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Your search keyword '"Wang, Chelsia Qiuxia"' showing total 11 results
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11 results on '"Wang, Chelsia Qiuxia"'

1. Integrin-α9 overexpression underlies the niche-independent maintenance of leukemia stem cells in acute myeloid leukemia

Author

Niibori-Nambu, Akiko, Wang, Chelsia Qiuxia, Chin, Desmond Wai Loon, Chooi, Jing Yuan, Hosoi, Hiroki, Sonoki, Takashi, Tham, Cheng-Yong, Nah, Giselle Sek Suan, Cirovic, Branko, Tan, Darren Qiancheng, Takizawa, Hitoshi, Sashida, Goro, Goh, Yufen, Tng, Jiaqi, Fam, Wee Nih, Fullwood, Melissa Jane, Suda, Toshio, Yang, Henry, Tergaonkar, Vinay, Taniuchi, Ichiro, Li, Shang, Chng, Wee Joo, and Osato, Motomi

Published
2024
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2. Activation of NOTCH signaling impedes cell proliferation and survival in acute megakaryoblastic leukemia

Author

Ong, Kelly Ooi Kee, Mok, Michelle Meng Huang, Niibori-Nambu, Akiko, Du, Linsen, Yanagida, Masatoshi, Wang, Chelsia Qiuxia, Bahirvani, Avinash Govind, Chin, Desmond Wai Loon, Koh, Cai Ping, Ng, King Pan, Yamashita, Namiko, Jacob, Bindya, Yokomizo, Tomomasa, Takizawa, Hitoshi, Matsumura, Takayoshi, Suda, Toshio, Lau, Jie-ying Amelia, Tan, Tuan Zea, Mori, Seiichi, Yang, Henry, Iwasaki, Masayuki, Minami, Takashi, Asou, Norio, Sun, Qiao-Yang, Ding, Ling-Wen, Koeffler, H. Phillip, Tenen, Daniel G., Shimizu, Ritsuko, Yamamoto, Masayuki, Ito, Yoshiaki, Kham, Shirley Kow Yin, Yeoh, Allen Eng-Juh, Chng, Wee Joo, and Osato, Motomi

Published
2024
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3. Highly efficient Runx1 enhancer eR1-mediated genetic engineering for fetal, child and adult hematopoietic stem cells

Author

Koh, Cai Ping, Bahirvani, Avinash Govind, Wang, Chelsia Qiuxia, Yokomizo, Tomomasa, Ng, Cherry Ee Lin, Du, Linsen, Tergaonkar, Vinay, Voon, Dominic Chih-Cheng, Kitamura, Hiroaki, Hosoi, Hiroki, Sonoki, Takashi, Michelle, Mok Meng Huang, Tan, Lii Jye, Niibori-Nambu, Akiko, Zhang, Yi, Perkins, Archibald S., Hossain, Zakir, Tenen, Daniel G., Ito, Yoshiaki, Venkatesh, Byrappa, and Osato, Motomi

Published
2023
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4. RUNX1-ETO (RUNX1-RUNX1T1) induces myeloid leukemia in mice in an age-dependent manner

Author

Abdallah, Mohamed Gaber, Niibori-Nambu, Akiko, Morii, Mariko, Yokomizo, Takako, Yokomizo, Tomomasa, Ideue, Takako, Kubota, Sho, Teoh, Vania Swee Imm, Mok, Michelle Meng Huang, Wang, Chelsia Qiuxia, Omar, Abdellah Ali, Tokunaga, Kenji, Iwanaga, Eisaku, Matsuoka, Masao, Asou, Norio, Nakagata, Naomi, Araki, Kimi, AboElenin, Mabrouk, Madboly, Sayed Hamada, Sashida, Goro, and Osato, Motomi

Published
2021
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5. Rap1 regulates hematopoietic stem cell survival and affects oncogenesis and response to chemotherapy

Author

Khattar, Ekta, Maung, Kyaw Ze Ya, Chew, Chen Li, Ghosh, Arkasubhra, Mok, Michelle Meng Huang, Lee, Pei, Zhang, Jun, Chor, Wei Hong Jeff, Cildir, Gökhan, Wang, Chelsia Qiuxia, Mohd-Ismail, Nur Khairiah, Chin, Desmond Wai Loon, Lee, Soo Chin, Yang, Henry, Shin, Yong-Jae, Nam, Do-Hyun, Chen, Liming, Kumar, Alan Prem, Deng, Lih Wen, Ikawa, Masahito, Gunaratne, Jayantha, Osato, Motomi, and Tergaonkar, Vinay

Published
2019
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6. An Inhibitory Role for Human CD96 Endodomain in T Cell Anti-Tumor Responses.

Author

Wang, Chelsia Qiuxia, Choy, Fong Chan, Sanny, Arleen, Murakami, Takashi, Tan, Andy Hee-Meng, and Lam, Kong-Peng

Subjects
*CYTOTOXIC T cells, *T cells, *EPIDERMAL growth factor receptors, *IMMUNE checkpoint proteins, *PROGRAMMED cell death 1 receptors, *IMMUNE checkpoint inhibitors, *CHIMERIC antigen receptors
Abstract

Immune checkpoint blockade (ICB) therapy involves the inhibition of immune checkpoint regulators which reverses their limitation of T cell anti-tumor responses and results in long-lasting tumor regression. However, poor clinical response or tumor relapse was observed in some patients receiving such therapy administered via antibodies blocking the cytotoxic T lymphocyte-associated protein 4 (CTLA-4) or the programmed cell death 1 (PD-1) pathway alone or in combination, suggesting the involvement of additional immune checkpoints. CD96, a possible immune checkpoint, was previously shown to suppress natural killer (NK) cell anti-tumor activity but its role in human T cells remains controversial. Here, we demonstrate that CRISPR/Cas9-based deletion of CD96 in human T cells enhanced their killing of leukemia cells in vitro. T cells engineered with a chimeric antigen receptor (CAR) comprising human epidermal growth factor receptor 2 (EGFR2/HER2)-binding extracellular region and intracellular regions of CD96 and CD3ζ (4D5-96z CAR-T cells) were less effective in suppressing the growth of HER2-expressing tumor cells in vitro and in vivo compared with counterparts bearing CAR that lacked CD96 endodomain (4D5-z CAR-T cells). Together, our findings implicate a role for CD96 endodomain in attenuating T cell cytotoxicity and support combination tumor immunotherapy targeting multiple rather than single immune checkpoints. [ABSTRACT FROM AUTHOR]

Published
2023
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10. Disruption of Runx1 and Runx3 Leads to Bone Marrow Failure and Leukemia Predisposition due to Transcriptional and DNA Repair Defects.

Author

Wang, Chelsia Qiuxia, Krishnan, Vaidehi, Tay, Lavina Sierra, Chin, Desmond Wai Loon, Koh, Cai Ping, Chooi, Jing Yuan, Nah, Giselle Sek Suan, Du, Linsen, Jacob, Bindya, Yamashita, Namiko, Lai, Soak Kuan, Tan, Tuan Zea, Mori, Seiichi, Tanuichi, Ichiro, Tergaonkar, Vinay, Ito, Yoshiaki, and Osato, Motomi

Abstract

The RUNX genes encode transcription factors involved in development and human disease. RUNX1 and RUNX3 are frequently associated with leukemias, yet the basis for their involvement in leukemogenesis is not fully understood. Here, we show that Runx1;Runx3 double-knockout (DKO) mice exhibited lethal phenotypes due to bone marrow failure and myeloproliferative disorder. These contradictory clinical manifestations are reminiscent of human inherited bone marrow failure syndromes such as Fanconi anemia (FA), caused by defective DNA repair. Indeed, Runx1;Runx3 DKO cells showed mitomycin C hypersensitivity, due to impairment of monoubiquitinated-FANCD2 recruitment to DNA damage foci, although FANCD2 monoubiquitination in the FA pathway was unaffected. RUNX1 and RUNX3 interact with FANCD2 independently of CBFβ, suggesting a nontranscriptional role for RUNX in DNA repair. These findings suggest that RUNX dysfunction causes DNA repair defect, besides transcriptional misregulation, and promotes the development of leukemias and other cancers. [ABSTRACT FROM AUTHOR]

Published
2014
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11. RUNX1 point mutations potentially identify a subset of early immature T-cell acute lymphoblastic leukaemia that may originate from differentiated T-cells.

Author

Mok, Michelle Meng Huang, Du, Linsen, Wang, Chelsia Qiuxia, Tergaonkar, Vinay, Liu, Te Chih, Yin Kham, Shirley Kow, Sanda, Takaomi, Yeoh, Allen Eng-Juh, and Osato, Motomi

Subjects
*RUNX proteins, *POINT mutation (Biology), *LYMPHOBLASTIC leukemia, *T cells, *NUCLEOTIDE sequencing, *CHILD patients, *CELL lines, *CELL differentiation
Abstract

Abstract: The RUNX1/AML1 gene is among the most frequently mutated genes in human leukaemia. However, its association with T-cell acute lymphoblastic leukaemia (T-ALL) remains poorly understood. In order to examine RUNX1 point mutations in T-ALL, we conducted an amplicon-based deep sequencing in 65 Southeast Asian childhood patients and 20 T-ALL cell lines, and detected RUNX1 mutations in 6 patients (9.2%) and 5 cell lines (25%). Interestingly, RUNX1-mutated T-ALL cases seem to constitute a subset of early immature T-ALL that may originate from differentiated T-cells. This result provides a deeper insight into the mechanistic basis for leukaemogenesis. [Copyright &y& Elsevier]

Published
2014
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