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Your search keyword '"Yim, So-young"' showing total 634 results
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634 results on '"Yim, So-young"'

1. Asian Pacific Association for the Study of the Liver clinical practice guidelines on liver transplantation

Author

Kim, Dong-Sik, Yoon, Young-In, Kim, Beom Kyung, Choudhury, Ashok, Kulkarni, Anand, Park, Jun Yong, Kim, Jongman, Sinn, Dong Hyun, Joo, Dong Jin, Choi, YoungRok, Lee, Jeong-Hoon, Choi, Ho Joong, Yoon, Ki Tae, Yim, Sun Young, Park, Cheon-Soo, Kim, Deok-Gie, Lee, Hae Won, Choi, Won-Mook, Chon, Young Eun, Kang, Woo-Hyoung, Rhu, Jinsoo, Lee, Jae Geun, Cho, Yuri, Sung, Pil Soo, Lee, Han Ah, Kim, Ji Hoon, Bae, Si Hyun, Yang, Jin Mo, Suh, Kyung-Suk, Al Mahtab, Mamun, Tan, Soek Siam, Abbas, Zaigham, Shresta, Ananta, Alam, Shahinul, Arora, Anil, Kumar, Ashish, Rathi, Pravin, Bhavani, Ruveena, Panackel, Charles, Lee, Kuei Chuan, Li, Jun, Yu, Ming-Lung, George, Jacob, Tanwandee, Tawesak, Hsieh, Sen-Yung, Yong, Chee Chien, Rela, Mohamed, Lin, H. C., Omata, Masao, and Sarin, Shiv Kumar

Published
2024
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4. Clinically conserved genomic subtypes of gastric adenocarcinoma

Author

Jeong, Yun Seong, Eun, Young-Gyu, Lee, Sung Hwan, Kang, Sang-Hee, Yim, Sun Young, Kim, Eui Hyun, Noh, Joo Kyung, Sohn, Bo Hwa, Woo, Seon Rang, Kong, Moonkyoo, Nam, Deok Hwa, Jang, Hee-Jin, Lee, Hyun-Sung, Song, Shumei, Oh, Sang Cheul, Lee, Jeeyun, Ajani, Jaffer A., and Lee, Ju-Seog

Published
2023
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7. OS-111 Predictive genomic biomarkers for Atezolizumab plus Bevacizumab combination immunotherapy response in liver cancer: insights from the IMbrave150 trial

Author

Yim, Sun Young, primary, Baek, Seung-Woo, additional, Lee, Sung-Hwan, additional, Sohn, BoHwa, additional, Jeong, Yun Seong, additional, Kang, Sang-Hee, additional, Park, Kena, additional, Park, Hyewon, additional, Lee, Sunyoung, additional, Kaseb, Ahmed, additional, Kim, Ji Hoon, additional, Chu, In-Sun, additional, and Lee, Ju-Seog, additional

Published
2024
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8. Convolutional Neural Network Quantization using Generalized Gamma Distribution

Author

Kim, Doyun, Yim, Han Young, Ha, Sanghyuck, Lee, Changgwun, and Kang, Inyup

Subjects
Computer Science - Neural and Evolutionary Computing, Computer Science - Artificial Intelligence, Computer Science - Machine Learning
Abstract

As edge applications using convolutional neural networks (CNN) models grow, it is becoming necessary to introduce dedicated hardware accelerators in which network parameters and feature-map data are represented with limited precision. In this paper we propose a novel quantization algorithm for energy-efficient deployment of the hardware accelerators. For weights and biases, the optimal bit length of the fractional part is determined so that the quantization error is minimized over their distribution. For feature-map data, meanwhile, their sample distribution is well approximated with the generalized gamma distribution (GGD), and accordingly the optimal quantization step size can be obtained through the asymptotical closed form solution of GGD. The proposed quantization algorithm has a higher signal-to-quantization-noise ratio (SQNR) than other quantization schemes previously proposed for CNNs, and even can be more improved by tuning the quantization parameters, resulting in efficient implementation of the hardware accelerators for CNNs in terms of power consumption and memory bandwidth.

Published
2018

9. Integrated Genomic Comparison of Mouse Models Reveals Their Clinical Resemblance to Human Liver Cancer

Author

Yim, Sun Young, Shim, Jae-Jun, Shin, Ji-Hyun, Jeong, Yun Seong, Kang, Sang-Hee, Kim, Sang-Bae, Eun, Young Gyu, Lee, Dong Jin, Conner, Elizabeth A, Factor, Valentina M, Moore, David D, Johnson, Randy L, Thorgeirsson, Snorri S, and Lee, Ju-Seog

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Liver Disease, Genetics, Liver Cancer, Orphan Drug, Biotechnology, Rare Diseases, Human Genome, Cancer, Digestive Diseases, Aetiology, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, 2.1 Biological and endogenous factors, Good Health and Well Being, Animals, Carcinoma, Hepatocellular, Disease Models, Animal, Genomics, Humans, Liver Neoplasms, Liver Neoplasms, Experimental, Mice, Prognosis, Developmental Biology, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Hepatocellular carcinoma (HCC) is a heterogeneous disease. Mouse models are commonly used as preclinical models to study hepatocarcinogenesis, but how well these models recapitulate molecular subtypes of human HCC is unclear. Here, integration of genomic signatures from molecularly and clinically defined human HCC (n = 11) and mouse models of HCC (n = 9) identified the mouse models that best resembled subtypes of human HCC and determined the clinical relevance of each model. Mst1/2 knockout (KO), Sav1 KO, and SV40 T antigen mouse models effectively recapitulated subtypes of human HCC with a poor prognosis, whereas the Myc transgenic model best resembled human HCCs with a more favorable prognosis. The Myc model was also associated with activation of β-catenin. E2f1, E2f1/Myc, E2f1/Tgfa, and diethylnitrosamine (DEN)-induced models were heterogeneous and were unequally split into poor and favorable prognoses. Mst1/2 KO and Sav1 KO models best resemble human HCC with hepatic stem cell characteristics. Applying a genomic predictor for immunotherapy, the six-gene IFNγ score, the Mst1/2 KO, Sav1 KO, SV40, and DEN models were predicted to be the least responsive to immunotherapy. Further analysis showed that elevated expression of immune-inhibitory genes (Cd276 and Nectin2/Pvrl2) in Mst1/2 KO, Sav1 KO, and SV40 models and decreased expression of immune stimulatory gene (Cd86) in the DEN model might be accountable for the lack of predictive response to immunotherapy.Implication: The current genomic approach identified the most relevant mouse models to human liver cancer and suggests immunotherapeutic potential for the treatment of specific subtypes. Mol Cancer Res; 16(11); 1713-23. ©2018 AACR.

Published
2018

10. Reduced Risk of Hepatocellular Carcinoma in Patients with Chronic Hepatitis B Receiving Long-Term Besifovir Therapy

Author

Yim, Hyung Joon, primary, Kang, Seong Hee, additional, Jung, Young Kul, additional, Ahn, Sang Hoon, additional, Kim, Won, additional, Yang, Jin Mo, additional, Jang, Jae Young, additional, Kweon, Yong Oh, additional, Cho, Yong Kyun, additional, Kim, Yoon Jun, additional, Hong, Gun Young, additional, Kim, Dong Joon, additional, Sohn, Joo Hyun, additional, Lee, Jin Woo, additional, Park, Sung Jae, additional, Yim, Sun Young, additional, Park, Jin Kyung, additional, and Um, Soon Ho, additional

Published
2024
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12. Platelets reduce anoikis and promote metastasis by activating YAP1 signaling.

Author

Haemmerle, Monika, Taylor, Morgan L, Gutschner, Tony, Pradeep, Sunila, Cho, Min Soon, Sheng, Jianting, Lyons, Yasmin M, Nagaraja, Archana S, Dood, Robert L, Wen, Yunfei, Mangala, Lingegowda S, Hansen, Jean M, Rupaimoole, Rajesha, Gharpure, Kshipra M, Rodriguez-Aguayo, Cristian, Yim, Sun Young, Lee, Ju-Seog, Ivan, Cristina, Hu, Wei, Lopez-Berestein, Gabriel, Wong, Stephen T, Karlan, Beth Y, Levine, Douglas A, Liu, Jinsong, Afshar-Kharghan, Vahid, and Sood, Anil K

Subjects
Blood Platelets, Cell Line, Tumor, Animals, Mice, Inbred C57BL, Humans, Mice, Nude, Ovarian Neoplasms, Neoplasm Metastasis, Adaptor Proteins, Signal Transducing, Phosphoproteins, Transplantation, Heterologous, Coculture Techniques, Gene Expression Profiling, Signal Transduction, Anoikis, RNA Interference, Female, Transcription Factors, Rare Diseases, Cancer, 2.1 Biological and endogenous factors, Cell Line, Tumor, Mice, Inbred C57BL, Nude, Adaptor Proteins, Signal Transducing, Transplantation, Heterologous
Abstract

Thrombocytosis is present in more than 30% of patients with solid malignancies and correlates with worsened patient survival. Tumor cell interaction with various cellular components of the tumor microenvironment including platelets is crucial for tumor growth and metastasis. Although it is known that platelets can infiltrate into tumor tissue, secrete pro-angiogenic and pro-tumorigenic factors and thereby increase tumor growth, the precise molecular interactions between platelets and metastatic cancer cells are not well understood. Here we demonstrate that platelets induce resistance to anoikis in vitro and are critical for metastasis in vivo. We further show that platelets activate RhoA-MYPT1-PP1-mediated YAP1 dephosphorylation and promote its nuclear translocation which induces a pro-survival gene expression signature and inhibits apoptosis. Reduction of YAP1 in cancer cells in vivo protects against thrombocytosis-induced increase in metastasis. Collectively, our results indicate that cancer cells depend on platelets to avoid anoikis and succeed in the metastatic process.Platelets have been associated with increased tumor growth and metastasis but the mechanistic details of this interaction are still unclear. Here the authors show that platelets improve anoikis resistance of cancer cells and increase metastasis by activating Yap through a RhoA/MYPT-PP1 pathway.

Published
2017

13. Comprehensive and Integrative Genomic Characterization of Hepatocellular Carcinoma

Author

Ally, Adrian, Balasundaram, Miruna, Carlsen, Rebecca, Chuah, Eric, Clarke, Amanda, Dhalla, Noreen, Holt, Robert A, Jones, Steven JM, Lee, Darlene, Ma, Yussanne, Marra, Marco A, Mayo, Michael, Moore, Richard A, Mungall, Andrew J, Schein, Jacqueline E, Sipahimalani, Payal, Tam, Angela, Thiessen, Nina, Cheung, Dorothy, Wong, Tina, Brooks, Denise, Robertson, A Gordon, Bowlby, Reanne, Mungall, Karen, Sadeghi, Sara, Xi, Liu, Covington, Kyle, Shinbrot, Eve, Wheeler, David A, Gibbs, Richard A, Donehower, Lawrence A, Wang, Linghua, Bowen, Jay, Gastier-Foster, Julie M, Gerken, Mark, Helsel, Carmen, Leraas, Kristen M, Lichtenberg, Tara M, Ramirez, Nilsa C, Wise, Lisa, Zmuda, Erik, Gabriel, Stacey B, Meyerson, Matthew, Cibulskis, Carrie, Murray, Bradley A, Shih, Juliann, Beroukhim, Rameen, Cherniack, Andrew D, Schumacher, Steven E, Saksena, Gordon, Pedamallu, Chandra Sekhar, Chin, Lynda, Getz, Gad, Noble, Michael, Zhang, Hailei, Heiman, David, Cho, Juok, Gehlenborg, Nils, Voet, Douglas, Lin, Pei, Frazer, Scott, Defreitas, Timothy, Meier, Sam, Lawrence, Michael, Kim, Jaegil, Creighton, Chad J, Muzny, Donna, Doddapaneni, HarshaVardhan, Hu, Jianhong, Wang, Min, Morton, Donna, Korchina, Viktoriya, Han, Yi, Dinh, Huyen, Lewis, Lora, Bellair, Michelle, Liu, Xiuping, Santibanez, Jireh, Glenn, Robert, Lee, Sandra, Hale, Walker, Parker, Joel S, Wilkerson, Matthew D, Hayes, D Neil, Reynolds, Sheila M, Shmulevich, Ilya, Zhang, Wei, Liu, Yuexin, Iype, Lisa, Makhlouf, Hala, Torbenson, Michael S, Kakar, Sanjay, Yeh, Matthew M, Jain, Dhanpat, Kleiner, David E, Dhanasekaran, Renumathy, El-Serag, Hashem B, and Yim, Sun Young

Subjects
Human Genome, Digestive Diseases, Biotechnology, Rare Diseases, Genetics, Liver Disease, Liver Cancer, Cancer, Aetiology, 2.1 Biological and endogenous factors, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Good Health and Well Being, Carcinoma, Hepatocellular, DNA Methylation, Genomics, Humans, Isocitrate Dehydrogenase, Liver Neoplasms, MicroRNAs, Mutation, Cancer Genome Atlas Research Network. Electronic address: wheeler@bcm.edu, Cancer Genome Atlas Research Network, IDH1/2, TP53, cancer subtyping, expression profile, hepatocellular carcinoma, metabolic reprogramming, promoter hypermethylation, significantly mutated genes, sonic hedgehog signaling, stem cell phenotype, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Liver cancer has the second highest worldwide cancer mortality rate and has limited therapeutic options. We analyzed 363 hepatocellular carcinoma (HCC) cases by whole-exome sequencing and DNA copy number analyses, and we analyzed 196 HCC cases by DNA methylation, RNA, miRNA, and proteomic expression also. DNA sequencing and mutation analysis identified significantly mutated genes, including LZTR1, EEF1A1, SF3B1, and SMARCA4. Significant alterations by mutation or downregulation by hypermethylation in genes likely to result in HCC metabolic reprogramming (ALB, APOB, and CPS1) were observed. Integrative molecular HCC subtyping incorporating unsupervised clustering of five data platforms identified three subtypes, one of which was associated with poorer prognosis in three HCC cohorts. Integrated analyses enabled development of a p53 target gene expression signature correlating with poor survival. Potential therapeutic targets for which inhibitors exist include WNT signaling, MDM4, MET, VEGFA, MCL1, IDH1, TERT, and immune checkpoint proteins CTLA-4, PD-1, and PD-L1.

Published
2017

16. Elevated Response to Type I IFN Enhances RANKL-Mediated Osteoclastogenesis in Usp18-Knockout Mice

Author

Yim, Hwa Young, Park, Cheolkyu, Lee, Yong Deok, Arimoto, Kei-Ichiro, Jeon, Raok, Baek, Sung Hee, Zhang, Dong-Er, Kim, Hong-Hee, and Kim, Keun Il

Subjects
Osteoporosis, Aetiology, 2.1 Biological and endogenous factors, Inflammatory and immune system, Musculoskeletal, Animals, Cell Differentiation, Cells, Cultured, Chemokine CXCL10, Interferon Type I, Macrophages, Mice, Mice, 129 Strain, Mice, Knockout, NFATC Transcription Factors, Osteoclasts, Osteogenesis, RANK Ligand, Ubiquitin Thiolesterase, Immunology
Abstract

A balance between bone formation and bone resorption is critical for the maintenance of bone mass. In many pathological conditions, including chronic inflammation, uncontrolled activation of osteoclast differentiation often causes excessive bone resorption that results in osteoporosis. In this study, we identified the osteopenia phenotype of mice lacking Usp18 (also called Ubp43), which is a deISGylating enzyme and is known as a negative regulator of type I IFN signaling. The expression of Usp18 was induced in preosteoclasts upon receptor activator of NF-κB ligand (RANKL) treatment. In an in vitro osteoclast-differentiation assay, bone marrow macrophages from Usp18-deficient mice exhibited an enhanced differentiation to multinucleated cells, elevated activation of NFATc1, and an increased expression of osteoclast marker genes upon RANKL treatment. Furthermore, in vitro quantification of bone resorption revealed a great increase in osteoclastic activities in Usp18-deficient cells. Interestingly, proinflammatory cytokine genes, such as IP-10 (CXCL10), were highly expressed in Usp18-deficient bone marrow macrophages upon RANKL treatment compared with wild-type cells. In addition, serum cytokine levels, especially IP-10, were significantly high in Usp18-knockout mice. In sum, we suggest that, although type I IFN is known to restrict osteoclast differentiation, the exaggerated activation of the type I IFN response in Usp18-knockout mice causes an osteopenia phenotype in mice.

Published
2016

22. Epidemiology and Effects of Bacterial Infections in Patients With Cirrhosis Worldwide

Author

Bartoletti, Michele, Brodersen, Carlos, Bruns, Tony, de Man, Robert A., Fialla, Annette Dam, Gambino, Carmine, Gautam, Vikas, Girala, Marcos, Juanola, Adria, Kim, Jeong Han, Kim, Tae Hun, Kumar, Pramod, Lattanzi, Barbara, Lee, Tae Hee, Rinaldi Lesmana, Cosmas A., Moreau, Richard, Nath, Preetam, Navarro, Gustavo, Park, Ji-Won, Pinero, Gisela, Pyrsopoulos, Nikolaos T., Restellini, Sophie, Romero, Gustavo, Sacco, Marco, Sevá-Pereira, Tiago, Simón-Talero, Macarena, Song, Do Seon, Suk, Ki Tae, Van Vlierberghe, Hans, Yim, Sun Young, Yoon, Eileen Laurel, Zaccherini, Giacomo, Piano, Salvatore, Singh, Virendra, Caraceni, Paolo, Maiwall, Rakhi, Alessandria, Carlo, Fernandez, Javier, Soares, Elza Cotrim, Kim, Dong Joon, Kim, Sung Eun, Marino, Monica, Vorobioff, Julio, Barea, Rita de Cassia Ribeiro, Merli, Manuela, Elkrief, Laure, Vargas, Victor, Krag, Aleksander, Singh, Shivaram Prasad, Lesmana, Laurentius Adrianto, Toledo, Claudio, Marciano, Sebastian, Verhelst, Xavier, Wong, Florence, Intagliata, Nicolas, Rabinowich, Liane, Colombato, Luis, Kim, Sang Gyune, Gerbes, Alexander, Durand, Francois, Roblero, Juan Pablo, Bhamidimarri, Kalyan Ram, Boyer, Thomas D., Maevskaya, Marina, Fassio, Eduardo, Kim, Hyoung Su, Hwang, Jae Seok, Gines, Pere, Gadano, Adrian, Sarin, Shiv Kumar, and Angeli, Paolo

Published
2019
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28. Dynamics of liver stiffness-based risk prediction model during antiviral therapy in patients with chronic hepatitis B

Author

Chon, Hye Yeon, Seo, Yeon Seok, Lee, Jung il, Kim, Byung Seok, Jang, Byoung Kuk, Kim, Sang Gyune, Suk, Ki Tae, Kim, In Hee, Lee, Jin-Woo, Chon, Young Eun, Kim, Moon Young, Jeong, Soung Won, Lee, Han Ah, Yim, Sun Young, Um, Soon Ho, Lee, Hyun Woong, Lee, Kwan Sik, Song, Jeong Eun, Lee, Chang Hyeong, Chung, Woo Jin, Hwang, Jae Seok, Yoo, Jeong-Ju, Kim, Young Seok, Kim, Dong Joon, Lee, Chang Hun, Yu, Jung Hwan, Ha, Yeon Jung, Kim, Mi Na, Lee, Joo Ho, Hwang, Seong Gyu, Kang, Seong Hee, Baik, Soon Koo, Jang, Jae Young, Suh, Sang Jun, Jung, Young Kul, Kim, Beom Kyung, Park, Jun Yong, Kim, Do Young, Ahn, Sang Hoon, Han, Kwang-Hyub, Yim, Hyung Joon, and Kim, Seung Up

Published
2020
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40. Propensity score-matched analysis of physician-controlled wire-guided cannulation as an effective technique against difficult cannulation in endoscopic retrograde cholangiopancreatography: A retrospective study

Author

Jeon, Han Jo, primary, Lee, Jae Min, additional, Yim, Sun Young, additional, Choi, Hyuk Soon, additional, Kim, Eun Sun, additional, Keum, Bora, additional, Seo, Yeon Seok, additional, Jeen, Yoon Tae, additional, Chun, Hoon Jai, additional, and Lee, Hong Sik, additional

Published
2023
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43. Data from Integrated Genomic Comparison of Mouse Models Reveals Their Clinical Resemblance to Human Liver Cancer

Author

Yim, Sun Young, primary, Shim, Jae-Jun, primary, Shin, Ji-Hyun, primary, Jeong, Yun Seong, primary, Kang, Sang-Hee, primary, Kim, Sang-Bae, primary, Eun, Young Gyu, primary, Lee, Dong Jin, primary, Conner, Elizabeth A., primary, Factor, Valentina M., primary, Moore, David D., primary, Johnson, Randy L., primary, Thorgeirsson, Snorri S., primary, and Lee, Ju-Seog, primary

Published
2023
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44. Supplementary Figure 2 from Integrated Analysis of Transcriptomes of Cancer Cell Lines and Patient Samples Reveals STK11/LKB1–Driven Regulation of cAMP Phosphodiesterase-4D

Author

He, Ningning, primary, Kim, Nayoung, primary, Song, Mee, primary, Park, Choa, primary, Kim, Somin, primary, Park, Eun Young, primary, Yim, Hwa Young, primary, Kim, Kyunga, primary, Park, Jong Hoon, primary, Kim, Keun Il, primary, Zhang, Fan, primary, Mills, Gordon B., primary, and Yoon, Sukjoon, primary

Published
2023
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45. Supplementary Table 2 from Integrated Analysis of Transcriptomes of Cancer Cell Lines and Patient Samples Reveals STK11/LKB1–Driven Regulation of cAMP Phosphodiesterase-4D

Author

He, Ningning, primary, Kim, Nayoung, primary, Song, Mee, primary, Park, Choa, primary, Kim, Somin, primary, Park, Eun Young, primary, Yim, Hwa Young, primary, Kim, Kyunga, primary, Park, Jong Hoon, primary, Kim, Keun Il, primary, Zhang, Fan, primary, Mills, Gordon B., primary, and Yoon, Sukjoon, primary

Published
2023
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46. Supplementary Table 4 from Integrated Analysis of Transcriptomes of Cancer Cell Lines and Patient Samples Reveals STK11/LKB1–Driven Regulation of cAMP Phosphodiesterase-4D

Author

He, Ningning, primary, Kim, Nayoung, primary, Song, Mee, primary, Park, Choa, primary, Kim, Somin, primary, Park, Eun Young, primary, Yim, Hwa Young, primary, Kim, Kyunga, primary, Park, Jong Hoon, primary, Kim, Keun Il, primary, Zhang, Fan, primary, Mills, Gordon B., primary, and Yoon, Sukjoon, primary

Published
2023
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47. Supplemental Data from Integrated Genomic Comparison of Mouse Models Reveals Their Clinical Resemblance to Human Liver Cancer

Author

Yim, Sun Young, primary, Shim, Jae-Jun, primary, Shin, Ji-Hyun, primary, Jeong, Yun Seong, primary, Kang, Sang-Hee, primary, Kim, Sang-Bae, primary, Eun, Young Gyu, primary, Lee, Dong Jin, primary, Conner, Elizabeth A., primary, Factor, Valentina M., primary, Moore, David D., primary, Johnson, Randy L., primary, Thorgeirsson, Snorri S., primary, and Lee, Ju-Seog, primary

Published
2023
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48. Supplementary Table 3 from Integrated Analysis of Transcriptomes of Cancer Cell Lines and Patient Samples Reveals STK11/LKB1–Driven Regulation of cAMP Phosphodiesterase-4D

Author

He, Ningning, primary, Kim, Nayoung, primary, Song, Mee, primary, Park, Choa, primary, Kim, Somin, primary, Park, Eun Young, primary, Yim, Hwa Young, primary, Kim, Kyunga, primary, Park, Jong Hoon, primary, Kim, Keun Il, primary, Zhang, Fan, primary, Mills, Gordon B., primary, and Yoon, Sukjoon, primary

Published
2023
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49. Supplementary Figure 1 from Integrated Analysis of Transcriptomes of Cancer Cell Lines and Patient Samples Reveals STK11/LKB1–Driven Regulation of cAMP Phosphodiesterase-4D

Author

He, Ningning, primary, Kim, Nayoung, primary, Song, Mee, primary, Park, Choa, primary, Kim, Somin, primary, Park, Eun Young, primary, Yim, Hwa Young, primary, Kim, Kyunga, primary, Park, Jong Hoon, primary, Kim, Keun Il, primary, Zhang, Fan, primary, Mills, Gordon B., primary, and Yoon, Sukjoon, primary

Published
2023
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50. Data from Integrated Analysis of Transcriptomes of Cancer Cell Lines and Patient Samples Reveals STK11/LKB1–Driven Regulation of cAMP Phosphodiesterase-4D

Author

He, Ningning, primary, Kim, Nayoung, primary, Song, Mee, primary, Park, Choa, primary, Kim, Somin, primary, Park, Eun Young, primary, Yim, Hwa Young, primary, Kim, Kyunga, primary, Park, Jong Hoon, primary, Kim, Keun Il, primary, Zhang, Fan, primary, Mills, Gordon B., primary, and Yoon, Sukjoon, primary

Published
2023
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