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2,013 results on '"Wong, Kwok-Kin"'

51. Supplementary Figure 1 from EZH2 Inhibition Promotes Tumor Immunogenicity in Lung Squamous Cell Carcinomas

Author

DuCote, Tanner J., primary, Song, Xiulong, primary, Naughton, Kassandra J., primary, Chen, Fan, primary, Plaugher, Daniel R., primary, Childress, Avery R., primary, Gellert, Abigail R., primary, Skaggs, Erika M., primary, Qu, Xufeng, primary, Liu, Jinze, primary, Liu, Jinpeng, primary, Li, Fei, primary, Wong, Kwok-Kin, primary, and Brainson, Christine F., primary

Published
2024
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52. FIGURE 3 from EZH2 Inhibition Promotes Tumor Immunogenicity in Lung Squamous Cell Carcinomas

Author

DuCote, Tanner J., primary, Song, Xiulong, primary, Naughton, Kassandra J., primary, Chen, Fan, primary, Plaugher, Daniel R., primary, Childress, Avery R., primary, Gellert, Abigail R., primary, Skaggs, Erika M., primary, Qu, Xufeng, primary, Liu, Jinze, primary, Liu, Jinpeng, primary, Li, Fei, primary, Wong, Kwok-Kin, primary, and Brainson, Christine F., primary

Published
2024
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53. Supplementary Figure 5 from EZH2 Inhibition Promotes Tumor Immunogenicity in Lung Squamous Cell Carcinomas

Author

DuCote, Tanner J., primary, Song, Xiulong, primary, Naughton, Kassandra J., primary, Chen, Fan, primary, Plaugher, Daniel R., primary, Childress, Avery R., primary, Gellert, Abigail R., primary, Skaggs, Erika M., primary, Qu, Xufeng, primary, Liu, Jinze, primary, Liu, Jinpeng, primary, Li, Fei, primary, Wong, Kwok-Kin, primary, and Brainson, Christine F., primary

Published
2024
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54. Data from EZH2 Inhibition Promotes Tumor Immunogenicity in Lung Squamous Cell Carcinomas

Author

DuCote, Tanner J., primary, Song, Xiulong, primary, Naughton, Kassandra J., primary, Chen, Fan, primary, Plaugher, Daniel R., primary, Childress, Avery R., primary, Gellert, Abigail R., primary, Skaggs, Erika M., primary, Qu, Xufeng, primary, Liu, Jinze, primary, Liu, Jinpeng, primary, Li, Fei, primary, Wong, Kwok-Kin, primary, and Brainson, Christine F., primary

Published
2024
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55. A Phase 1/2 multicenter trial of DKN-01 as monotherapy or in combination with docetaxel for the treatment of metastatic castration-resistant prostate cancer (mCRPC)

Author

Wise, David R., primary, Pachynski, Russell K., additional, Denmeade, Samuel R., additional, Aggarwal, Rahul R., additional, Deng, Jiehui, additional, Febles, Victor Adorno, additional, Balar, Arjun V., additional, Economides, Minas P., additional, Loomis, Cynthia, additional, Selvaraj, Shanmugapriya, additional, Haas, Michael, additional, Kagey, Michael H., additional, Newman, Walter, additional, Baum, Jason, additional, Troxel, Andrea B., additional, Griglun, Sarah, additional, Leis, Dayna, additional, Yang, Nina, additional, Aranchiy, Viktoriya, additional, Machado, Sabrina, additional, Waalkes, Erika, additional, Gargano, Gabrielle, additional, Soamchand, Nadia, additional, Puranik, Amrutesh, additional, Chattopadhyay, Pratip, additional, Fedal, Ezeddin, additional, Deng, Fang-Ming, additional, Ren, Qinghu, additional, Chiriboga, Luis, additional, Melamed, Jonathan, additional, Sirard, Cynthia A., additional, and Wong, Kwok-Kin, additional

Published
2024
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56. EZH2 inhibition promotes tumor immunogenicity in lung squamous cell carcinomas

Author

DuCote, Tanner J, primary, Song, Xiulong, additional, Naughton, Kassandra J, additional, Chen, Fan, additional, Plaugher, Daniel R, additional, Childress, Avery R, additional, Gellert, Abigail R, additional, Skaggs, Erika M, additional, Qu, Xufeng, additional, Liu, Jinze, additional, Liu, Jinpeng, additional, Li, Fei, additional, Wong, Kwok-Kin, additional, and Brainson, Christine F., additional

Published
2024
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58. STK11/LKB1 Deficiency Promotes Neutrophil Recruitment and Proinflammatory Cytokine Production to Suppress T-cell Activity in the Lung Tumor Microenvironment

Author

Koyama, Shohei, Akbay, Esra A, Li, Yvonne Y, Aref, Amir R, Skoulidis, Ferdinandos, Herter-Sprie, Grit S, Buczkowski, Kevin A, Liu, Yan, Awad, Mark M, Denning, Warren L, Diao, Lixia, Wang, Jing, Parra-Cuentas, Edwin R, Wistuba, Ignacio I, Soucheray, Margaret, Thai, Tran, Asahina, Hajime, Kitajima, Shunsuke, Altabef, Abigail, Cavanaugh, Jillian D, Rhee, Kevin, Gao, Peng, Zhang, Haikuo, Fecci, Peter E, Shimamura, Takeshi, Hellmann, Matthew D, Heymach, John V, Hodi, F Stephen, Freeman, Gordon J, Barbie, David A, Dranoff, Glenn, Hammerman, Peter S, and Wong, Kwok-Kin

Subjects
Clinical Research, Lung, Cancer, Lung Cancer, 5.1 Pharmaceuticals, 2.1 Biological and endogenous factors, Aetiology, Development of treatments and therapeutic interventions, AMP-Activated Protein Kinase Kinases, AMP-Activated Protein Kinases, Animals, B7-H1 Antigen, Cytokines, Humans, Lung Neoplasms, Lymphocytes, Tumor-Infiltrating, Mice, Mutation, Neutrophil Infiltration, Protein Serine-Threonine Kinases, T-Lymphocytes, Tumor Microenvironment, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

STK11/LKB1 is among the most commonly inactivated tumor suppressors in non-small cell lung cancer (NSCLC), especially in tumors harboring KRAS mutations. Many oncogenes promote immune escape, undermining the effectiveness of immunotherapies, but it is unclear whether the inactivation of tumor suppressor genes, such as STK11/LKB1, exerts similar effects. In this study, we investigated the consequences of STK11/LKB1 loss on the immune microenvironment in a mouse model of KRAS-driven NSCLC. Genetic ablation of STK11/LKB1 resulted in accumulation of neutrophils with T-cell-suppressive effects, along with a corresponding increase in the expression of T-cell exhaustion markers and tumor-promoting cytokines. The number of tumor-infiltrating lymphocytes was also reduced in LKB1-deficient mouse and human tumors. Furthermore, STK11/LKB1-inactivating mutations were associated with reduced expression of PD-1 ligand PD-L1 in mouse and patient tumors as well as in tumor-derived cell lines. Consistent with these results, PD-1-targeting antibodies were ineffective against Lkb1-deficient tumors. In contrast, treating Lkb1-deficient mice with an IL6-neutralizing antibody or a neutrophil-depleting antibody yielded therapeutic benefits associated with reduced neutrophil accumulation and proinflammatory cytokine expression. Our findings illustrate how tumor suppressor mutations can modulate the immune milieu of the tumor microenvironment, and they offer specific implications for addressing STK11/LKB1-mutated tumors with PD-1-targeting antibody therapies.

Published
2016

59. Notch inhibition overcomes resistance to tyrosine kinase inhibitors in EGFR-driven lung adenocarcinoma

Author

Mur, Emilie Bousquet, Bernardo, Sara, Papon, Laura, Mancini, Maicol, Fabbrizio, Eric, Goussard, Marion, Ferrer, Irene, Giry, Anais, Quantin, Xavier, Pujol, Jean-Louis, Calvayrac, Olivier, Moll, Herwig P., Glasson, Yael, Pirot, Nelly, Turtoi, Andrei, Canamero, Marta, Wong, Kwok-Kin, Yarden, Yosef, Casanova, Emilio, Soria, Jean-Charles, Colinge, Jacques, Siebel, Christian W., Mazieres, Julien, Favre, Gilles, Paz-Ares, Luis, and Maraver, Antonio

Subjects
Cancer treatment -- Health aspects, Adenocarcinoma -- Development and progression -- Health aspects, Osimertinib -- Health aspects, Tyrosine -- Health aspects, Antineoplastic agents -- Health aspects, Phenols (Class of compounds) -- Health aspects, Gefitinib, Chemotherapy, Tumors, Diseases, Health care industry
Abstract

EGFR-mutated lung adenocarcinoma patients treated with gefitinib and osimertinib show a therapeutic benefit limited by the appearance of secondary mutations, such as [EGFR.sup.T790M] and [EGFR.sup.C7975]. It is generally assumed that these secondary mutations render EGFR completely unresponsive to the inhibitors, but contrary to this, we uncovered here that gefitinib and osimertinib increased STAT3 phosphorylation (p-STAT3) in [EGFR.sup.T790M] and [EGFR.sup.C7975] tumoral cells. Interestingly, we also found that concomitant Notch inhibition with gefitinib or osimertinib treatment induced a p-STAT3-dependent strong reduction in the levels of the transcriptional repressor HES1. Importantly, we showed that tyrosine kinase inhibitor-resistant tumors, with [EGFR.sup.T790M] and [EGFR.sup.C7975] mutations, were highly responsive to the combined treatment of Notch inhibitors with gefitinib or osimertinib, respectively. Finally, in patients with EGFR mutations treated with tyrosine kinase inhibitors, HES1 protein levels increased during relapse and correlated with shorter progression-free survival. Therefore, our results offer a proof of concept for an alternative treatment to chemotherapy in lung adenocarcinoma osimertinib- treated patients after disease progression., Introduction Lung cancer kills approximately 1 million people every year worldwide and is the leading cause of death by cancer in the world. Lung cancer consists of 2 main types: [...]

Published
2020
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61. PD-L1 engagement on T cells promotes self-tolerance and suppression of neighboring macrophages and effector T cells in cancer

Author

Diskin, Brian, Adam, Salma, Cassini, Marcelo F., Sanchez, Gustavo, Liria, Miguel, Aykut, Berk, Buttar, Chandan, Li, Eric, Sundberg, Belen, Salas, Ruben D., Chen, Ruonan, Wang, Junjie, Kim, Mirhee, Farooq, Mohammad Saad, Nguy, Susanna, Fedele, Carmine, Tang, Kwan Ho, Chen, Ting, Wang, Wei, Hundeyin, Mautin, Rossi, Juan A. Kochen, Kurz, Emma, Haq, Muhammad Israr Ul, Karlen, Jason, Kruger, Emma, Sekendiz, Zennur, Wu, Dongling, Shadaloey, Sorin A. A., Baptiste, Gillian, Werba, Gregor, Selvaraj, Shanmugapriya, Loomis, Cynthia, Wong, Kwok-Kin, Leinwand, Joshua, and Miller, George

Published
2020
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63. Exact meromorphic stationary solutions of the real cubic Swift-Hohenberg equation

Author

Conte, Robert, Ng, Tuen-Wai, and Wong, Kwok-Kin

Subjects
Nonlinear Sciences - Exactly Solvable and Integrable Systems, Mathematics - Classical Analysis and ODEs, 35Q53
Abstract

We show that all meromorphic solutions of the stationary reduction of the real cubic Swift-Hohenberg equation are elliptic or degenerate elliptic. We then obtain them all explicitly by the subequation method, and one of them appears to be a new elliptic solution., Comment: 15 pages, 3 figures, to appear, Studies in Applied Mathematics

Published
2012
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64. SOX2 and p63 colocalize at genetic loci in squamous cell carcinomas

Author

Watanabe, Hideo, Ma, Qiuping, Peng, Shouyong, Adelmant, Guillaume, Swain, Danielle, Song, Wenyu, Fox, Cameron, Francis, Joshua M, Pedamallu, Chandra Sekhar, DeLuca, David S, Brooks, Angela N, Wang, Su, Que, Jianwen, Rustgi, Anil K, Wong, Kwok-kin, Ligon, Keith L, Liu, X Shirley, Marto, Jarrod A, Meyerson, Matthew, and Bass, Adam J

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Genetics, Biological Sciences, Cancer, Stem Cell Research - Embryonic - Non-Human, Regenerative Medicine, Stem Cell Research, Human Genome, Biotechnology, 2.1 Biological and endogenous factors, Aetiology, Adenovirus E1A Proteins, Binding Sites, Carcinoma, Squamous Cell, Cell Line, Cell Line, Tumor, Chromatiaceae, Embryonic Stem Cells, Gene Amplification, Gene Expression Regulation, Neoplastic, Humans, Octamer Transcription Factor-3, Oncogenes, Pluripotent Stem Cells, Protein Binding, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-ets, SOXB1 Transcription Factors, Transcription Factors, Transcriptome, Tumor Suppressor Proteins, Medical and Health Sciences, Immunology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

The transcription factor SOX2 is an essential regulator of pluripotent stem cells and promotes development and maintenance of squamous epithelia. We previously reported that SOX2 is an oncogene and subject to highly recurrent genomic amplification in squamous cell carcinomas (SCCs). Here, we have further characterized the function of SOX2 in SCC. Using ChIP-seq analysis, we compared SOX2-regulated gene profiles in multiple SCC cell lines to ES cell profiles and determined that SOX2 binds to distinct genomic loci in SCCs. In SCCs, SOX2 preferentially interacts with the transcription factor p63, as opposed to the transcription factor OCT4, which is the preferred SOX2 binding partner in ES cells. SOX2 and p63 exhibited overlapping genomic occupancy at a large number of loci in SCCs; however, coordinate binding of SOX2 and p63 was absent in ES cells. We further demonstrated that SOX2 and p63 jointly regulate gene expression, including the oncogene ETV4, which was essential for SOX2-amplified SCC cell survival. Together, these findings demonstrate that the action of SOX2 in SCC differs substantially from its role in pluripotency. The identification of the SCC-associated interaction between SOX2 and p63 will enable deeper characterization the downstream targets of this interaction in SCC and normal squamous epithelial physiology.

Published
2014

65. D-2-hydroxyglutarate produced by mutant IDH2 causes cardiomyopathy and neurodegeneration in mice.

Author

Akbay, Esra, Moslehi, Javid, Christensen, Camilla, Saha, Supriya, Tchaicha, Jeremy, Ramkissoon, Shakti, Stewart, Kelly, Carretero, Julian, Kikuchi, Eiki, Zhang, Haikuo, Cohoon, Travis, Murray, Stuart, Liu, Wei, Uno, Kazumasa, Fisch, Sudeshna, Jones, Kristen, Gurumurthy, Sushma, Gliser, Camelia, Choe, Sung, Keenan, Marie, Son, Jaekyoung, Stanley, Illana, Losman, Julie, Padera, Robert, Bronson, Roderick, Asara, John, Abdel-Wahab, Omar, Amrein, Philip, Fathi, Amir, Danial, Nika, Kimmelman, Alec, Kung, Andrew, Ligon, Keith, Yen, Katharine, Kaelin, William, Bardeesy, Nabeel, and Wong, Kwok-Kin

Subjects
D-2HG, D2HGA, IDH2, cardiomyopathy, glycogen, myopathy, vacuolar leukoencephalopathy, Animals, Cardiomyopathies, Cell Line, Gene Expression Profiling, Gene Expression Regulation, Developmental, Glutarates, Heart, Humans, Isocitrate Dehydrogenase, Mice, Mice, Inbred BALB C, Mice, Nude, Mutation, Neurodegenerative Diseases
Abstract

Mutations in isocitrate dehydrogenase 1 and 2 (IDH1/2) have been discovered in several cancer types and cause the neurometabolic syndrome D2-hydroxyglutaric aciduria (D2HGA). The mutant enzymes exhibit neomorphic activity resulting in production of D2-hydroxyglutaric acid (D-2HG). To study the pathophysiological consequences of the accumulation of D-2HG, we generated transgenic mice with conditionally activated IDH2(R140Q) and IDH2(R172K) alleles. Global induction of mutant IDH2 expression in adults resulted in dilated cardiomyopathy, white matter abnormalities throughout the central nervous system (CNS), and muscular dystrophy. Embryonic activation of mutant IDH2 resulted in more pronounced phenotypes, including runting, hydrocephalus, and shortened life span, recapitulating the abnormalities observed in D2HGA patients. The diseased hearts exhibited mitochondrial damage and glycogen accumulation with a concordant up-regulation of genes involved in glycogen biosynthesis. Notably, mild cardiac hypertrophy was also observed in nude mice implanted with IDH2(R140Q)-expressing xenografts, suggesting that 2HG may potentially act in a paracrine fashion. Finally, we show that silencing of IDH2(R140Q) in mice with an inducible transgene restores heart function by lowering 2HG levels. Together, these findings indicate that inhibitors of mutant IDH2 may be beneficial in the treatment of D2HGA and suggest that 2HG produced by IDH mutant tumors has the potential to provoke a paraneoplastic condition.

Published
2014

66. Supplementary Table S9 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRASG12C Inhibitor Efficacy

Author

Mukhopadhyay, Suman, primary, Huang, Hsin-Yi, primary, Lin, Ziyan, primary, Ranieri, Michela, primary, Li, Shuai, primary, Sahu, Soumyadip, primary, Liu, Yingzhuo, primary, Ban, Yi, primary, Guidry, Kayla, primary, Hu, Hai, primary, Lopez, Alfonso, primary, Sherman, Fiona, primary, Tan, Yi Jer, primary, Lee, Yeuan Ting, primary, Armstrong, Amanda P., primary, Dolgalev, Igor, primary, Sahu, Priyanka, primary, Zhang, Tinghu, primary, Lu, Wenchao, primary, Gray, Nathanael S., primary, Christensen, James G., primary, Tang, Tracy T., primary, Velcheti, Vamsidhar, primary, Khodadadi-Jamayran, Alireza, primary, Wong, Kwok-Kin, primary, and Neel, Benjamin G., primary

Published
2023
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67. Supplementary Figure Legend from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRASG12C Inhibitor Efficacy

Author

Mukhopadhyay, Suman, primary, Huang, Hsin-Yi, primary, Lin, Ziyan, primary, Ranieri, Michela, primary, Li, Shuai, primary, Sahu, Soumyadip, primary, Liu, Yingzhuo, primary, Ban, Yi, primary, Guidry, Kayla, primary, Hu, Hai, primary, Lopez, Alfonso, primary, Sherman, Fiona, primary, Tan, Yi Jer, primary, Lee, Yeuan Ting, primary, Armstrong, Amanda P., primary, Dolgalev, Igor, primary, Sahu, Priyanka, primary, Zhang, Tinghu, primary, Lu, Wenchao, primary, Gray, Nathanael S., primary, Christensen, James G., primary, Tang, Tracy T., primary, Velcheti, Vamsidhar, primary, Khodadadi-Jamayran, Alireza, primary, Wong, Kwok-Kin, primary, and Neel, Benjamin G., primary

Published
2023
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68. Supplementary Figures 1-7 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRASG12C Inhibitor Efficacy

Author

Mukhopadhyay, Suman, primary, Huang, Hsin-Yi, primary, Lin, Ziyan, primary, Ranieri, Michela, primary, Li, Shuai, primary, Sahu, Soumyadip, primary, Liu, Yingzhuo, primary, Ban, Yi, primary, Guidry, Kayla, primary, Hu, Hai, primary, Lopez, Alfonso, primary, Sherman, Fiona, primary, Tan, Yi Jer, primary, Lee, Yeuan Ting, primary, Armstrong, Amanda P., primary, Dolgalev, Igor, primary, Sahu, Priyanka, primary, Zhang, Tinghu, primary, Lu, Wenchao, primary, Gray, Nathanael S., primary, Christensen, James G., primary, Tang, Tracy T., primary, Velcheti, Vamsidhar, primary, Khodadadi-Jamayran, Alireza, primary, Wong, Kwok-Kin, primary, and Neel, Benjamin G., primary

Published
2023
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69. Correction to: Identification of TAZ as the essential molecular switch in orchestrating SCLC phenotypic transition and metastasis

Author

Jin, Yujuan, primary, Zhao, Qiqi, additional, Zhu, Weikang, additional, Feng, Yan, additional, Xiao, Tian, additional, Zhang, Peng, additional, Jiang, Liyan, additional, Hou, Yingyong, additional, Guo, Chenchen, additional, Huang, Hsinyi, additional, Chen, Yabin, additional, Tong, Xinyuan, additional, Cao, Jiayu, additional, Li, Fei, additional, Zhu, Xueliang, additional, Qin, Jun, additional, Gao, Dong, additional, Liu, Xin-Yuan, additional, Zhang, Hua, additional, Chen, Luonan, additional, Thomas, Roman K, additional, Wong, Kwok-Kin, additional, Zhang, Lei, additional, Wang, Yong, additional, Hu, Liang, additional, and Ji, Hongbin, additional

Published
2023
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70. Data from A Multivalent Peptoid Conjugate Modulates Androgen Receptor Transcriptional Activity to Inhibit Therapy-resistant Prostate Cancer

Author

Habault, Justine, primary, Schneider, Jeffrey A., primary, Ha, Susan, primary, Ruoff, Rachel, primary, Pereira, Luiza D., primary, Puccini, Joseph, primary, Ranieri, Michela, primary, Ayasun, Ruveyda, primary, Deng, Jiehui, primary, Kasper, Amanda C., primary, Bar-Sagi, Dafna, primary, Wong, Kwok-Kin, primary, Zoubeidi, Amina, primary, Claessens, Frank, primary, Wise, David R., primary, Logan, Susan K., primary, Kirshenbaum, Kent, primary, and Garabedian, Michael J., primary

Published
2023
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71. Supplementary Figure Legends from A Multivalent Peptoid Conjugate Modulates Androgen Receptor Transcriptional Activity to Inhibit Therapy-resistant Prostate Cancer

Author

Habault, Justine, primary, Schneider, Jeffrey A., primary, Ha, Susan, primary, Ruoff, Rachel, primary, Pereira, Luiza D., primary, Puccini, Joseph, primary, Ranieri, Michela, primary, Ayasun, Ruveyda, primary, Deng, Jiehui, primary, Kasper, Amanda C., primary, Bar-Sagi, Dafna, primary, Wong, Kwok-Kin, primary, Zoubeidi, Amina, primary, Claessens, Frank, primary, Wise, David R., primary, Logan, Susan K., primary, Kirshenbaum, Kent, primary, and Garabedian, Michael J., primary

Published
2023
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72. Figure S4 from A Multivalent Peptoid Conjugate Modulates Androgen Receptor Transcriptional Activity to Inhibit Therapy-resistant Prostate Cancer

Author

Habault, Justine, primary, Schneider, Jeffrey A., primary, Ha, Susan, primary, Ruoff, Rachel, primary, Pereira, Luiza D., primary, Puccini, Joseph, primary, Ranieri, Michela, primary, Ayasun, Ruveyda, primary, Deng, Jiehui, primary, Kasper, Amanda C., primary, Bar-Sagi, Dafna, primary, Wong, Kwok-Kin, primary, Zoubeidi, Amina, primary, Claessens, Frank, primary, Wise, David R., primary, Logan, Susan K., primary, Kirshenbaum, Kent, primary, and Garabedian, Michael J., primary

Published
2023
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73. PROSPECTIVE EVALUATION OF CELL-FREE DNA FRAGMENTATION PROFILES FOR LUNG CANCER DETECTION

Author

J. MAZZONE, PETER, primary, WONG, KWOK-KIN, additional, TSAY, JAMES, additional, VACHANI, ANIL, additional, THOMPSON, JEFFREY, additional, RYAN, ALLISON, additional, CAREY, JACOB, additional, WU, TONY, additional, ZONG, YUHUA, additional, PORTWOOD, CARTER, additional, LUMBARD, KEITH, additional, CATALLINI, JOSEPH, additional, ARJUNGI, KAVITA, additional, BIRCH, ASHLEY, additional, BACH, PETER, additional, SCHARPF, ROBERT, additional, DRACOPOLI, NICHOLAS, additional, and VELCULESCU, VICTOR E, additional

Published
2023
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78. Cullin5 deficiency promotes small-cell lung cancer metastasis by stabilizing integrin [beta]1

Author

Zhao, Gaoxiang, Gong, Liyan, Su, Dan, Jin, Yujuan, Guo, Chenchen, Yue, Meiting, Yao, Shun, Qin, Zhen, Ye, Yi, Tang, Ying, Wu, Qibiao, Zhang, Jian, Cui, Binghai, Ding, Qiurong, Huang, Hsinyi, Hu, Liang, Chen, Yuting, Zhang, Peiyuan, Hu, Guohong, Chen, Luonan, Wong, Kwok-Kin, Gao, Daming, and Ji, Hongbin

Subjects
CRISPR-Cas technology -- Usage, Cancer metastasis -- Research, Genetic testing -- Usage, Small cell lung cancer -- Care and treatment -- Prognosis, Integrins, Death, Drug approval, Ligases, Libraries, Genomics, Lung cancer, Dasatinib, Cytokines, Ubiquitin, Genomes, Health care industry
Abstract

Metastasis is the dominant cause of patient death in small-cell lung cancer (SCLC), and a better understanding of the molecular mechanisms underlying SCLC metastasis may potentially improve clinical treatment. Through genome-scale screening for key regulators of mouse [Rb1.sup.-/-] [Trp53.sup.-/-] SCLC metastasis using the pooled CRISPR/Cas9 library, we identified Cullin5 (CUL5) and suppressor of cytokine signaling 3 (SOCS3), two components of the Cullin-RING E3 ubiquitin ligase complex, as top candidates. Mechanistically, the deficiency of CUL5 or SOCS3 disrupted the functional formation of the E3 ligase complex and prevented the degradation of integrin [beta]1, which stabilized integrin [beta]1 and activated downstream focal adhesion kinase/SRC (FAK/SRC) signaling and eventually drove SCLC metastasis. Low expression levels of CUL5 and SOCS3 were significantly associated with high integrin [beta]1 levels and poor prognosis in a large cohort of 128 clinical patients with SCLC. Moreover, the CUL5-deficient SCLCs were vulnerable to the treatment of the FDA-approved SRC inhibitor dasatinib. Collectively, this work identifies the essential role of CUL5- and SOCS3- mediated integrin [beta]1 turnover in controlling SCLC metastasis, which might have therapeutic implications., Introduction Small-cell lung cancer (SCLC) is the most aggressive and highly metastatic subtype of lung cancer and accounts for approximately 15% of all lung cancer cases (1). The 5-year survival [...]

Published
2019
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82. Evidence for an alternative fatty acid desaturation pathway increasing cancer plasticity

Author

Vriens, Kim, Christen, Stefan, Parik, Sweta, Broekaert, Dorien, Yoshinaga, Kazuaki, Talebi, Ali, Dehairs, Jonas, Escalona-Noguero, Carmen, Schmieder, Roberta, Cornfield, Thomas, Charlton, Catriona, Romero-Pérez, Laura, Rossi, Matteo, Rinaldi, Gianmarco, Orth, Martin F., Boon, Ruben, Kerstens, Axelle, Kwan, Suet Ying, Faubert, Brandon, Méndez-Lucas, Andrés, Kopitz, Charlotte C., Chen, Ting, Fernandez-Garcia, Juan, Duarte, João A. G., Schmitz, Arndt A., Steigemann, Patrick, Najimi, Mustapha, Hägebarth, Andrea, Van Ginderachter, Jo A., Sokal, Etienne, Gotoh, Naohiro, Wong, Kwok-Kin, Verfaillie, Catherine, Derua, Rita, Munck, Sebastian, Yuneva, Mariia, Beretta, Laura, DeBerardinis, Ralph J., Swinnen, Johannes V., Hodson, Leanne, Cassiman, David, Verslype, Chris, Christian, Sven, Grünewald, Sylvia, Grünewald, Thomas G. P., and Fendt, Sarah-Maria

Published
2019
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83. High-Resolution Genomic Profiles of Human Lung Cancer

Author

Tonon, Giovanni, Wong, Kwok-Kin, Maulik, Gautam, Brennan, Cameron, Feng, Bin, Zhang, Yunyu, Khatry, Deepak B., Protopopov, Alexei, You, Mingjian James, Aguirre, Andrew J., Martin, Eric S., Yang, Zhaohui, Ji, Hongbin, Chin, Lynda, DePinho, Ronald A., and Cavenee, Webster K.

Published
2005

84. Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRASG12C Inhibitor Efficacy

Author

Mukhopadhyay, Suman, primary, Huang, Hsin-Yi, additional, Lin, Ziyan, additional, Ranieri, Michela, additional, Li, Shuai, additional, Sahu, Soumyadip, additional, Liu, Yingzhuo, additional, Ban, Yi, additional, Guidry, Kayla, additional, Hu, Hai, additional, Lopez, Alfonso, additional, Sherman, Fiona, additional, Tan, Yi Jer, additional, Lee, Yeuan Ting, additional, Armstrong, Amanda P., additional, Dolgalev, Igor, additional, Sahu, Priyanka, additional, Zhang, Tinghu, additional, Lu, Wenchao, additional, Gray, Nathanael S., additional, Christensen, James G., additional, Tang, Tracy T., additional, Velcheti, Vamsidhar, additional, Khodadadi-Jamayran, Alireza, additional, Wong, Kwok-Kin, additional, and Neel, Benjamin G., additional

Published
2023
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85. A multivalent peptoid conjugate modulates androgen receptor transcriptional activity to inhibit therapy-resistant prostate cancer

Author

Habault, Justine, primary, Schneider, Jeffrey A., additional, Ha, Susan, additional, Ruoff, Rachel, additional, Doro Pereira, Luiza D., additional, Puccini, Joseph, additional, Ranieri, Michela, additional, Ayasun, Ruveyda, additional, Deng, Jiehui, additional, Kasper, Amanda C., additional, Bar-Sagi, Dafna, additional, Wong, Kwok-Kin, additional, Zoubeidi, Amina, additional, Claessens, Frank, additional, Wise, David R., additional, Logan, Susan K., additional, Kirshenbaum, Kent, additional, and Garabedian, Michael J., additional

Published
2023
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86. Tumor-intrinsic LKB1-LIF signaling axis establishes a myeloid niche to promote immune evasion and tumor growth

Author

Rashidfarrokhi, Ali, primary, Pillai, Ray, additional, Hao, Yuan, additional, Wu, Warren, additional, Karadal-Ferrena, Burcu, additional, dimitriadoy, Sofia G, additional, Cross, Michael, additional, Yeaton, Anna H, additional, Ming Huang, Shih, additional, Bhutkar, Arjun J, additional, Herrera, Alberto, additional, Rajalingam, Sahith, additional, Hayashi, Makiko, additional, Huang, Kuan-lin, additional, Bartnicki, Eric, additional, Zavitsanou, Anastasia-Maria, additional, Wohlhieter, Corrin, additional, Leboeuf, Sarah E, additional, Chen, Ting, additional, Loomis, Cynthia, additional, Mezzano, Valeria, additional, Kulicke, Ruth, additional, Davis, Fred P, additional, Stransky, Nicolas, additional, Smolen, Gromoslaw A, additional, Rudin, Charles M, additional, Moreira, Andre L, additional, Khanna, Kamal M, additional, Pass, Harvey I, additional, Wong, Kwok-Kin, additional, Koide, Shohei, additional, Tsirigos, Aristotelis, additional, Koralov, Sergei B, additional, and Papagiannakopoulos, Thales, additional

Published
2023
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87. Potent and Selective Covalent Quinazoline Inhibitors of KRAS G12C

Author

Zeng, Mei, Lu, Jia, Li, Lianbo, Feru, Frederic, Quan, Chunshan, Gero, Thomas W., Ficarro, Scott B., Xiong, Yuan, Ambrogio, Chiara, Paranal, Raymond M., Catalano, Marco, Shao, Jay, Wong, Kwok-Kin, Marto, Jarrod A., Fischer, Eric S., Jänne, Pasi A., Scott, David A., Westover, Kenneth D., and Gray, Nathanael S.

Published
2017
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88. Interleukin-17A Promotes Lung Tumor Progression through Neutrophil Attraction to Tumor Sites and Mediating Resistance to PD-1 Blockade

Author

Akbay, Esra A., Koyama, Shohei, Liu, Yan, Dries, Ruben, Bufe, Lauren E., Silkes, Michael, Alam, MD Maksudul, Magee, Dillon M., Jones, Robert, Jinushi, Masahisa, Kulkarni, Meghana, Carretero, Julian, Wang, Xiaoen, Warner-Hatten, Tiquella, Cavanaugh, Jillian D., Osa, Akio, Kumanogoh, Atsushi, Freeman, Gordon J., Awad, Mark M., Christiani, David C., Bueno, Raphael, Hammerman, Peter S., Dranoff, Glenn, and Wong, Kwok-Kin

Published
2017
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91. Quasi-Projective Manifolds Uniformized by Carathéodory Hyperbolic Manifolds and Hyperbolicity of Their Subvarieties.

Author

Wong, Kwok-Kin and Yeung, Sai-Kee

Subjects
*HYPERBOLIC spaces
Abstract

Let |$M$| be a Carathéodory hyperbolic complex manifold. We show that |$M$| supports a real-analytic bounded strictly plurisubharmonic function. If |$M$| is also complete Kähler, we show that |$M$| admits the Bergman metric. When |$M$| is strongly Carathéodory hyperbolic and is the universal covering of a quasi-projective manifold |$X$|⁠ , the Bergman metric can be estimated in terms of a Poincaré-type metric on |$X$|⁠. It is also proved that any quasi-projective (resp. projective) subvariety of |$X$| is of log-general type (resp. general type), a result consistent with a conjecture of Lang. [ABSTRACT FROM AUTHOR]

Published
2024
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92. JAK2/IDH-mutant-driven myeloproliferative neoplasm is sensitive to combined targeted inhibition

Author

McKenney, Anna Sophia, Lau, Allison N., Somasundara, Amritha Varshini Hanasoge, Spitzer, Barbara, Intlekofer, Andrew M., Ahn, Jihae, Shank, Kaitlyn, Rapaport, Franck T., Patel, Minal A., Papalexi, Efthymia, Shih, Alan H., Chiu, April, Freinkman, Elizaveta, Akbay, Esra A., Steadman, Mya, Nagaraja, Raj, Yen, Katharine, Teruya-Feldstein, Julie, Wong, Kwok-Kin, Rampal, Raajit, Heiden, Matthew G. Vander, Thompson, Craig B., and Levine, Ross L.

Subjects
Gene mutation -- Health aspects, Tumors -- Genetic aspects -- Development and progression -- Care and treatment, Myeloproliferative disorders -- Genetic aspects -- Development and progression -- Care and treatment, Health care industry
Abstract

Patients with myeloproliferative neoplasms (MPNs) frequently progress to bone marrow failure or acute myeloid leukemia (AML), and mutations in epigenetic regulators such as the metabolic enzyme isocitrate dehydrogenase (IDH) are associated with poor outcomes. Here, we showed that combined expression of [Jak2.sup.V617F] and mutant [IDH1.sup.R132H] or [Idh2.sup.R140Q] induces MPN progression, alters stem/progenitor cell function, and impairs differentiation in mice. [Jak2.sup.V617F] [Idh2.sup.R140Q]-mutant MPNs were sensitive to small-molecule inhibition of IDH. Combined inhibition of JAK2 and IDH2 normalized the stem and progenitor cell compartments in the murine model and reduced disease burden to a greater extent than was seen with JAK inhibition alone. In addition, combined JAK2 and IDH2 inhibitor treatment also reversed aberrant gene expression in MPN stem cells and reversed the metabolite perturbations induced by concurrent JAK2 and IDH2 mutations. Combined JAK2 and IDH2 inhibitor therapy also showed cooperative efficacy in cells from MPN patients with both [JAK2.sup.mut] and [IDH2.sup.mut] mutations. Taken together, these data suggest that combined JAK and IDH inhibition may offer a therapeutic advantage in this high-risk MPN subtype., Introduction Myeloproliferative neoplasms (MPNs) are clonal myeloid malignancies characterized by somatic mutations acquired in hematopoietic stem/progenitor cells, which drive the expansion of 1 or more myeloid lineages. Although patients with [...]

Published
2018
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93. Genomic correlates of response to immune checkpoint blockade in microsatellite-stable solid tumors

Author

Miao, Diana, Margolis, Claire A., Vokes, Natalie I., Liu, David, Taylor-Weiner, Amaro, Wankowicz, Stephanie M., Adeegbe, Dennis, Keliher, Daniel, Schilling, Bastian, Tracy, Adam, Manos, Michael, Chau, Nicole G., Hanna, Glenn J., Polak, Paz, Rodig, Scott J., Signoretti, Sabina, Sholl, Lynette M., Engelman, Jeffrey A., Getz, Gad, Jänne, Pasi A., Haddad, Robert I., Choueiri, Toni K., Barbie, David A., Haq, Rizwan, Awad, Mark M., Schadendorf, Dirk, Hodi, F. Stephen, Bellmunt, Joaquim, Wong, Kwok-Kin, Hammerman, Peter, and Van Allen, Eliezer M.

Published
2018
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95. Targeting wild-type KRAS-amplified gastroesophageal cancer through combined MEK and SHP2 inhibition

Author

Wong, Gabrielle S., Zhou, Jin, Liu, Jie Bin, Wu, Zhong, Xu, Xinsen, Li, Tianxia, Xu, David, Schumacher, Steven E., Puschhof, Jens, McFarland, James, Zou, Charles, Dulak, Austin, Henderson, Les, Xu, Peng, O’Day, Emily, Rendak, Rachel, Liao, Wei-li, Cecchi, Fabiola, Hembrough, Todd, Schwartz, Sarit, Szeto, Christopher, Rustgi, Anil K., Wong, Kwok-Kin, Diehl, J. Alan, Jensen, Karin, Graziano, Francesco, Ruzzo, Annamaria, Fereshetian, Shaunt, Mertins, Philipp, Carr, Steven A., Beroukhim, Rameen, Nakamura, Kenichi, Oki, Eiji, Watanabe, Masayuki, Baba, Hideo, Imamura, Yu, Catenacci, Daniel, and Bass, Adam J.

Published
2018
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96. The dTAG system for immediate and target-specific protein degradation

Author

Nabet, Behnam, Roberts, Justin M., Buckley, Dennis L., Paulk, Joshiawa, Dastjerdi, Shiva, Yang, Annan, Leggett, Alan L., Erb, Michael A., Lawlor, Matthew A., Souza, Amanda, Scott, Thomas G., Vittori, Sarah, Perry, Jennifer A., Qi, Jun, Winter, Georg E., Wong, Kwok-Kin, Gray, Nathanael S., and Bradner, James E.

Published
2018
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97. Mechanisms and clinical activity of an EGFR and HER2 exon 20–selective kinase inhibitor in non–small cell lung cancer

Author

Robichaux, Jacqulyne P., Elamin, Yasir Y., Tan, Zhi, Carter, Brett W., Zhang, Shuxing, Liu, Shengwu, Li, Shuai, Chen, Ting, Poteete, Alissa, Estrada-Bernal, Adriana, Le, Anh T., Truini, Anna, Nilsson, Monique B., Sun, Huiying, Roarty, Emily, Goldberg, Sarah B., Brahmer, Julie R., Altan, Mehmet, Lu, Charles, Papadimitrakopoulou, Vassiliki, Politi, Katerina, Doebele, Robert C., Wong, Kwok-Kin, and Heymach, John V.

Published
2018
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98. Glutamine antagonist DRP-104 suppresses tumor growth and enhances response to checkpoint blockade inKEAP1mutant lung cancer

Author

Pillai, Ray, primary, LeBoeuf, Sarah E., additional, Hao, Yuan, additional, New, Connie, additional, Blum, Jenna L. E., additional, Rashidfarrokhi, Ali, additional, Huang, Shih Ming, additional, Bahamon, Christian, additional, Wu, Warren L., additional, Karadal-Ferrena, Burcu, additional, Herrera, Alberto, additional, Ivanova, Ellie, additional, Cross, Michael, additional, Bossowski, Jozef P., additional, Ding, Hongyu, additional, Hayashi, Makiko, additional, Rajalingam, Sahith, additional, Karakousi, Triantafyllia, additional, Sayin, Volkan I., additional, Khanna, Kamal M., additional, Wong, Kwok-Kin, additional, Wild, Robert, additional, Tsirigos, Aristotelis, additional, Poirier, John T., additional, Rudin, Charles M., additional, Davidson, Shawn M., additional, Koralov, Sergei B., additional, and Papagiannakopoulos, Thales, additional

Published
2023
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99. Acquired Cross-resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification ofMYCparalogs

Author

Choudhuri, Shreoshi Pal, primary, Girard, Luc, additional, Lim, Jun Yi Stanley, additional, Wise, Jillian F., additional, Freitas, Braeden, additional, Yang, Di, additional, Wong, Edmond, additional, Hamilton, Seth, additional, Chien, Victor D., additional, Gilbreath, Collin, additional, Zhong, Jun, additional, Phat, Sarah, additional, Myers, David T., additional, Christensen, Camilla L., additional, Stanzione, Marcello, additional, Wong, Kwok-Kin, additional, Farago, Anna F., additional, Meador, Catherine B., additional, Dyson, Nicholas J., additional, Lawrence, Michael S., additional, Wu, Sihan, additional, and Drapkin, Benjamin J., additional

Published
2023
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100. EZH2 inhibition promotes tumor immunogenicity in lung squamous cell carcinomas

Author

DuCote, Tanner J., primary, Song, Xiulong, additional, Naughton, Kassandra J., additional, Chen, Fan, additional, Plaugher, Daniel R., additional, Childress, Avery R., additional, Edgin, Abigail R., additional, Qu, Xufeng, additional, Liu, Jinze, additional, Liu, Jinpeng, additional, Li, Fei, additional, Wong, Kwok-Kin, additional, and Brainson, Christine F., additional

Published
2023
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