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288 results on '"Hongeng, Suradej"'

7. Retinoblastoma in Asia: Clinical Presentation and Treatment Outcomes in 2112 Patients from 33 Countries

Author

Kaliki, Swathi, Vempuluru, Vijitha S., Mohamed, Ashik, Abdulqader, Rula Ahmed, Aggarwal, Priyanka, Ahmad, Alia, Akib, Marliyanti Nur Rahmah, Al Mesfer, Saleh A., Al Ani, Mouroge Hashim, Al-Badri, Safaa A.Faraj, Angeles Alcasabas, Ana Patricia, Al-Dahmash, Saad A., Al-Haddad, Christiane, Yahya Al-Hussaini, Hamoud Hodeish, Al-Jadiry, Mazin Faisal, Al-Jumaily, Usama, Alkatan, Hind Manaa, Razzaq Mahmood Al-Mafrachi, Ali Abdul, Samad Majeed Al-Shaheen, Athar Abdul, Al-Shammary, Entissar Hadi, Amiruddin, Primawita Oktarima, Armytasari, Inggar, Astbury, Nicholas John, Atalay, Hatice Tuba, Ataseven, Eda, Atchaneeyasakul, La-ongsri, Balayeva, Ruhengiz, Bascaran, Covadonga, Begimkulova, Ainura Suranovna, Bhaduri, Anirban, Bhat, Sunil, Bhattacharyya, Arpita, Blum, Sharon, Bowman, Richard, Buaboonnam, Jassada, Burton, Matthew J., Caspi, Shani, Chaudhry, Shabana, Chawla, Bhavna, Chen, Wensi, Chuluunbat, Tsengelmaa, Dangboon, Wantanee, Das, Anirban, Das, Pranab, Das, Sima, Du, Yi, Dudeja, Gagan, Eka Sutyawan, I Wayan, Fadoo, Zehra, Faranoush, Mohammad, Foster, Allen, Frenkel, Shahar, Ghassemi, Fariba, Gomel, Nir, Gunasekera, D Sanjeeva, Gündüz, Ahmet K., Gupta, Himika, Gupta, Sanjiv, Gupta, Vineeta, Hamid, Syed Ahmer, Hamzah, Norhafizah, Hasanreisoglu, Murat, Hassan, Shadab, Haydar, Huda Awni, Hongeng, Suradej, Hussein Al-Janabi, Allawi Noor, Islamov, Ziyavuddin, Janjua, Teyyeb Azeem, Jeeva, Irfan, Ji, Xunda, Jo, Dong Hyun, Kantar, Mehmet, Kapelushnik, Noa, Kebudi, Rejin, Keomisy, Jonny, Khan, Zohora Jameela, Khaqan, Hussain Ahmed, Khetan, Vikas, Khodabande, Alireza, Kim, Jeong Hun, Kiratli, Hayyam, Koç, Irem, Kulvichit, Kittisak, Kuntorini, Mayasari Wahyu, Li, Cairui, Li, Kaijun, Limbu, Ben, Liu, ChunHsiu, Lutfi, Delfitri, Mahajan, Amita, Maitra, Puja, Makimbetov, Emil Kojoshovich, Maktabi, Azza M.Y., Manzhuova, Lyazat, Masud, Sidra, Mehrvar, Azim, Menon, Vikas, John V Mercado, Gary, Chandra Mishra, Divyansh Kailash, Mohammad, Mona Tayseer, Mudaliar, Sangeeta Sanjay, Mushtaq, Asma, Nair, Akshay Gopinathan, Natarajan, Sundaram, Nency, Yetty Movieta, Neroev, Vladimir, Nuruddin, Murtuza, Pagarra, Halimah, Palanivelu, Mahesh Shanmugam, Papyan, Ruzanna, Pe'er, Jacob, Polyakov, Vladimir, Qadir, Ali Omer, Qayyum, Seema, Qian, Jiang, Quah, BoonLong, Rahman, Ardizal, Rajkarnikar, Purnima, Ramanjulu, Rajesh, Rashid, Riffat, Rojanaporn, Duangnate, Roy, Soma Rani, Saab, Raya Hamad, Saakyan, Svetlana, Sabhan, Ahmed Hatem, Saiju, Rohit, Sayalith, Phayvanh, Sedaghat, Ahad, Seth, Rachna, Shakoor, Shawkat Ara, Sharma, Manoj Kumar, Siddiqui, Sorath Noorani, Singh, Usha, Singha, Penny, Sitorus, Rita S., Soebagjo, Hendrian D., Sultana, Sadia, Sun, Xiantao, Supriyadi, Eddy, Surukrattanaskul, Supawan, Suzuki, Shigenobu, Tan, Deborah, Tang, Jing, Tashvighi, Maryam, Teh, Kok Hoi, Tehuteru, Edi Setiawan, Thawaba, Abdullah Dahan M., Toledano, Helen, Le Trang, Doan, Tripathy, Devjyoti, Tuncer, Samuray, Unal, Emel, Ushakova, Tatiana L., Usmanov, Rustam, Verma, Nishant, Victor, Andi Arus, Vishnevskia-Dai, Victoria, Wang, Yi-Zhuo, Wangtiraumnuay, Nutsuchar, Riono, Widiarti Pandu, Wiwatwongwana, Atchareeya, Wiwatwongwana, Damrong, Wong, Emily S., Wongwai, Phanthipha, Wu, Si-qi, Xiang, Daoman, Xiao, Yishuang, Xu, Bing, Xue, Kang, Yam, Jason C., Yang, Huasheng, Yaqub, Muhammad Amer, Yarovaya, Vera A., Yarovoy, Andrey A., Ye, Huijing, Yousef, Yacoub Abdallah, Yuliawati, Putu, Zhang, Yi, Zia, Nida, Zondervan, Marcia, Fabian, Ido Didi, and Sthapit, Purnima Rajkarnikar

Published
2024
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9. Invivo evaluation of Andrographis paniculata and Boesenbergia rotunda extract activity against SARS-CoV-2 Delta variant in Golden Syrian hamsters: Potential herbal alternative for COVID-19 treatment

Author

Kongsomros, Supasek, Boonyarattanasoonthorn, Tussapon, Phongphaew, Wallaya, Kasorndorkbua, Chaiyan, Sunyakumthorn, Piyanate, Im-Erbsin, Rawiwan, Lugo-Roman, Luis A., Kongratanapasert, Teetat, Paha, Jiraporn, Manopwisedjaroen, Suwimon, Kwankhao, Pakakrong, Supannapan, Kittitach, Ngamkhae, Nittaya, Srimongkolpithak, Nitipol, Vivithanaporn, Pornpun, Hongeng, Suradej, Thitithanyanont, Arunee, and Khemawoot, Phisit

Published
2024
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14. MINERVA: A CubeSat for demonstrating DNA damage mitigation against space radiation in C. elegans by using genetic modification

Author

Klomchitcharoen, Sumeth, Tangwattanasirikun, Tanchanok, Gallup, Sean, Smerwong, Noparin, Arunwiriyakit, Peetimon, Tachavises, Pisitchai, Tangkijngamwong, Jin, Phatthanaanukun, Pichamon, Jirapanyalerd, Benjamard, Chattanupakorn, Siripak, Rungpongvanich, Visarut, Nangsue, Norawit, Meemon, Krai, Wongtrakoonkate, Patompon, Hongeng, Suradej, and Wongsawat, Yodchanan

Published
2022
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15. The Global Retinoblastoma Outcome Study: a prospective, cluster-based analysis of 4064 patients from 149 countries

Author

Fabian, Ido Didi, Abdallah, Elhassan, Abdullahi, Shehu U, Abdulqader, Rula A, Abdulrahaman, Aminatu A, Abouelnaga, Sherif, Ademola-Popoola, Dupe S, Adio, Adedayo, Afifi, Mahmoud A, Afshar, Armin R, Aggarwal, Priyanka, Aghaji, Ada E, Ahmad, Alia, Akib, Marliyanti NR, Akinsete, Adeseye, Al Harby, Lamis, Al Mesfer, Saleh, Al Ani, Mouroge H, Alarcón Portabella, Silvia, Al-Badri, Safaa AF, Alcasabas, Ana Patricia A, Al-Dahmash, Saad A, Alejos, Amanda, Alemany-Rubio, Ernesto, Alfa Bio, Amadou I, Alfonso Carreras, Yvania, Al-Haddad, Christiane E, Al-Hussaini, Hamoud HY, Ali, Amany M, Alia, Donjeta B, Al-Jadiry, Mazin F, Al-Jumaily, Usama, Alkatan, Hind M, All-Eriksson, Charlotta, Al-Mafrachi, Ali ARM, Almeida, Argentino A, Alsawidi, Khalifa M, Al-Shaheen, Athar ASM, Al-Shammary, Entissar H, Amankwaa-Frempong, Doreen, Amiruddin, Primawita O, Armytasari, Inggar, Astbury, Nicholas J, Atalay, Hatice T, Ataseven, Eda, Atchaneeyasakul, La-ongsri, Atsiaya, Rose, Autrata, Rudolf, Balaguer, Julia, Balayeva, Ruhengiz, Barranco, Honorio, Bartoszek, Paulina, Bartuma, Katarina, Bascaran, Covadonga, Bechrakis, Nikolaos E, Beck Popovic, Maja, Begimkulova, Ainura S, Benmiloud, Sarra, Berete, Rokia C, Berry, Jesse L, Bhaduri, Anirban, Bhat, Sunil, Bhattacharyya, Arpita, Biewald, Eva M, Binkley, Elaine, Blum, Sharon, Bobrova, Nadia, Boldt, H.C., Bonanomi, Maria Teresa BC, Bouda, Gabrielle C, Bouguila, Hédi, Brennan, Rachel C, Brichard, Bénédicte G, Buaboonnam, Jassada, Budiongo, Aléine, Burton, Matthew J, Calderón-Sotelo, Patricia, Calle Jara, Doris A, Camuglia, Jayne E, Cano, Miriam R, Capra, Michael, Caspi, Shani, Cassoux, Nathalie, Castela, Guilherme, Castillo, Luis, Català-Mora, Jaume, Cavieres, Isabel, Chandramohan, Arthika, Chantada, Guillermo L, Chaudhry, Shabana, Chawla, Bhavna, Chen, Wensi, Chiwanga, Faraja S, Chuluunbat, Tsengelmaa, Cieslik, Krzysztof, Clark, Antony, Cockcroft, Ruellyn L, Comsa, Codruta, Correa Llano, Maria G, Corson, Timothy W, Couitchere, Line, Cowan-Lyn, Kristin E, Csóka, Monika, Dangboon, Wantanee, Das, Anirban, Das, Pranab, Das, Sima, Davanzo, Jacquelyn M, Davidson, Alan, De Francesco, Sonia, De Potter, Patrick, Quintero D, Karina, Demirci, Hakan, Desjardins, Laurence, Díaz Coronado, Rosdali Y, Dimaras, Helen, Dodgshun, Andrew J, Donato Macedo, Carla R, Dragomir, Monica D, Du, Yi, Du Bruyn, Magritha, Du Plessis, Johannes, Dudeja, Gagan, Eerme, Katrin, Eka Sutyawan, I Wayan, El Kettani, Asmaa, Elbahi, Amal M, Elder, James E, Elhaddad, Alaa M, Elhassan, Moawia MA, Elzembely, Mahmoud M, Ericksen, Connor, Essuman, Vera A, Evina, Ted Grimbert A, Ezegwui, Ifeoma R, Fadoo, Zehra, Fandiño, Adriana C, Faranoush, Mohammad, Fasina, Oluyemi, Fernández, Delia DPG, Fernández-Teijeiro, Ana, Foster, Allen, Frenkel, Shahar, Fu, Ligia D, Fuentes-Alabi, Soad L, Garcia, Juan L, García Aldana, David, Garcia Pacheco, Henry N, Geel, Jennifer A, Ghassemi, Fariba, Girón, Ana V, Goenz, Marco A, Gold, Aaron S, Goldberg, Hila, Gole, Glen A, Gomel, Nir, Gonzalez, Efren, Gonzalez Perez, Graciela, González-Rodríguez, Liudmira, Gorfine, Malka, Graells, Jaime, Gregersen, Pernille A, Grigorovski, Nathalia DAK, Guedenon, Koffi M, Gunasekera, D Sanjeeva, Gündüz, Ahmet K, Gupta, Himika, Gupta, Sanjiv, Gupta, Vineeta, Hadjistilianou, Theodora, Hamel, Patrick, Hamid, Syed A, Hamzah, Norhafizah, Hansen, Eric D, Harbour, J William, Hartnett, M. Elizabeth, Hasanreisoglu, Murat, Muhammad, Hassan, Hassan, Sadiq, Hassan, Shadab, Hautz, Wojciech, Haydar, Huda, Hederova, Stanislava, Hessissen, Laila, Hongeng, Suradej, Hordofa, Diriba F, Hubbard, G. Baker, Hummelen, Marlies, Husakova, Kristina, Hussein Al-Janabi, Allawi N, Ibanga, Affiong, Ida, Russo, Ilic, Vesna R, Islamov, Ziyavuddin, Jairaj, Vivekaraj, Janjua, Teyyeb, Jeeva, Irfan, Ji, Xunda, Jo, Dong Hyun, Jones, Michael M, Kabesha Amani, Theophile B, Kabore, Rolande L, Kaliki, Swathi, Kalinaki, Abubakar, Kamsang, Pius, Kantar, Mehmet, Kapelushnik, Noa, Kardava, Tamar, Kebudi, Rejin, Keomisy, Jonny, Kepak, Tomas, Ketteler, Petra, Khan, Zohora J, Khaqan, Hussain A, Khetan, Vikas, Khodabande, Alireza, Khotenashvili, Zaza, Kim, Jonathan W, Kim, Jeong Hun, Kiratli, Hayyam, Kivela, Tero T., Klett, Artur, Koç, Irem, Kosh Komba Palet, Jess Elio, Krivaitiene, Dalia, Kruger, Mariana, Kulvichit, Kittisak, Kuntorini, Mayasari W, Kyara, Alice, Lam, Geoffrey C, Larson, Scott A, Latinović, Slobodanka, Laurenti, Kelly D, Lavy, Yotam, Lavric Groznik, Alenka, Leverant, Amy A, Li, Cairui, Li, Kaijun, Limbu, Ben, Liu, Chun-Hsiu, Quah, BoonLong, López, Juan P, Lukamba, Robert M, Luna-Fineman, Sandra, Lutfi, Delfitri, Lysytsia, Lesia, Madgar, Shiran, Magrath, George N, Mahajan, Amita, Maitra, Puja, Maka, Erika, Makimbetov, Emil K, Maktabi, Azza, Maldonado, Carlos, Mallipatna, Ashwin, Manudhane, Rebecca, Manzhuova, Lyazat, Martín-Begue, Nieves, Masud, Sidra, Matende, Ibrahim O, Mattosinho, Clarissa CDS, Matua, Marchelo, Mayet, Ismail, Mbumba, Freddy B, McKenzie, John D, Mehrvar, Azim, Mengesha, Aemero A, Menon, Vikas, Mercado, Gary John V, Mets, Marilyn B, Midena, Edoardo, Miller, Audra, Mishra, Divyansh KC, Mndeme, Furahini G, Mohamedani, Ahmed A, Mohammad, Mona T, Moll, Annette C, Montero, Margarita M, Moreira, Claude, Mruthyunjaya, Prithvi, Msina, Mchikirwa S, Msukwa, Gerald, Mudaliar, Sangeeta S, Muma, Kangwa I M, Munier, Francis L, Murray, Timothy G, Musa, Kareem O, Mushtaq, Asma, Musika, Anne A, Mustak, Hamzah, Mustapha, Tajudeen, Muyen, Okwen M, Myezo, Khumo H, Naidu, Gita, Naidu, Natasha, Nair, Akshay Gopinathan, Natarajan, Sundaram, Naumenko, Larisa, Ndoye Roth, Paule Aïda, Nency, Yetty M, Neroev, Vladimir, Ng, Yvonne, Nikitovic, Marina, Nkanga, Elizabeth D, Nkumbe, Henry E, Numbi, Marcel N, Nummi, Kalle, Nuruddin, Murtuza, Nyaywa, Mutale, Nyirenda, Chinsisi, Obono-Obiang, Ghislaine, Oliver, Scott CN, Oporto, Joaquin, Ortega-Hernández, Miriam, Oscar, Alexander H, Ossandon, Diego, Pagarra, Halimah, Paintsil, Vivian, Paiva, Luisa, Palanivelu, Mahesh Shanmugam, Papyan, Ruzanna, Parrozzani, Raffaele, Pascual Morales, Claudia R, Paton, Katherine E, Pe'er, Jacob, Peralta Calvo, Jesús, Perić, Sanja, Pham, Chau TM, Philbert, Remezo, Plager, David A, Pochop, Pavel, Polania, Rodrigo A., Polyakov, Vladimir, Ponce, Jimena, Qadir, Ali O, Qayyum, Seema, Qian, Jiang, Refaeli, David, Rahman, Ardizal, Rajkarnikar, Purnima, Ramanjulu, Rajesh, Ramasubramanian, Aparna, Ramirez-Ortiz, Marco A, Randhawa, Jasmeen K, Randrianarisoa, Hoby Lalaina, Raobela, Léa, Rashid, Riffat, Reddy, M.A., Renner, Lorna A, Reynders, David, Ribadu, Dahiru, Ritter-Sovinz, Petra, Rogowska, Anna, Rojanaporn, Duangnate, Romero, Livia, Roy, Soma R, Saab, Raya H, Saakyan, Svetlana, Sabhan, Ahmed H, Sagoo, Mandeep S, Said, Azza MA, Saiju, Rohit, Salas, Beatriz, San Román Pacheco, Sonsoles, Sánchez, Gissela L, Sanchez Orozco, Alma Janeth, Sayalith, Phayvanh, Scanlan, Trish A, Schlüter, Sabrina, Schwab, Christoph, Sedaghat, Ahad, Seth, Rachna, Sgroi, Mariana, Shah, Ankoor S, Shakoor, Shawkat A, Sharma, Manoj K, Sherief, Sadik T, Shields, Carol L, Sia, David, Siddiqui, Sorath Noorani, Sidi cheikh, Sidi, Silva, Sónia, Singh, Arun D, Singh, Usha, Singha, Penny, Sitorus, Rita S, Skalet, Alison H, Soebagjo, Hendrian D, Sorochynska, Tetyana, Ssali, Grace, Stacey, Andrew W, Staffieri, Sandra E, Stahl, Erin D, Steinberg, David M, Stones, David K, Strahlendorf, Caron, Suarez, Maria Estela Coleoni, Sultana, Sadia, Sun, Xiantao, Superstein, Rosanne, Supriyadi, Eddy, Surukrattanaskul, Supawan, Suzuki, Shigenobu, Svojgr, Karel, Sylla, Fatoumata, Tamamyan, Gevorg, Tan, Deborah, Tandili, Alketa, Tang, Jing, Tarrillo Leiva, Fanny F, Tashvighi, Maryam, Tateshi, Bekim, Teh, Kok Hoi, Tehuteru, Edi S, Teixeira, Luiz F, Tekavcic Pompe, Manca, Thawaba, Abdullah Dahan M, Theophile, Tuyisabe, Toledano, Helen, Trang, Doan L, Traoré, Fousseyni, Tripathy, Devjyoti, Tuncer, Samuray, Tyau-Tyau, Harba, Umar, Ali B, Unal, Emel, Uner, Ogul E, Urbak, Steen F, Ushakova, Tatiana L, Usmanov, Rustam H, Valeina, Sandra, Valente, Paola, van Hoefen Wijsard, Milo, Vasquez Anchaya, Jacqueline Karina, Vaughan, Leon O, Veleva-Krasteva, Nevyana V, Verma, Nishant, Victor, Andi A, Viksnins, Maris, Villacís Chafla, Edwin G, Villegas, Victor M, Vishnevskia-Dai, Victoria, Waddell, Keith, Wali, Amina H, Wang, Yi-Zhuo, Wangtiraumnuay, Nutsuchar, Wetter, Julie, Widiarti, Widiarti, Wilson, Matthew W, Wime, Amelia DC, Wiwatwongwana, Atchareeya, Wiwatwongwana, Damrong, Wolley Dod, Charlotte, Wong, Emily S, Wongwai, Phanthipha, Wu, Si-qi, Xiang, Daoman, Xiao, Yishuang, Xu, Bing, Xue, Kang, Yaghy, Antonio, Yam, Jason C, Yang, Huasheng, Yanga, Jenny M, Yaqub, Muhammad A, Yarovaya, Vera A, Yarovoy, Andrey A, Ye, Huijing, Yee, Roberto I, Yousef, Yacoub A, Yuliawati, Putu, Zapata López, Arturo M, Zein, Ekhtelbenina, Zhang, Yi, Zhilyaeva, Katsiaryna, Zia, Nida, Ziko, Othman AO, Zondervan, Marcia, and Bowman, Richard

Published
2022
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20. Therapeutic delivery of recombinant glucocerebrosidase enzyme-containing extracellular vesicles to human cells from Gaucher disease patients.

Author

Janpipatkul, Keatdamrong, Sutjarit, Nareerat, Tangprasittipap, Amornrat, Chaiamarit, Tai, Innachai, Pawarit, Suksen, Kanoknetr, Chokpanuwat, Tanida, Tim-Aroon, Thipwimol, Anurathapan, Usanarat, Jearawiriyapaisarn, Natee, Tubsuwan, Alisa, Bowornpinyo, Supareak, Asavapanumas, Nithi, Chairoungdua, Arthit, Bhukhai, Kanit, and Hongeng, Suradej

Abstract

Background: Gaucher disease (GD) is one of the most common types of lysosomal storage diseases (LSDs) caused by pathogenic variants of lysosomal β-glucocerebrosidase gene (GBA1), resulting in the impairment of Glucocerebrosidase (GCase) enzyme function and the accumulation of a glycolipid substrate, glucosylceramide (GlcCer) within lysosomes. Current therapeutic approaches such as enzyme replacement therapy and substrate reduction therapy cannot fully rescue GD pathologies, especially neurological symptoms. Meanwhile, delivery of lysosomal enzymes to the endocytic compartment of affected human cells is a promising strategy for treating neuropathic LSDs. Result: Here, we describe a novel approach to restore GCase enzyme in cells from neuropathic GD patients by producing extracellular vesicle (EVs)-containing GCase from cells overexpressing GBA1 gene. Lentiviral vectors containing modified GBA1 were introduced into HEK293T cells to produce a stable cell line that provides a sustainable source of functional GCase enzyme. The GBA1-overexpressing cells released EV-containing GCase enzyme, that is capable of entering into and localizing in the endocytic compartment of recipient cells, including THP-1 macrophage, SH-SY5Y neuroblastoma, and macrophages and neurons derived from induced pluripotent stem cells (iPSCs) of neuropathic GD patients. Importantly, the recipient cells exhibit higher GCase enzyme activity. Conclusion: This study presents a promising therapeutic strategy to treat severe types of LSDs. It involves delivering lysosomal enzymes to the endocytic compartment of human cells affected by conditions such as GDs with neurological symptoms, as well as potentially other neurological disorders impacting lysosomes. [ABSTRACT FROM AUTHOR]

Published
2024
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21. Investigating the impact of botulinum toxin type a on the migration of normal human dermal fibroblasts: An in vitro wound healing assay.

Author

Thanasarnaksorn, Wilai, Pomsoong, Cherrin, Kanjanasirirat, Phongthon, Jearawuttanakul, Kedchin, Borwornpinyo, Suparerk, Hongeng, Suradej, Ratanapokasatit, Yanisa, and Rattananukrom, Teerapong

Subjects
BOTULINUM toxin, HYPERTROPHIC scars, BOTULINUM A toxins, KELOIDS, WOUND healing
Abstract

Background: Botulinum toxin A (BoNT‐A) is widely utilized in the management of hypertrophic and keloid scars. One proposed mechanism for scar prevention involves the inhibition of fibroblast migration in scars by BoNT‐A. However, the data regarding the effect of BoNT‐A on the migration of normal human dermal fibroblasts (NHDF) is limited. Objectives: The aim of this study was to investigate the inhibitory effect of different types and dilutions of BoNT‐A on the migration of NHDF. Methods: In vitro scratch wound assay, NHDF cells were cultured, incubated, and subjected to scratching using a sterile tip. Subsequently, the scratched NHDF monolayer was treated with different types of BoNT‐A, including onabotulinumtoxinA (ONA), incobotulinumtoxinA (INCO), prabotulinumtoxinA (PRABO), or letibotulinumtoxinA (LETI), at varying concentrations of 10, 20, 25, 40, 50, and 100 units/milliliter (U/mL). Additionally, abobotulinumtoxinA (ABO) was administered at concentrations of 33, 50, 66, 71, 100, 150, 300, and 500 U/mL. Normal saline solution (NSS) served as a negative control. The extent of NHDF migration was evaluated by comparing each dilution of BoNT‐A with the controls using high‐content imaging at the 48‐h time point. Furthermore, the viability of the of NHDF was assessed. Results: The concentrations of 25, 40, and 50 U/mL of ONA (p < 0.001) and 25 U/mL of LETI (p < 0.05) demonstrated significantly inhibited NHDF migration in comparison to the control group. Conversely, all dilutions of PRABO, INCO, and ABO exhibited comparable NHDF migration to that of the control group. Regarding NHDF viability, no significant decrease was observed across any of the BoNT‐A types and dilutions. Conclusion: Different types and dilutions of BoNT‐A demonstrated variable inhibitory effects on NHDF migration in vitro. The selection of BoNT‐A formulation may significantly impact the clinical outcome of scar prevention related to fibroblast migration. [ABSTRACT FROM AUTHOR]

Published
2024
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22. Whole-Exome Sequencing Reveals Novel Candidate Driver Mutations and Potential Druggable Mutations in Patients with High-Risk Neuroblastoma.

Author

Nokchan, Natakorn, Suthapot, Praewa, Choochuen, Pongsakorn, Khongcharoen, Natthapon, Hongeng, Suradej, Anurathapan, Usanarat, Surachat, Komwit, and Sangkhathat, Surasak

Subjects
CANCER genes, MISSENSE mutation, OVERALL survival, GENETIC mutation, SURVIVAL rate, NEUROBLASTOMA
Abstract

Neuroblastoma is the most prevalent solid tumor in early childhood, with a 5-year overall survival rate of 40–60% in high-risk cases. Therefore, the identification of novel biomarkers for the diagnosis, prognosis, and therapy of neuroblastoma is crucial for improving the clinical outcomes of these patients. In this study, we conducted the whole-exome sequencing of 48 freshly frozen tumor samples obtained from the Biobank. Somatic variants were identified and selected using a bioinformatics analysis pipeline. The mutational signatures were determined using the Mutalisk online tool. Cancer driver genes and druggable mutations were predicted using the Cancer Genome Interpreter. The most common mutational signature was single base substitution 5. MUC4, MUC16, and FLG were identified as the most frequently mutated genes. Using the Cancer Genome Interpreter, we identified five recurrent cancer driver mutations spanning MUC16, MUC4, ALK, and CTNND1, with the latter being novel and containing a missense mutation, R439C. We also identified 11 putative actionable mutations including NF1 Q1798*, Q2616*, and S636X, ALK F1174L and R1275Q, SETD2 P10L and Q1829E, BRCA1 R612S, NOTCH1 D1670V, ATR S1372L, and FGFR1 N577K. Our findings provide a comprehensive overview of the novel information relevant to the underlying molecular pathogenesis and therapeutic targets of neuroblastoma. [ABSTRACT FROM AUTHOR]

Published
2024
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23. Disturbance of Immune Microenvironment in Androgenetic Alopecia through Spatial Transcriptomics.

Author

Charoensuksira, Sasin, Tantiwong, Supasit, Pongklaokam, Juthapa, Hanvivattanakul, Sirashat, Surinlert, Piyaporn, Krajarng, Aungkana, Thanasarnaksorn, Wilai, Hongeng, Suradej, and Ponnikorn, Saranyoo

Subjects
T helper cells, GENE expression, TRANSCRIPTOMES, HAIR follicles, PROTEIN-protein interactions, T cells
Abstract

Androgenetic alopecia (AGA) is characterized by microinflammation and abnormal immune responses, particularly in the upper segment of hair follicles (HFs). However, the precise patterns of immune dysregulation remain unclear, partly due to limitations in current analysis techniques to preserve tissue architecture. The infundibulum, a major part of the upper segment of HFs, is associated with significant clusters of immune cells. In this study, we investigated immune cells around the infundibulum, referred to as peri-infundibular immune infiltration (PII). We employed spatial transcriptome profiling, a high-throughput analysis technology, to investigate the immunological disruptions within the PII region. Our comprehensive analysis included an evaluation of overall immune infiltrates, gene set enrichment analysis (GSEA), cellular deconvolution, differential expression analysis, over-representation analysis, protein-protein interaction (PPI) networks, and upstream regulator analysis to identify cell types and molecular dysregulation in immune cells. Our results demonstrated significant differences in immune signatures between the PII of AGA patients (PII-A) and the PII of control donors (PII-C). Specifically, PII-A exhibited an enrichment of CD4+ helper T cells, distinct immune response patterns, and a bias toward a T helper (Th) 2 response. Immunohistochemistry revealed disruptions in T cell subpopulations, with more CD4+ T cells displaying an elevated Th2 response and a reduced Th1-cytotoxic response compared to PII-C. These findings reveal the unique immune landscapes of PII-A and PII-C, suggesting potential for the development of innovative treatment approaches. [ABSTRACT FROM AUTHOR]

Published
2024
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27. Proteomic analysis reveals plasma haptoglobin, interferon-γ, and interleukin-1β as potential biomarkers of pediatric refractory epilepsy

Author

Saengow, Vitchayaporn Emarach, Chiangjong, Wararat, Khongkhatithum, Chaiyos, Changtong, Channarong, Chokchaichamnankit, Daranee, Weeraphan, Churat, Kaewboonruang, Patcharin, Thampratankul, Lunliya, Manuyakorn, Wiparat, Hongeng, Suradej, Srisomsap, Chantragan, Svasti, Jisnuson, Chutipongtanate, Somchai, and Visudtibhan, Anannit

Published
2021
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30. Immortalized hepatocyte-like cells: A competent hepatocyte model for studying clinical HCV isolate infection.

Author

Pewkliang, Yongyut, Thongsri, Piyanoot, Suthivanich, Phichaya, Thongbaiphet, Nipa, Keatkla, Jiraporn, Pasomsub, Ekawat, Anurathapan, Usanarat, Borwornpinyo, Suparerk, Wongkajornsilp, Adisak, Hongeng, Suradej, and Sa-ngiamsuntorn, Khanit

Subjects
HUMAN stem cells, LIFE cycles (Biology), MESENCHYMAL stem cells, ANTIVIRAL agents, LIVER diseases, APOPTOSIS
Abstract

More than 58 million individuals worldwide are inflicted with chronic HCV. The disease carries a high risk of end stage liver disease, i.e., cirrhosis and hepatocellular carcinoma. Although direct-acting antiviral agents (DAAs) have revolutionized therapy, the emergence of drug-resistant strains has become a growing concern. Conventional cellular models, Huh7 and its derivatives were very permissive to only HCVcc (JFH-1), but not HCV clinical isolates. The lack of suitable host cells had hindered comprehensive research on patient-derived HCV. Here, we established a novel hepatocyte model for HCV culture to host clinically pan-genotype HCV strains. The immortalized hepatocyte-like cell line (imHC) derived from human mesenchymal stem cell carries HCV receptors and essential host factors. The imHC outperformed Huh7 as a host for HCV (JFH-1) and sustained the entire HCV life cycle of pan-genotypic clinical isolates. We analyzed the alteration of host markers (i.e., hepatic markers, cellular innate immune response, and cell apoptosis) in response to HCV infection. The imHC model uncovered the underlying mechanisms governing the action of IFN-α and the activation of sofosbuvir. The insights from HCV-cell culture model hold promise for understanding disease pathogenesis and novel anti-HCV development. [ABSTRACT FROM AUTHOR]

Published
2024
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31. CRISPR/Cas9 genome editing of CCR5 combined with C46 HIV-1 fusion inhibitor for cellular resistant to R5 and X4 tropic HIV-1.

Author

Khamaikawin, Wannisa, Saisawang, Chonticha, Tassaneetrithep, Boonrat, Bhukhai, Kanit, Phanthong, Phetcharat, Borwornpinyo, Suparerk, Phuphuakrat, Angsana, Pasomsub, Ekawat, Chaisavaneeyakorn, Sujittra, Anurathapan, Usanarat, Apiwattanakul, Nopporn, and Hongeng, Suradej

Abstract

Hematopoietic stem-cell (HSC) transplantation using a donor with a homozygous mutation in the HIV co-receptor CCR5 (CCR5Δ32/Δ32) holds great promise as a cure for HIV-1. Previously, there were three patients that had been reported to be completely cured from HIV infection by this approach. However, finding a naturally suitable Human Leukocyte Antigen (HLA)-matched homozygous CCR5Δ32 donor is very difficult. The prevalence of this allele is only 1% in the Caucasian population. Therefore, additional sources of CCR5Δ32/Δ32 HSCs are required. The Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/CRISPR-associated (Cas) system is one method to mediate CCR5 knockout in HSCs that has been successfully employed as a gene editing tool in clinical trials. Additional anti-HIV-1 strategies are still required for broad-spectrum inhibition of HIV-1 replication. Here in this study, we combined an additional anti-HIV-1 therapy, which is C46, a cell membrane-anchored HIV-1 fusion inhibitor with the CRISPR/Cas9 mediated knockout CCR5. The combined HIV-1 therapeutic genes were investigated for the potential prevention of both CCR5 (R5)- and CXCR4 (X4)-tropic HIV-1 infections in the MT4CCR5 cell line. The combinatorial CRISPR/Cas9 therapies were superior compared to single method therapy for achieving the HIV-1 cure strategy and shows potential for future applications. [ABSTRACT FROM AUTHOR]

Published
2024
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32. The translational gap for gene therapies in low- and middle-income countries.

Author

Doxzen, Kevin W., Adair, Jennifer E., Fonseca Bazzo, Yris Maria, Bukini, Daima, Cornetta, Kenneth, Dalal, Varsha, Guerino-Cunha, Renato Luiz, Hongeng, Suradej, Jotwani, Geeta, Kityo-Mutuluuza, Cissy, Lakshmanan, Krishnamurti, Mahlangu, Johnny, Makani, Julie, Mathews, Vikram, Ozelo, Margareth C., Rangarajan, Savita, Scholefield, Janine, Batista Silva Júnior, João, and McCune, Joseph M.

Subjects
GENE therapy, MIDDLE-income countries, TECHNOLOGICAL innovations, ROOT diseases, GENETIC disorders
Abstract

Gene therapies are designed to address the root cause of disease. As scientific understanding of disease prevention, diagnosis, and treatment improves in tandem with technological innovation, gene therapies have the potential to become safe and effective treatment options for a wide range of genetic and nongenetic diseases. However, as the medical scope of gene therapies expands, consideration must be given to those who will benefit and what proactive steps must be taken to widen development and access potential, particularly in regions carrying a high disease burden. [ABSTRACT FROM AUTHOR]

Published
2024
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33. Extracellular Vesicles for Childhood Cancer Liquid Biopsy.

Author

Singhto, Nilubon, Pongphitcha, Pongpak, Jinawath, Natini, Hongeng, Suradej, and Chutipongtanate, Somchai

Subjects
BRAIN tumor diagnosis, DIAGNOSIS of tumors in children, EXTRACELLULAR vesicles, TUMORS in children, BODY fluid examination, MINIMALLY invasive procedures, TUMOR markers, TREATMENT effectiveness, INDIVIDUALIZED medicine, PATIENT monitoring
Abstract

Simple Summary: Liquid biopsy is a technique that uses minimally invasive or noninvasive methods to detect disease biomarkers in biofluids, such as blood and urine. For childhood cancers, this approach is promising, especially when tissue biopsies are challenging. By analyzing tiny particles called extracellular vesicles, the small particles in biofluids which carry genetic and molecular information from cancer cells, this liquid biopsy technique can aid early diagnosis, treatment monitoring, and outcome prediction, potentially improving the outcomes of childhood cancers. This review article introduces the concept of extracellular vesicle liquid biopsy, summarizes the progress that is being made in the diagnosis of multiple types of pediatric malignancies, and provides prospects for using this extracellular vesicle method to guide the development of novel cancer therapeutics. Liquid biopsy involves the utilization of minimally invasive or noninvasive techniques to detect biomarkers in biofluids for disease diagnosis, monitoring, or guiding treatments. This approach is promising for the early diagnosis of childhood cancer, especially for brain tumors, where tissue biopsies are more challenging and cause late detection. Extracellular vesicles offer several characteristics that make them ideal resources for childhood cancer liquid biopsy. Extracellular vesicles are nanosized particles, primarily secreted by all cell types into body fluids such as blood and urine, and contain molecular cargos, i.e., lipids, proteins, and nucleic acids of original cells. Notably, the lipid bilayer-enclosed structure of extracellular vesicles protects their cargos from enzymatic degradation in the extracellular milieu. Proteins and nucleic acids of extracellular vesicles represent genetic alterations and molecular profiles of childhood cancer, thus serving as promising resources for precision medicine in cancer diagnosis, treatment monitoring, and prognosis prediction. This review evaluates the recent progress of extracellular vesicles as a liquid biopsy platform for various types of childhood cancer, discusses the mechanistic roles of molecular cargos in carcinogenesis and metastasis, and provides perspectives on extracellular vesicle-guided therapeutic intervention. Extracellular vesicle-based liquid biopsy for childhood cancer may ultimately contribute to improving patient outcomes. [ABSTRACT FROM AUTHOR]

Published
2024
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34. Hematopoietic Stem Cell Transplantation for Severe Thalassemia Patients from Haploidentical Donors Using a Novel Conditioning Regimen

Author

Anurathapan, Usanarat, Hongeng, Suradej, Pakakasama, Samart, Songdej, Duantida, Sirachainan, Nongnuch, Pongphitcha, Pongpak, Chuansumrit, Ampaiwan, Charoenkwan, Pimlak, Jetsrisuparb, Arunee, Sanpakit, Kleebsabai, Rujkijyanont, Piya, Meekaewkunchorn, Arunotai, Lektrakul, Yujinda, Iamsirirak, Pornchanok, Surapolchai, Pacharapan, Sirireung, Somtawin, Sruamsiri, Rosarin, Wahidiyat, Pustika Amalia, and Andersson, Borje S.

Published
2020
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37. Pediatric primary central nervous system tumors registry in Thailand under National Health Security Office schemes

Author

Pongtanakul, Bunchoo, Sirachainan, Nongnuch, Surapolchai, Pacharapan, Charoenkwan, Pimlak, Choeyprasert, Worawut, Komwilaisak, Patcharee, Chainansamit, Su-on, Witsanuyothin, Nittaya, Lertrakul, Yujinda, Rujkijyanont, Piya, Kanjanapongkul, Somjai, Sosothikul, Darintr, Sanpakit, Kleebsabai, Chotsampancharoen, Thirachit, Wangruangsathit, Somporn, Thokanit, Nintita Sripaiboonkij, Tabjareon, Sommaphun, and Hongeng, Suradej

Published
2020
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39. An increase in ER stress and unfolded protein response in iPSCs-derived neuronal cells from neuronopathic Gaucher disease patients.

Author

Pornsukjantra, Tanapat, Saikachain, Nongluk, Sutjarit, Nareerat, Khongkrapan, Arthaporn, Tubsuwan, Alisa, Bhukhai, Kanit, Tim-Aroon, Thipwimol, Anurathapan, Usanarat, Hongeng, Suradej, and Asavapanumas, Nithi

Abstract

Gaucher disease (GD) is a lysosomal storage disorder caused by a mutation in the GBA1 gene, responsible for encoding the enzyme Glucocerebrosidase (GCase). Although neuronal death and neuroinflammation have been observed in the brains of individuals with neuronopathic Gaucher disease (nGD), the exact mechanism underlying neurodegeneration in nGD remains unclear. In this study, we used two induced pluripotent stem cells (iPSCs)-derived neuronal cell lines acquired from two type-3 GD patients (GD3-1 and GD3-2) to investigate the mechanisms underlying nGD by biochemical analyses. These iPSCs-derived neuronal cells from GD3-1 and GD3-2 exhibit an impairment in endoplasmic reticulum (ER) calcium homeostasis and an increase in unfolded protein response markers (BiP and CHOP), indicating the presence of ER stress in nGD. A significant increase in the BAX/BCL-2 ratio and an increase in Annexin V-positive cells demonstrate a notable increase in apoptotic cell death in GD iPSCs-derived neurons, suggesting downstream signaling after an increase in the unfolded protein response. Our study involves the establishment of iPSCs-derived neuronal models for GD and proposes a possible mechanism underlying nGD. This mechanism involves the activation of ER stress and the unfolded protein response, ultimately leading to apoptotic cell death in neurons. [ABSTRACT FROM AUTHOR]

Published
2024
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40. Ceftriaxone exerts antitumor effects in MYCN‐driven retinoblastoma and neuroblastoma by targeting DDX3X for translation repression.

Author

Chittavanich, Pamorn, Saengwimol, Duangporn, Roytrakul, Sittiruk, Rojanaporn, Duangnate, Chaitankar, Vijender, Srimongkol, Atthapol, Anurathapan, Usanarat, Hongeng, Suradej, and Kaewkhaw, Rossukon

Abstract

MYCN proto‐oncogene, bHLH transcription factor (MYCN) amplification is associated with aggressive retinoblastoma (RB) and neuroblastoma (NB) cancer recurrence that is resistant to chemotherapies. Therefore, there is an urgent need to identify new therapeutic tools. This study aimed to evaluate the potential repurposing of ceftriaxone for the treatment of MYCN‐amplified RB and NB, based on the clinical observations that the drug was serendipitously found to decrease the volume of the MYCN‐driven RB subtype. Using patient‐derived tumor organoids and tumor cell lines, we demonstrated that ceftriaxone is a potent and selective growth inhibitor targeting MYCN‐driven RB and NB cells. Profiling of drug‐induced transcriptomic changes, cell‐cycle progression, and apoptotic death indicated cell‐cycle arrest and death of drug‐treated MYCN‐amplified tumor cells. Drug target identification, using an affinity‐based proteomic and molecular docking approach, and functional studies of the target proteins revealed that ceftriaxone targeted DEAD‐box helicase 3 X‐linked (DDX3X), thereby inhibiting translation in MYCN‐amplified tumors but not in MYCN‐nonamplified cells. The data suggest the feasibility of repurposing ceftriaxone as an anticancer drug and provide insights into the mechanism of drug action, highlighting DDX3X as a potential target for treating MYCN‐driven tumors. [ABSTRACT FROM AUTHOR]

Published
2024
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41. Improving hematopoietic differentiation from human induced pluripotent stem cells by the modulation of Hippo signaling with a diarylheptanoid derivative.

Author

Thongsa-ad, Umnuaychoke, Wongpan, Anongnat, Wongkummool, Wasinee, Chaiwijit, Phaewa, Uppakara, Kwanchanok, Chaiyakitpattana, Gorawin, Singpant, Passanan, Tong-ngam, Pirut, Chukhan, Amnat, Pabuprappap, Wachirachai, Wongniam, Sirapope, Suksamrarn, Apichart, Hongeng, Suradej, Anurathapan, Usanarat, Kulkeaw, Kasem, Tubsuwan, Alisa, and Bhukhai, Kanit

Subjects
INDUCED pluripotent stem cells, HIPPO signaling pathway, HEMATOPOIETIC stem cells, PROGENITOR cells, BLOOD cells, HEMORHEOLOGY, REGENERATIVE medicine
Abstract

Background: The diarylheptanoid ASPP 049 has improved the quality of adult hematopoietic stem cell (HSC) expansion ex vivo through long-term reconstitution in animal models. However, its effect on hematopoietic regeneration from human induced pluripotent stem cells (hiPSCs) is unknown. Method: We utilized a defined cocktail of cytokines without serum or feeder followed by the supplementation of ASPP 049 to produce hematopoietic stem/progenitor cells (HSPCs). Flow cytometry and trypan blue exclusion analysis were used to identify nonadherent and adherent cells. Nonadherent cells were harvested to investigate the effect of ASPP 049 on multipotency using LTC-IC and CFU assays. Subsequently, the mechanism of action was explored through transcriptomic profiles, which were validated by qRT-PCR, immunoblotting, and immunofluorescence analysis. Result: The supplementation of ASPP 049 increased the number of phenotypically defined primitive HSPCs (CD34+CD45+CD90+) two-fold relative to seeded hiPSC colonies, indicating enhanced HSC derivation from hiPSCs. Under ASPP 049-supplemented conditions, we observed elevated HSPC niches, including CD144+CD73− hemogenic- and CD144+CD73+ vascular-endothelial progenitors, during HSC differentiation. Moreover, harvested ASPP 049-treated cells exhibited improved self-renewal and a significantly larger proportion of different blood cell colonies with unbiased lineages, indicating enhanced HSC stemness properties. Transcriptomics and KEGG analysis of sorted CD34+CD45+ cells-related mRNA profiles revealed that the Hippo signaling pathway is the most significant in responding to WWTR1/TAZ, which correlates with the validation of the protein expression. Interestingly, ASPP 049-supplemented HSPCs upregulated 11 genes similarly to umbilical cord blood-derived HSPCs. Conclusion: These findings suggest that ASPP 049 can improve HSC-generating protocols with proliferative potentials, self-renewal ability, unbiased differentiation, and a definable mechanism of action for the clinical perspective of hematopoietic regenerative medicine. [ABSTRACT FROM AUTHOR]

Published
2024
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42. Unveiling the Antiviral Properties of Panduratin A through SARS-CoV-2 Infection Modeling in Cardiomyocytes.

Author

Linn, Aung Khine, Manopwisedjaroen, Suwimon, Kanjanasirirat, Phongthon, Borwornpinyo, Suparerk, Hongeng, Suradej, Phanthong, Phetcharat, and Thitithanyanont, Arunee

Subjects
ANTIVIRAL agents, SARS-CoV-2, DRUG discovery, ANGIOTENSIN converting enzyme, CYTOTOXINS, INFECTION
Abstract

Establishing a drug-screening platform is critical for the discovery of potential antiviral agents against SARS-CoV-2. In this study, we developed a platform based on human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) to investigate SARS-CoV-2 infectivity, with the aim of evaluating potential antiviral agents for anti-SARS-CoV-2 activity and cardiotoxicity. Cultured myocytes of iPSC-CMs and immortalized human cardiomyocyte cell line (AC-16) were primarily characterized for the expression of cardiac markers and host receptors of SARS-CoV-2. An infectivity model for the wild-type SARS-CoV-2 strain was then established. Infection modeling involved inoculating cells with SARS-CoV-2 at varying multiplicities of infection (MOIs) and then quantifying infection using immunofluorescence and plaque assays. Only iPSC-CMs, not AC16 cells, expressed angiotensin-converting enzyme 2 (ACE-2), and quantitative assays confirmed the dose-dependent infection of iPSC-CMs by SARS-CoV-2, unlike the uninfectable AC16 cells lacking the expression of ACE2. Cytotoxicity was evaluated using MTT assays across a concentration range. An assessment of the plant-derived compound panduratin A (panA) showed cytotoxicity at higher doses (50% cytotoxic concentration (CC50) 10.09 μM) but promising antiviral activity against SARS-CoV-2 (50% inhibition concentration (IC50) 0.8–1.6 μM), suppressing infection at concentrations 10 times lower than its CC50. Plaque assays also showed decreased viral production following panA treatment. Overall, by modeling cardiac-specific infectivity, this iPSC-cardiomyocyte platform enables the reliable quantitative screening of compound cytotoxicity alongside antiviral efficacy. By combining disease pathogenesis and pharmacology, this system can facilitate the evaluation of potential novel therapeutics, such as panA, for drug discovery applications. [ABSTRACT FROM AUTHOR]

Published
2024
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43. Cytotoxicity and exhaustion markers of chimeric antigen receptor T cells targeting BCMA in multiple myeloma cell lines between patients and healthy donors.

Author

Prasongtanakij, Somsak, Preedagasamzin, Sarinthip, Jittorntrum, Bunyada, Anurathapan, Usanarat, Puavilai, Teeraya, Niparuck, Pimjai, Chantrathammachart, Pichika, Piyajaroenkij, Thanakrit, Uaesoontrachoon, Kitipong, Uchibori, Ryosuke, Ozawa, Keiya, Ohmine, Ken, and Hongeng, Suradej

Subjects
CHIMERIC antigen receptors, FATIGUE (Physiology), MONONUCLEAR leukocytes, MULTIPLE myeloma, CYTOTOXINS
Abstract

Objectives: Multiple myeloma (MM) accounts for 10% of hematologic malignancies. However, most of the patients suffered from relapsed/refractory disease. We would like to expand CAR T cell therapy to treat MM using our current platform. Methods: BCMA CAR T lymphocytes were generated for volunteers or MM patients. The transduction efficiency was detected by the ddPCR technique. Immunophenotyping and exhaustion markers were monitored by flow cytometry. The efficacy of BCMA CAR T cells was tested using coculturing with BCMA CAR or mock, and the positive and negative targets, K562/hBCMA‐ECTM and K562, respectively. Results: BCMA CAR T cells were generated from consented volunteers or MM patients and could be detected CAR BCMA expression at a mean of 4.07 ± 1.95 or 4.65 ± 1.21 copies/cell, respectively. Those modified T cells were primarily effector memory T cells. Our BCMA CAR T cells could explicitly eradicate the K562/hBCMA‐ECTM cell line while the K562 cell line survived. Interestingly, the BCMA CAR, mock T cells, and peripheral blood mononuclear cells from MM patients expressed similar levels of the exhaustion makers, TIM‐3, LAG‐3, and PD1. Conclusions: Our BCMA CAR T cells, mainly effector/effector memory, could eliminate BCMA‐expressing cells in vitro and had similar levels of exhaustion markers among different populations. [ABSTRACT FROM AUTHOR]

Published
2024
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47. High-content screening of Thai medicinal plants reveals Boesenbergia rotunda extract and its component Panduratin A as anti-SARS-CoV-2 agents

Author

Kanjanasirirat, Phongthon, Suksatu, Ampa, Manopwisedjaroen, Suwimon, Munyoo, Bamroong, Tuchinda, Patoomratana, Jearawuttanakul, Kedchin, Seemakhan, Sawinee, Charoensutthivarakul, Sitthivut, Wongtrakoongate, Patompon, Rangkasenee, Noppawan, Pitiporn, Supaporn, Waranuch, Neti, Chabang, Napason, Khemawoot, Phisit, Sa-ngiamsuntorn, Khanit, Pewkliang, Yongyut, Thongsri, Piyanoot, Chutipongtanate, Somchai, Hongeng, Suradej, Borwornpinyo, Suparerk, and Thitithanyanont, Arunee

Published
2020
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49. Phase II, multi-center, open-label, single-arm clinical trial evaluating the efficacy and safety of Mycophenolate Mofetil in patients with high-grade locally advanced or metastatic osteosarcoma (ESMMO): rationale and design of the ESMMO trial

Author

Koonrungsesomboon, Nut, Ngamphaiboon, Nuttapong, Townamchai, Natavudh, Teeyakasem, Pimpisa, Charoentum, Chaiyut, Charoenkwan, Pimlak, Natesirinilkul, Rungrote, Sathitsamitphong, Lalita, Ativitavas, Touch, Chaiyawat, Parunya, Klangjorhor, Jeerawan, Hongeng, Suradej, and Pruksakorn, Dumnoensun

Published
2020
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