>T novel homoplasmic variant in a HCM patient) were predicted to alter tRNA secondary structure, possibly leading to abnormal tRNA function., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Woravatin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Published
2024
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35. Association between HLA alleles and beta-lactam antibiotics-related severe cutaneous adverse reactions.

Author

Wattanachai P, Amornpinyo W, Konyoung P, Purimart D, Khunarkornsiri U, Pattanacheewapull O, Tassaneeyakul W, and Nakkam N

Abstract

Introduction: Beta-lactam antibiotics are one of the most common causes of antibiotics-related severe cutaneous adverse reactions (SCARs) including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), drug reactions with eosinophilia and systemic symptoms (DRESS), and acute generalized exanthematous pustulosis (AGEP). Recent evidence demonstrated that the human leukocyte antigen ( HLA ) polymorphisms play important roles in the development of drug-related SCARs. This study aimed to extensively characterize the associations between HLA genetic polymorphisms and several phenotypes of SCARs related to beta-lactam antibiotics. Methods: Thirty-one Thai patients with beta-lactam antibiotics-related SCARs were enrolled in the study. A total of 183 unrelated native Thai subjects without any evidence of drug allergy were recruited as the control group. Genotyping of HLA class I and class II alleles was performed. Results: Six HLA alleles including HLA-A*01:01 , HLA-B*50:01 , HLA-C*06:02 , HLA-DRB1*15:01 , HLA-DQA1*03:01 , and HLA-DQB1*03:02 , were significantly associated with beta-lactam antibiotics-related SCARs. The highest risk of SCARs was observed in patients with the HLA-B*50:01 allele (OR = 12.6, 95% CI = 1.1-142.9, p = 0.042), followed by the HLA-DQB1*03:02 allele (OR = 5.8, 95% CI = 1.5-22.0, p = 0.012) and the HLA-C*06:02 allele (OR = 5.7, 95% CI = 1.6-19.9, p = 0.011). According to the phenotypes of SCARs related to beta-lactam antibiotics, the higher risk of SJS/TEN was observed in patients with HLA-A*03:02 , HLA-B*46:02 (OR = 17.5, 95% CI = 1.5-201.6, p = 0.033), HLA-A*02:06 , HLA-B*57:01 (OR = 9.5, 95% CI = 1.3-71.5, p = 0.028), HLA-DQB1*03:02 (OR = 7.5, 95% CI = 1.8-30.9, p = 0.008), or HLA-C*06:02 (OR = 4.9, 95% CI = 1.1-21.4, p = 0.008). While eight HLA alleles including HLA-A*02:05 , HLA-A*02:11 , HLA-B*37:01 , HLA-B*38:01 , HLA-B*50:01 , HLA-C*06:02 , HLA-C*03:09 , and HLA-DRB1*15:01 were associated with AGEP, the highest risk of AGEP was observed in patients with the HLA-B*50:01 allele (OR = 60.7, 95% CI = 4.8-765.00, p = 0.005). Among the four HLA alleles associated with DRESS including HLA-C*04:06 , HLA-DRB1*04:05 , HLA-DRB1*11:01 , and HLA-DQB1*04:01 , the HLA-C*04:06 allele had the highest risk of beta-lactam antibiotics-related DRESS (OR = 60.0, 95% CI = 3.0-1202.1, p = 0.043). However, these associations did not achieve statistical significance after Bonferroni's correction. Apart from the HLA risk alleles, the HLA-A*02:07 allele appeared to be a protective factor against beta-lactam antibiotic-related SCARs (OR = 0.1, 95% CI = 0.0-0.5, p = 3.7 × 10 -4 , Pc = 0.012). Conclusion: This study demonstrated the candidate HLA alleles that are significantly associated with several phenotypes of beta-lactam antibiotics-related SCARs. However, whether the HLA alleles observed in this study can be used as valid genetic markers for SCARs related to beta-lactam antibiotics needs to be further explored in other ethnicities and larger cohort studies., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Wattanachai, Amornpinyo, Konyoung, Purimart, Khunarkornsiri, Pattanacheewapull, Tassaneeyakul and Nakkam.)

Published
2023
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36. Cost-effectiveness analysis of HLA-B*13:01 screening for the prevention of co-trimoxazole-induced severe cutaneous adverse reactions among HIV-infected patients in Thailand.

Author

Kategeaw W, Nakkam N, Kiertiburanakul S, Sukasem C, Tassaneeyakul W, and Chaiyakunapruk N

Subjects
Humans, Cost-Effectiveness Analysis, Thailand, Cicatrix, Cost-Benefit Analysis, HLA-B Antigens genetics, Trimethoprim, Sulfamethoxazole Drug Combination adverse effects, HIV Infections drug therapy
Abstract

Studies found a strong association between HLA-B*13:01 allele and co-trimoxazole-induced severe cutaneous adverse reactions (SCARs). Genetic screening before initiation of co-trimoxazole may decrease the incidence of co-trimoxazole-induced SCARs. This study aims to evaluate the cost-effectiveness of HLA-B*13:01 screening before co-trimoxazole initiation in HIV-infected patients in Thailand. A combination of a decision tree model and a Markov model was used to estimate lifetime costs and outcomes of two strategies including 1) HLA-B*13:01 screening before co-trimoxazole initiation and 2) usual practice from a societal perspective. Alternative drugs are not considered because dapsone (the second-line drug) also presents a genetic risk. Input parameters were obtained from literature, government documents, and part of the TREAT Asia HIV Observational Database (TAHOD). One-way sensitivity analyses and probabilistic analyses were performed to determine robustness of the findings. HLA-B*13:01 screening resulted in 0.0061 quality-adjusted life years (QALYs) loss with an additional cost of 370 THB ($11.84). At the cost-effectiveness threshold of 160,000 THB ($5,112.85), the probability of the genetic screening strategy being cost-effective is 9.54%. This analysis demonstrated that HLA-B*13:01 allele screening before initiation of co-trimoxazole among HIV-infected patients is unlikely to be cost-effective in Thailand. Our findings will help policymakers make an evidence-informed decision making.

Published
2023
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37. Development of label-free electrochemical impedance spectroscopy for the detection of HLA-B*15:02 and HLA-B*15:21 for the prevention of carbamazepine-induced Stevens-Johnson syndrome.

Author

Chomean S, Nakkam N, Tassaneeyakul W, Attapong J, and Kaset C

Subjects
Humans, Anticonvulsants therapeutic use, Benzodiazepines, Genetic Predisposition to Disease, HLA-B Antigens chemistry, HLA-B Antigens genetics, HLA-B15 Antigen chemistry, HLA-B15 Antigen genetics, Carbamazepine adverse effects, Carbamazepine pharmacology, Dielectric Spectroscopy methods, Stevens-Johnson Syndrome diagnosis, Stevens-Johnson Syndrome etiology, Stevens-Johnson Syndrome genetics
Abstract

Background: Carbamazepine (CBZ) is an FDA-approved anticonvulsant that is widely used to treat epilepsy, bipolar disorder, trigeminal neuralgia and chronic pain. Several studies have reported a strong association between HLA-B*15:02 and carbamazepine-induced Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN). However, the HLA-B75 serotype (HLA-B*15:02, HLA-B*15:08, HLA-B*15:11 and HLA-B*15:21) has been found in patients with carbamazepine-induced SJS/TEN., Methods: This study aimed to develop label-free electrochemical impedance spectroscopy (EIS) for the detection of HLA-B*15:02 and HLA-B*15:21 after PCR-SSP amplification. A total of 208 DNA samples were tested. The impedance was measured and compared to standard gel electrophoresis., Results: The developed label-free EIS identified HLA-B*15:02 and HLA-B*15:21 alleles with 100% sensitivity (95% CI: 86.773%-100.000%) and 95.05% specificity (95% CI: 90.821%-97.714%), comparable to commercial DMSc 15:02 detection kits., Conclusions: We successfully developed a novel PCR-SSP associated with signal impedance changes to detect the HLA-B*15:02 allele and HLA-B*15:21 without downstream amplicon size analysis that is suitable for screening individuals before indication of CBZ therapy., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Published
2022
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38. Associations of HLA and drug-metabolizing enzyme genes in co-trimoxazole-induced severe cutaneous adverse reactions.

Author

Nakkam N, Saksit N, Konyoung P, Amornpinyo W, Khunarkornsiri U, Purimart D, Pattanacheewapull O, Naewla T, Wattanachai P, Khaeso K, Chumworathayi P, and Tassaneeyakul W

Subjects
Humans, Alleles, Anticonvulsants, HLA-B Antigens genetics, Polymorphism, Genetic, Stevens-Johnson Syndrome genetics, Trimethoprim, Sulfamethoxazole Drug Combination adverse effects
Abstract

Co-trimoxazole is mainly used as a first-line drug for treatment and prophylaxis against Pneumocystis jiroveci pneumonia. This drug, however, has been reported as the most common causative drug for severe cutaneous adverse reactions (SCARs). This study aimed to extensively elucidate the associations between genetic polymorphisms of HLA class I and genes involved in bioactivation and detoxification of co-trimoxazole on co-trimoxazole-induced SCARS in a large sample size and well-defined Thai SCARs patients. A total of 67 patients with co-trimoxazole-induced SCARs, consisting of 51 SJS/TEN patients and 16 DRESS patients, and 91 co-trimoxazole tolerant controls were enrolled in the study. The results clearly demonstrated that the HLA-B ∗ 13:01 allele was significantly associated with co-trimoxazole-induced SCARs, especially with DRESS (OR = 8.44, 95% CI = 2.66-26.77, P = 2.94 × 10 -4 , Pc = 0.0126). Moreover, the HLA-C ∗ 08:01 allele was significantly associated with co-trimoxazole-induced SJS/TEN in the HIV/AIDS patients with an OR of 8.51 (95% CI = 2.18-33.14, P = 8.60 × 10 -4 , Pc = 0.0241). None of the genes involved in the bioactivation and detoxification of co-trimoxazole investigated in this study play any major role in the development of all phenotypes of SCARs., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Japanese Society for the Study of Xenobiotics. Published by Elsevier Ltd. All rights reserved.)

Published
2022
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39. NUDT15 is a key genetic factor for prediction of hematotoxicity in pediatric patients who received a standard low dosage regimen of 6-mercaptopurine.

Author

Khaeso K, Komvilaisak P, Chainansamit SO, Nakkam N, Suwannaying K, Kuwatjanakul P, Hikino K, Dornsena A, Kanjanawart S, Laoaroon N, Vannaprasaht S, Taketani T, and Tassaneeyakul W

Subjects
Asian People, Child, Genotype, Humans, Methyltransferases genetics, Polymorphism, Genetic genetics, Mercaptopurine adverse effects, Mercaptopurine metabolism, Precursor Cell Lymphoblastic Leukemia-Lymphoma chemically induced, Precursor Cell Lymphoblastic Leukemia-Lymphoma drug therapy, Precursor Cell Lymphoblastic Leukemia-Lymphoma genetics
Abstract

6-Mercaptopurine (6-MP) is commonly used for treatment of acute lymphoblastic leukemia (ALL). The incidence of hematotoxicity caused by this drug is quite high in Asians even using a standard low dosage regimen. The present study was aimed to elucidate the impact of thiopurine S-methyltransferase (TPMT), a nucleoside diphosphate-linked moiety X-type motif 15 (NUDT15), inosine triphosphatase (ITPA) and ATP Binding Cassette Subfamily C Member 4 (ABCC4) polymorphisms on hematotoxicity in pediatric patients who received a standard low starting dose of 6-MP. One hundred and sixty-nine pediatric patients were enrolled and their genotypes were determined. Patients who carried NUDT15 ∗ 3 and NUDT15 ∗ 2 genotypes were at a 10-15 fold higher risk of severe neutropenia than those of the wild-type during the early months of the maintenance phase. Risk of neutropenia was not significantly increased in patients with other NUDT15 variants as well as in patients with TPMT, ITPA or ABCC4 variants. These results suggest that NUDT15 polymorphisms particularly, NUDT15 ∗ 3 and NUDT15 ∗ 2, play major roles in 6-MP-induced severe hematotoxicity even when using a standard low dosage of 6-MP and genotyping of these variants is necessary in order to obtain precise tolerance doses and avoid severe hematotoxicity in pediatric patients., Competing Interests: Declaration of competing interest The author declares no conflict of interest., (Copyright © 2021 The Japanese Society for the Study of Xenobiotics. Published by Elsevier Ltd. All rights reserved.)

Published
2022
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40. Genetic variants associated with severe cutaneous adverse drug reactions induced by carbamazepine.

Author

Nakkam N, Konyoung P, Amornpinyo W, Saksit N, Tiamkao S, Khunarkornsiri U, Khaeso K, Pattanacheewapull O, Jorns TP, Chumworathayi P, and Tassaneeyakul W

Subjects
Anticonvulsants adverse effects, Benzodiazepines, Carbamazepine adverse effects, Genetic Predisposition to Disease, HLA Antigens, HLA-A Antigens genetics, HLA-B Antigens genetics, Humans, Cicatrix chemically induced, Cicatrix complications, Cicatrix drug therapy, Stevens-Johnson Syndrome diagnosis, Stevens-Johnson Syndrome genetics
Abstract

Aims: Carbamazepine (CBZ) is one of the most common causative drugs of severe cutaneous adverse drug reactions (SCARs) including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN) and drug reactions with eosinophilia and systemic symptoms. Although genetic polymorphisms of the human leucocyte antigens (HLA) are well recognized key elements for the susceptibility to CBZ-induced SCARs, some evidence suggest that polymorphisms of microsomal epoxide hydrolase 1 (EPHX1) may also contribute to the risk of these SCARs. This study investigated the association between the HLA and EPHX1 polymorphisms on CBZ-induced SCARs in large sample sizes and well-defined SCARs patients., Methods: Ninety-one CBZ-induced SCARs Thai patients and 144 CBZ-tolerant patients were enrolled in the study. The genotypes of HLA-A, HLA-B and EPHX1 were determined., Results: Only 2 HLA alleles including HLA-B*15:02 and HLA-A*24:07 were statistically significant association with CBZ-induced SJS/TEN. The highest risk was observed in patients with HLA-B*15:02 allele (OR = 44.33, 95% confidence interval = 20.24-97.09, corrected P-value = 6.80 × 10 -29 ). Moreover, HLA-B75 serotypes were significantly associated with CBZ-induced SJS/TEN groups with an odds ratio of 81.00 (95% confidence interval = 32.39-202.56, corrected P-value = 3.84 × 10 -34 ). There is no association between EPHX1 c.337 T > C polymorphism and all phenotypes of CBZ-induced SCARs., Conclusion: The HLA-B*15:02 allele is the strongest genetic marker for the prediction of SJS/TEN induced by CBZ in Thai population. Screening for other alleles in the HLA-B75 serotype increases sensitivity for prediction of a life-threatening SCARs caused by CBZ., (© 2021 British Pharmacological Society.)

Published
2022
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41. Meta-Analysis of NUDT15 Genetic Polymorphism on Thiopurine-Induced Myelosuppression in Asian Populations.

Author

Khaeso K, Udayachalerm S, Komvilaisak P, Chainansamit SO, Suwannaying K, Laoaroon N, Kuwatjanakul P, Nakkam N, Sukasem C, Puangpetch A, Tassaneeyakul W, and Chaiyakunapruk N

Abstract

Backgound: The high incidence of thiopurine-induced myelosuppression in Asians is known to be attributable to genetic variation in thiopurine metabolism. A quantitative synthesis to summarize the genetic association with thiopurine-induced myelosuppression in Asians was therefore conducted. Methods: A Literature search was performed from January 2016 to May 2021 in the following databases: PubMed, Web of Science, and Embase and addition search included the studies from Zhang et al. Two reviewers independently extracted the following data: the author's name, year of publication, ethnicity, drugs, diseases, genetic polymorphisms, onset, type of myelosuppression and results of Hardy-Weinberg equilibrium. The Newcastle-Ottawa Scale was used to assess the quality of the studies. The pooled odds ratios (OR) and 95% confidence intervals (CI) were calculated to evaluate the associations of NUDT15 and the risk of thiopurine-induced myelosuppression stratified by onset and type of myelosuppressive. Subgroup analysis by NUDT15 genetic polymorphisms was performed. Results: A total of 30 studies was included in this meta-analysis. The overall OR for the relationship between NUDT15 genetic polymorphisms and thiopurine-induced early onset of leukopenia and neutropenia in Asian populations were 11.43 (95% CI 7.11-18.35) and 16.35 (95% CI 10.20-26.22). Among NUDT15 polymorphisms, NUDT15*3 showed a significantly increased risk of early leukopenia (OR 15.31; 95% CI 9.65-24.27) and early neutropenia (OR 15.85; 95% CI 8.80-28.53). A significantly higher thiopurine-induced early neutropenic risk was also found for NUDT15*2 (OR 37.51; 95% CI 1.99-708.69) . Whereas, NUDT15*5 and NUDT15*6 variants showed a lower risk of leukopenia. Conclusion: This study suggests that NUDT15*3 and NUDT15*2 are important genetic markers of thiopurine-induced early onset of myelotoxicity in Asians, therefore, early detection of these variants before initiating thiopurine therapy is necessary., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Khaeso, Udayachalerm, Komvilaisak, Chainansamit, Suwannaying, Laoaroon, Kuwatjanakul, Nakkam, Sukasem, Puangpetch, Tassaneeyakul and Chaiyakunapruk.)

Published
2021
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42. The Thai reference exome (T-REx) variant database.

Author

Shotelersuk V, Wichadakul D, Ngamphiw C, Srichomthong C, Phokaew C, Wilantho A, Pakchuen S, Nakhonsri V, Shaw PJ, Wasitthankasem R, Piriyapongsa J, Wangkumhang P, Assawapitaksakul A, Chetruengchai W, Lapphra K, Khuninthong A, Makarawate P, Suphapeetiporn K, Mahasirimongkol S, Satproedprai N, Porntaveetus T, Pisitkun P, Praphanphoj V, Kantaputra P, Tassaneeyakul W, and Tongsima S

Subjects
Computational Biology methods, DNA Copy Number Variations, Genetic Association Studies methods, Genetic Predisposition to Disease, Genetics, Population, Genomic Medicine methods, Humans, Molecular Sequence Annotation, Polymorphism, Single Nucleotide, Thailand, Exome Sequencing, Databases, Genetic, Exome, Genetic Variation
Abstract

To maximize the potential of genomics in medicine, it is essential to establish databases of genomic variants for ethno-geographic groups that can be used for filtering and prioritizing candidate pathogenic variants. Populations with non-European ancestry are poorly represented among current genomic variant databases. Here, we report the first high-density survey of genomic variants for the Thai population, the Thai Reference Exome (T-REx) variant database. T-REx comprises exome sequencing data of 1092 unrelated Thai individuals. The targeted exome regions common among four capture platforms cover 30.04 Mbp on autosomes and chromosome X. 345 681 short variants (18.27% of which are novel) and 34 907 copy number variations were found. Principal component analysis on 38 469 single nucleotide variants present worldwide showed that the Thai population is most genetically similar to East and Southeast Asian populations. Moreover, unsupervised clustering revealed six Thai subpopulations consistent with the evidence of gene flow from neighboring populations. The prevalence of common pathogenic variants in T-REx was investigated in detail, which revealed subpopulation-specific patterns, in particular variants associated with erythrocyte disorders such as the HbE variant in HBB and the Viangchan variant in G6PD. T-REx serves as a pivotal addition to the current databases for genomic medicine., (© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2021
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43. HLA-B*13 :01 Is a Predictive Marker of Dapsone-Induced Severe Cutaneous Adverse Reactions in Thai Patients.

Author

Satapornpong P, Pratoomwun J, Rerknimitr P, Klaewsongkram J, Nakkam N, Rungrotmongkol T, Konyoung P, Saksit N, Mahakkanukrauh A, Amornpinyo W, Khunarkornsiri U, Tempark T, Wantavornprasert K, Jinda P, Koomdee N, Jantararoungtong T, Rerkpattanapipat T, Wang CW, Naisbitt D, Tassaneeyakul W, Ariyachaipanich M, Roonghiranwat T, Pirmohamed M, Chung WH, and Sukasem C

Subjects
Adolescent, Adult, Aged, Asian People statistics & numerical data, Child, Child, Preschool, Cytochrome P-450 Enzyme System genetics, Female, Genetic Association Studies, Genetic Markers, Genotype, HLA-B Antigens classification, Humans, Male, Middle Aged, Molecular Docking Simulation, Prospective Studies, Young Adult, Alleles, Dapsone adverse effects, HLA-B Antigens genetics, Polymorphism, Genetic, Skin drug effects, Skin pathology
Abstract

HLA-B*13:01 allele has been identified as the genetic determinant of dapsone hypersensitivity syndrome (DHS) among leprosy and non-leprosy patients in several studies. Dapsone hydroxylamine (DDS-NHOH), an active metabolite of dapsone, has been believed to be responsible for DHS. However, studies have not highlighted the importance of other genetic polymorphisms in dapsone-induced severe cutaneous adverse reactions (SCAR). We investigated the association of HLA alleles and cytochrome P450 (CYP) alleles with dapsone-induced SCAR in Thai non-leprosy patients. A prospective cohort study, 16 Thai patients of dapsone-induced SCARs (5 SJS-TEN and 11 DRESS) and 9 Taiwanese patients of dapsone-induced SCARs (2 SJS-TEN and 7 DRESS), 40 dapsone-tolerant controls, and 470 general Thai population were enrolled. HLA class I and II alleles were genotyped using polymerase chain reaction-sequence specific oligonucleotides (PCR-SSOs). CYP2C9 , CYP2C19 , and CYP3A4 genotypes were determined by the TaqMan real-time PCR assay. We performed computational analyses of dapsone and DDS-NHOH interacting with HLA-B*13:01 and HLA-B*13:02 alleles by the molecular docking approach. Among all the HLA alleles, only HLA-B*13:01 allele was found to be significantly associated with dapsone-induced SCARs (OR = 39.00, 95% CI = 7.67-198.21, p = 5.3447 × 10 -7 ), SJS-TEN (OR = 36.00, 95% CI = 3.19-405.89, p = 2.1657 × 10 -3 ), and DRESS (OR = 40.50, 95% CI = 6.38-257.03, p = 1.0784 × 10 -5 ) as compared to dapsone-tolerant controls. Also , HLA-B*13:01 allele was strongly associated with dapsone-induced SCARs in Asians (OR = 36.00, 95% CI = 8.67-149.52, p = 2.8068 × 10 -7 ) and Taiwanese (OR = 31.50, 95% CI = 4.80-206.56, p = 2.5519 × 10 -3 ). Furthermore, dapsone and DDS-NHOH fit within the extra-deep sub pocket of the antigen-binding site of the HLA-B*13:01 allele and change the antigen-recognition site. However, there was no significant association between genetic polymorphism of cytochrome P450 ( CYP2C9 , CYP2C19 , and CYP3A4 ) and dapsone-induced SCARs (SJS-TEN and DRESS). The results of this study support the specific genotyping of the HLA-B*13:01 allele to avoid dapsone-induced SCARs including SJS-TEN and DRESS before initiating dapsone therapy in the Asian population., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer TB declared a past collaboration with the author W-HC to the handling editor., (Copyright © 2021 Satapornpong, Pratoomwun, Rerknimitr, Klaewsongkram, Nakkam, Rungrotmongkol, Konyoung, Saksit, Mahakkanukrauh, Amornpinyo, Khunarkornsiri, Tempark, Wantavornprasert, Jinda, Koomdee, Jantararoungtong, Rerkpattanapipat, Wang, Naisbitt, Tassaneeyakul, Ariyachaipanich, Roonghiranwat, Pirmohamed, Chung and Sukasem.)

Published
2021
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44. Characterization of T-Cell Responses to SMX and SMX-NO in Co-Trimoxazole Hypersensitivity Patients Expressing HLA-B*13:01 .

Author

Pratoomwun J, Thomson P, Jaruthamsophon K, Tiyasirichokchai R, Jinda P, Rerkpattanapipat T, Tassaneeyakul W, Nakkam N, Rerknimitr P, Klaewsongkram J, Srinoulprasert Y, Pirmohamed M, Naisbitt DJ, and Sukasem C

Subjects
Adult, Antigen Presentation immunology, Antigen-Presenting Cells immunology, Antigen-Presenting Cells metabolism, CD4-Positive T-Lymphocytes immunology, CD4-Positive T-Lymphocytes metabolism, Cells, Cultured, Drug Hypersensitivity metabolism, Female, Histocompatibility Antigens Class II genetics, Histocompatibility Antigens Class II immunology, Humans, Leukocytes, Mononuclear immunology, Leukocytes, Mononuclear metabolism, Lymphocyte Activation genetics, Lymphocyte Activation immunology, Male, T-Cell Antigen Receptor Specificity, Drug Hypersensitivity etiology, Gene Expression, HLA-B13 Antigen genetics, HLA-B13 Antigen immunology, T-Lymphocytes immunology, T-Lymphocytes metabolism, Trimethoprim, Sulfamethoxazole Drug Combination adverse effects
Abstract

HLA-B*13:01 -positive patients in Thailand can develop frequent co-trimoxazole hypersensitivity reactions. This study aimed to characterize drug-specific T cells from three co-trimoxazole hypersensitive patients presenting with either Stevens-Johnson syndrome or drug reaction with eosinophilia and systemic symptoms. Two of the patients carried the HLA allele of interest, namely HLA-B*13:01 . Sulfamethoxazole and nitroso sulfamethoxazole specific T cell clones were generated from T cell lines of co-trimoxazole hypersensitive HLA-B*13:01 -positive patients. Clones were characterized for antigen specificity and cross-reactivity with structurally related compounds by measuring proliferation and cytokine release. Surface marker expression was characterized via flow cytometry. Mechanistic studies were conducted to assess pathways of T cell activation in response to antigen stimulation. Peripheral blood mononuclear cells from all patients were stimulated to proliferate and secrete IFN-γ with nitroso sulfamethoxazole. All sulfamethoxazole and nitroso sulfamethoxazole specific T cell clones expressed the CD4+ phenotype and strongly secreted IL-13 as well as IFN-γ, granzyme B and IL-22. No secretion of IL-17 was observed. A number of nitroso sulfamethoxazole-specific clones cross-reacted with nitroso dapsone but not sulfamethoxazole whereas sulfamethoxazole specific clones cross-reacted with nitroso sulfamethoxazole only. The nitroso sulfamethoxazole specific clones were activated in both antigen processing-dependent and -independent manner, while sulfamethoxazole activated T cell responses via direct HLA binding. Furthermore, activation of nitroso sulfamethoxazole-specific, but not sulfamethoxazole-specific, clones was blocked with glutathione. Sulfamethoxazole and nitroso sulfamethoxazole specific T cell clones from hypersensitive patients were CD4+ which suggests that HLA-B*13:01 is not directly involved in the iatrogenic disease observed in co-trimoxazole hypersensitivity patients., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Pratoomwun, Thomson, Jaruthamsophon, Tiyasirichokchai, Jinda, Rerkpattanapipat, Tassaneeyakul, Nakkam, Rerknimitr, Klaewsongkram, Srinoulprasert, Pirmohamed, Naisbitt and Sukasem.)

Published
2021
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45. Whole genome sequencing identifies genetic variants associated with co-trimoxazole hypersensitivity in Asians.

Author

Wang CW, Tassaneeyakul W, Chen CB, Chen WT, Teng YC, Huang CY, Sukasem C, Lu CW, Lee YS, Choon SE, Nakkam N, Hui RC, Huang YH, Chang YC, Lin YY, Chang CJ, Chiu TM, Chantratita W, Konyoung P, Lee CN, Klaewsongkram J, Rerkpattanapipat T, Amornpinyo W, Saksit N, Rerknimitr P, Huang YH, Lin SH, Hsu CK, Chan CC, Lin YJ, Hung SI, and Chung WH

Subjects
Adolescent, Adult, Aged, Case-Control Studies, Female, Humans, Malaysia epidemiology, Male, Middle Aged, Polymorphism, Single Nucleotide, Taiwan epidemiology, Thailand epidemiology, Whole Genome Sequencing, Young Adult, Anti-Bacterial Agents adverse effects, Anti-Infective Agents, Urinary adverse effects, Asian People genetics, Drug Hypersensitivity genetics, Genetic Predisposition to Disease, HLA-B Antigens genetics, Trimethoprim, Sulfamethoxazole Drug Combination adverse effects
Abstract

Background: Co-trimoxazole, a sulfonamide antibiotic, is used to treat a variety of infections worldwide, and it remains a common first-line medicine for prophylaxis against Pneumocystis jiroveci pneumonia. However, it can cause severe cutaneous adverse reaction (SCAR), including Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug reaction with eosinophilia and systemic symptoms. The pathomechanism of co-trimoxazole-induced SCAR remains unclear., Objective: We aimed to investigate the genetic predisposition of co-trimoxazole-induced SCAR., Methods: We conducted a multicountry case-control association study that included 151 patients with of co-trimoxazole-induced SCAR and 4631 population controls from Taiwan, Thailand, and Malaysia, as well as 138 tolerant controls from Taiwan. Whole-genome sequencing was performed for the patients and population controls from Taiwan; it further validated the results from Thailand and Malaysia., Results: The whole-genome sequencing study (43 case patients vs 507 controls) discovered that the single-nucleotide polymorphism rs41554616, which is located between the HLA-B and MICA loci, had the strongest association with co-trimoxazole-induced SCAR (P = 8.2 × 10 -9 ; odds ratio [OR] = 7.7). There were weak associations of variants in co-trimoxazole-related metabolizing enzymes (CYP2D6, GSTP1, GCLC, N-acetyltransferase [NAT2], and CYP2C8). A replication study using HLA genotyping revealed that HLA-B∗13:01 was strongly associated with co-trimoxazole-induced SCAR (the combined sample comprised 91 case patients vs 2545 controls [P = 7.2 × 10 -21 ; OR = 8.7]). A strong HLA association was also observed in the case patients from Thailand (P = 3.2 × 10 -5 ; OR = 3.6) and Malaysia (P = .002; OR = 12.8), respectively. A meta-analysis and phenotype stratification study further indicated a strong association between HLA-B∗13:01 and co-trimoxazole-induced drug reaction with eosinophilia and systemic symptoms (P = 4.2 × 10 -23 ; OR = 40.1)., Conclusion: This study identified HLA-B∗13:01 as an important genetic factor associated with co-trimoxazole-induced SCAR in Asians., (Copyright © 2020 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)

Published
2021
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46. Genetic Polymorphisms of Drug-Metabolizing Enzymes Involved in 6-Mercaptopurine-Induced Myelosuppression in Thai Pediatric Acute Lymphoblastic Leukemia Patients.

Author

Khaeso K, Nakkam N, Komwilaisak P, Wongmast P, Chainansamit SO, Dornsena A, Kanjanawart S, Vannaprasaht S, and Tassaneeyakul W

Abstract

Genetic polymorphisms of thiopurine S-methyltransferase (TPMT) and nucleoside diphosphate-linked moiety X-type motif 15 ( NUDT15 ) genes have been proposed as key determinants of 6-mercaptopurine (6-MP)-induced myelosuppression in pediatric acute lymphoblastic leukemia (ALL). In the present study, genotypes of TPMT and NUDT15 were investigated in 178 Thai pediatric patients with ALL by the TaqMan SNP genotyping assay and DNA sequencing. The frequency of TPMT*3C was 0.034. Among NUDT15 variants, NUDT15*3 is the most common variant with the allele frequency of 0.073, whereas those of NUDT15*2 , NUDT15*5 , and NUDT15*6 variants were 0.022, 0.011, and 0.039. These data suggest that a high proportion of Thai pediatric ALL patients may be at risk of thiopurine-induced myelosuppression., Competing Interests: Conflict of Interest None declared., (Thieme. All rights reserved.)

Published
2021
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47. Genetic Association of Co-Trimoxazole-Induced Severe Cutaneous Adverse Reactions Is Phenotype-Specific: HLA Class I Genotypes and Haplotypes.

Author

Sukasem C, Pratoomwun J, Satapornpong P, Klaewsongkram J, Rerkpattanapipat T, Rerknimitr P, Lertpichitkul P, Puangpetch A, Nakkam N, Konyoung P, Khunarkornsiri U, Disphanurat W, Srisuttiyakorn C, Pattanacheewapull O, Kanjanawart S, Kongpan T, Chumworathayi P, Saksit N, Bruminhent J, Tassaneeyakul W, Chantratita W, and Pirmohamed M

Subjects
Adolescent, Adult, Aged, Case-Control Studies, Drug Hypersensitivity Syndrome diagnosis, Drug Hypersensitivity Syndrome immunology, Female, Genetic Association Studies, Genetic Predisposition to Disease, HIV Infections immunology, HLA Antigens immunology, Haplotypes, Humans, Male, Middle Aged, Phenotype, Prospective Studies, Risk Assessment, Risk Factors, Severity of Illness Index, Stevens-Johnson Syndrome diagnosis, Stevens-Johnson Syndrome immunology, Thailand, Young Adult, Anti-Bacterial Agents adverse effects, Drug Hypersensitivity Syndrome genetics, HLA Antigens genetics, Stevens-Johnson Syndrome genetics, Trimethoprim, Sulfamethoxazole Drug Combination adverse effects
Abstract

Co-trimoxazole (CTX) causes various forms of severe cutaneous adverse reactions (SCARs). This case-control study was conducted to investigate the involvement between genetic variants of human leukocyte antigen (HLA) and CYP2C9 in CTX-induced SCARs, including Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) and drug reaction with eosinophilia and systemic symptoms (DRESS) in Thai patients. Thirty cases of CTX-induced SCARs were enrolled and compared with 91 CTX-tolerant controls and 150 people from the general Thai population. Cases comprised 18 SJS/TEN and 12 DRESS patients. This study demonstrated that genetic association of CTX-induced SCARs was phenotype-specific. HLA-B*15:02 and HLA-C*08:01 alleles were significantly associated with CTX-induced SJS/TEN, whereas the HLA-B*13:01 allele was significantly associated with CTX-induced DRESS. In addition, a significant higher frequency of HLA-A*11:01-B*15:02 and HLA-B*13:01-C*03:04 haplotypes were detected in the group of CTX-induced Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) and DRESS cases, respectively. Genetic association of CTX-induced SCARs is phenotype-specific. Interestingly, these association was observed only in HIV-infected patients but not in non-HIV-infected patients., (© 2020 The Authors Clinical Pharmacology & Therapeutics © 2020 American Society for Clinical Pharmacology and Therapeutics.)

Published
2020
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48. Identification of drug-specific public TCR driving severe cutaneous adverse reactions.

Author

Pan RY, Chu MT, Wang CW, Lee YS, Lemonnier F, Michels AW, Schutte R, Ostrov DA, Chen CB, Phillips EJ, Mallal SA, Mockenhaupt M, Bellón T, Tassaneeyakul W, White KD, Roujeau JC, Chung WH, and Hung SI

Subjects
Adoptive Transfer, Adult, Aged, Animals, Disease Models, Animal, Female, HLA-B15 Antigen genetics, HLA-B15 Antigen immunology, Humans, Male, Mice, Transgenic, Middle Aged, Receptor-CD3 Complex, Antigen, T-Cell immunology, Receptors, Antigen, T-Cell, alpha-beta immunology, Severity of Illness Index, Skin immunology, Skin pathology, Stevens-Johnson Syndrome diagnosis, Stevens-Johnson Syndrome pathology, T-Lymphocytes, Cytotoxic metabolism, T-Lymphocytes, Cytotoxic transplantation, Carbamazepine adverse effects, Receptor-CD3 Complex, Antigen, T-Cell metabolism, Receptors, Antigen, T-Cell, alpha-beta metabolism, Stevens-Johnson Syndrome immunology, T-Lymphocytes, Cytotoxic immunology
Abstract

Drug hypersensitivity such as severe cutaneous adverse reactions (SCAR), including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), could be life-threatening. Here, we enroll SCAR patients to investigate the T cell receptor (TCR) repertoire by next-generation sequencing. A public αβTCR is identified from the cytotoxic T lymphocytes of patients with carbamazepine-SJS/TEN, with its expression showing drug/phenotype-specificity and an bias for HLA-B*15:02. This public αβTCR has binding affinity for carbamazepine and its structural analogs, thereby mediating the immune response. Adoptive transfer of T cell expressing this public αβTCR to HLA-B*15:02 transgenic mice receiving oral administration of carbamazepine induces multi-organ injuries and symptoms mimicking SCAR, including hair loss, erythema, increase of inflammatory lymphocytes in the skin and blood, and liver and kidney dysfunction. Our results not only demonstrate an essential role of TCR in the immune synapse mediating SCAR, but also implicate potential clinical applications and development of therapeutics.

Published
2019
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49. Roles of pharmacogenomics in non-anthracycline antineoplastic-induced cardiovascular toxicities: A systematic review and meta-analysis of genotypes effect.

Author

Leong SL, Chaiyakunapruk N, Tassaneeyakul W, Arunmanakul P, Nathisuwan S, and Lee SWH

Subjects
Anthracyclines, Humans, Pharmacogenetics trends, Antineoplastic Agents adverse effects, Cardiotoxins adverse effects, Cardiovascular Diseases chemically induced, Cardiovascular Diseases genetics, Genotype, Pharmacogenetics methods
Abstract

Background: Exploration on genetic roles in antineoplastic-related cardiovascular toxicity has increased with the advancement of genotyping technology. However, knowledge on the extent of genetic determinants in affecting the susceptibility to the cardiovascular toxicities of antineoplastic is limited. This study aims to identify potential single nucleotide polymorphism (SNP) in predicting non-anthracycline antineoplastic-related cardiovascular toxicity., Methods: We systematically searched for original research in PubMed, Cochrane Central Register of Controlled Studies, CINAHL Plus, EMBASE and HuGE Navigator from database inception until January 2018. Studies on association between polymorphism and antineoplastic-induced cardiovascular toxicity in patients treated for cancer of all antineoplastic agents were included except for anthracycline. Case reports, conference abstracts, reviews and non-patient studies were excluded. Data extracted by two independent reviewers were combined with random-effects model and reported according to PRISMA and MOOSE guidelines., Results: The 35 studies included examined a total of 219 SNPs in 80 genes, 11 antineoplastic and 5 types of cardiovascular toxicities. Meta-analyses showed that human epidermal growth factor receptor 2 (HER2) rs1136201, a risk variants (pooled OR: 2.43; 1.17-5.06, p = 0.018) is a potential predictors for trastuzumab-related cardiotoxicity. Gene dose effect analysis showed number of variant allele may contribute to the risk too., Conclusions: This review found that HER2 rs1136201 can have the potential in predicting trastuzumab-related heart failure. As such, further studies are needed to confirm the validity of these results as well as determine the economic aspect of using SNPs prior to its implementation as a clinical practice., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Published
2019
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50. HLA Alleles and CYP2C9*3 as Predictors of Phenytoin Hypersensitivity in East Asians.

Author

Su SC, Chen CB, Chang WC, Wang CW, Fan WL, Lu LY, Nakamura R, Saito Y, Ueta M, Kinoshita S, Sukasem C, Yampayon K, Kijsanayotin P, Nakkam N, Saksit N, Tassaneeyakul W, Aihara M, Lin YJ, Chang CJ, Wu T, Hung SI, and Chung WH

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Asian People, Child, Child, Preschool, Drug Eruptions epidemiology, Drug Eruptions genetics, Female, Humans, Infant, Infant, Newborn, Male, Middle Aged, Predictive Value of Tests, Risk Assessment, Sensitivity and Specificity, Taiwan, Young Adult, Anticonvulsants adverse effects, Cytochrome P-450 CYP2C9 genetics, Drug Hypersensitivity genetics, HLA Antigens genetics, Phenytoin adverse effects
Abstract

To develop a pre-emptive genetic test that comprises multiple predisposing alleles for the prevention of phenytoin-related severe cutaneous adverse reactions (SCARs), three sets of patients with phenytoin-SCAR and drug-tolerant controls from Taiwan, Thailand, and Japan, were enrolled for this study. In addition to cytochrome P450 (CYP)2C9*3, we found that HLA-B*13:01, HLA-B*15:02, and HLA-B*51:01 were significantly associated with phenytoin hypersensitivity with distinct phenotypic specificities. Strikingly, we showed an increase in predictive sensitivity of concurrently testing CYP2C9*3/HLA-B*13:01/HLA-B*15:02/HLA-B*51:01 from 30.5-71.9% for selecting the individuals with the risk of developing phenytoin-SCAR in Taiwanese cohorts, accompanied by a specificity of 77.7% (combined sensitivity, 64.7%; specificity, 71.9% for three Asian populations). Meta-analysis of the four combined risk alleles showed significant associations with phenytoin-SCAR in three Asian populations. In conclusion, combining the assessment of risk alleles of HLA and CYP2C9 potentiated the usefulness of predictive genetic tests to prevent phenytoin hypersensitivity in Asians., (© 2018 American Society for Clinical Pharmacology and Therapeutics.)

Published
2019
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