نتائج البحث - "YANG, PAN-CHYR"

1

دورية أكاديمية

Trends and predictors of changes in pulmonary function after treatment for pulmonary tuberculosis

المؤلفون: Chung, Kuei-Pin, Chen, Jung-Yueh, Lee, Chih-Hsin, Wu, Huey-Dong, Wang, Jann-Yuan, Lee, Li-Na, Yu, Chong-Jen, Yang, Pan-Chyr

المصدر: Clinics. January 2011 66(4)

مصطلحات موضوعية: completion of treatment, disease extent, pulmonary function, pulmonary tuberculosis

الوصف: OBJECTIVES: The present study aimed to investigate the trends in changes in pulmonary function and the risk factors for pulmonary function deterioration in patients with pulmonary tuberculosis after completing treatment. INTRODUCTION: Patients usually have pulmonary function abnormalities after completing treatment for pulmonary tuberculosis. The time course for changes in pulmonary function and the risk factors for deterioration have not been well studied. METHODS: A total of 115 patients with 162 pulmonary function results were analyzed. We retrieved demographic and clinical data, radiographic scores, bacteriological data, and pulmonary function data. A generalized additive model with a locally weighted scatterplot smoothing technique was used to evaluate the trends in changes in pulmonary function. A generalized estimating equation model was used to determine the risk factors associated with deterioration of pulmonary function. RESULTS: The median interval between the end of anti-tuberculosis treatment and the pulmonary function test was 16 months (range: 0 to 112 months). The nadir of pulmonary function occurred approximately 18 months after the completion of the treatment. The risk factors associated with pulmonary function deterioration included smear-positive disease, extensive pulmonary involvement prior to anti-tuberculosis treatment, prolonged anti-tuberculosis treatment, and reduced radiographic improvement after treatment. CONCLUSIONS: After the completion of anti-tuberculosis TB treatment, several risk factors predicted pulmonary function deterioration. For patients with significant respiratory symptoms and multiple risk factors, the pulmonary function test should be followed up to monitor the progression of functional impairment, especially within the first 18 months after the completion of anti-tuberculosis treatment.

وصف الملف: text/html

الوصول الحر: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1807-59322011000400005Test

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النص الكامل

2

دورية أكاديمية

Reduced symmetric dimethylation stabilizes vimentin and promotes metastasis in MTAP‐deficient lung cancer

المؤلفون: Chang, Wen‐Hsin, Chen, Yi‐Ju, Hsiao, Yi‐Jing, Chiang, Ching‐Cheng, Wang, Chia‐Yu, Chang, Ya‐Ling, Hong, Qi‐Sheng, Lin, Chien‐Yu, Lin, Shr‐Uen, Chang, Gee‐Chen, Chen, Hsuan‐Yu, Chen, Yu‐Ju, Chen, Ching‐Hsien, Yang, Pan‐Chyr, Yu, Sung‐Liang

المصدر: EMBO Reports. 23(8)

مصطلحات موضوعية: Cancer, Lung Cancer, Lung, Aetiology, 2.1 Biological and endogenous factors, Humans, Lung Neoplasms, Protein-Arginine N-Methyltransferases, Purine-Nucleoside Phosphorylase, Vimentin, Methylproteome, Methylthioadenosine, Post-translational modification, Protein arginine methyltransferase 5, Symmetric dimethylarginine, Biochemistry and Cell Biology, Developmental Biology

الوصف: The aggressive nature and poor prognosis of lung cancer led us to explore the mechanisms driving disease progression. Utilizing our invasive cell-based model, we identified methylthioadenosine phosphorylase (MTAP) and confirmed its suppressive effects on tumorigenesis and metastasis. Patients with low MTAP expression display worse overall and progression-free survival. Mechanistically, accumulation of methylthioadenosine substrate in MTAP-deficient cells reduce the level of protein arginine methyltransferase 5 (PRMT5)-mediated symmetric dimethylarginine (sDMA) modification on proteins. We identify vimentin as a dimethyl-protein whose dimethylation levels drop in response to MTAP deficiency. The sDMA modification on vimentin reduces its protein abundance but trivially affects its filamentous structure. In MTAP-deficient cells, lower sDMA modification prevents ubiquitination-mediated vimentin degradation, thereby stabilizing vimentin and contributing to cell invasion. MTAP and PRMT5 negatively correlate with vimentin in lung cancer samples. Taken together, we propose a mechanism for metastasis involving vimentin post-translational regulation.

وصف الملف: application/pdf

الوصول الحر: https://escholarship.org/uc/item/63x6g3gfTest

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3

دورية أكاديمية

Nano-modified viruses prime the tumor microenvironment and promote the photodynamic virotherapy in liver cancer

المؤلفون: Ou, Da-Liang, Liao, Zi-Xian, Kempson, Ivan M., Li, Lin, Yang, Pan-Chyr, Tseng, S.-Ja

المساهمون: National Science and Technology Council

المصدر: Journal of Biomedical Science ; volume 31, issue 1 ; ISSN 1423-0127

مصطلحات موضوعية: Pharmacology (medical), Biochemistry (medical), Cell Biology, Clinical Biochemistry, Molecular Biology, General Medicine, Endocrinology, Diabetes and Metabolism

الوصف: Background As of 2020, hepatocellular carcinoma (HCC), a form of liver cancer, stood as the third most prominent contributor to global cancer-related mortality. Combining immune checkpoint inhibitors (ICI) with other therapies has shown promising results for treating unresectable HCC, offering new opportunities. Recombinant adeno-associated viral type 2 (AAV2) virotherapy has been approved for clinical use but it efficacy is stifled through systemic administration. On the other hand, iron oxide nanoparticles (ION) can be cleared via the liver and enhance macrophage polarization, promoting infiltration of CD8 + T cells and creating a more favorable tumor microenvironment for immunotherapy. Methods To enhance the efficacy of virotherapy and promote macrophage polarization towards the M1-type in the liver, ION-AAV2 were prepared through the coupling of ION-carboxyl and AAV2-amine using 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide hydrochloride (EDC)/N-hydroxysulfosuccinimide (Sulfo-NHS). Efficacy after systemic delivery of ION-AAV2 in an orthotopic HCC model was evaluated. Results After 28 days, the tumor weight in mice treated with ION-AAV2 was significantly reduced by 0.56-fold compared to the control group. The ION-AAV2 treatment led to an approximate 1.80-fold increase in the level of tumor associated M1-type macrophages, while the number of M2-type macrophages was reduced by 0.88-fold. Moreover, a proinflammatory response increased the population of tumor-infiltrating CD8 + T cells in the ION-AAV2 group. This transformation converted cold tumors into hot tumors. Conclusions Our findings suggest that the conjugation of ION with AAV2 could be utilized in virotherapy while simultaneously exploiting macrophage-modulating cancer immunotherapies to effectively suppress HCC growth.

الإتاحة: https://doi.org/10.1186/s12929-023-00989-1Test

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4

دورية أكاديمية

Genome-wide association study of lung adenocarcinoma in East Asia and comparison with a European population

المؤلفون: Shi, Jianxin, Shiraishi, Kouya, Choi, Jiyeon, Matsuo, Keitaro, Chen, Tzu-Yu, Dai, Juncheng, Hung, Rayjean J, Chen, Kexin, Shu, Xiao-Ou, Kim, Young Tae, Landi, Maria Teresa, Lin, Dongxin, Zheng, Wei, Yin, Zhihua, Zhou, Baosen, Song, Bao, Wang, Jiucun, Seow, Wei Jie, Song, Lei, Chang, I-Shou, Hu, Wei, Chien, Li-Hsin, Cai, Qiuyin, Hong, Yun-Chul, Kim, Hee Nam, Wu, Yi-Long, Wong, Maria Pik, Richardson, Brian Douglas, Funderburk, Karen M, Li, Shilan, Zhang, Tongwu, Breeze, Charles, Wang, Zhaoming, Blechter, Batel, Bassig, Bryan A, Kim, Jin Hee, Albanes, Demetrius, Wong, Jason Y Y, Shin, Min-Ho, Chung, Lap Ping, Yang, Yang, An, She-Juan, Zheng, Hong, Yatabe, Yasushi, Zhang, Xu-Chao, Kim, Young-Chul, Caporaso, Neil E, Chang, Jiang, Ho, James Chung Man, Kubo, Michiaki, Daigo, Yataro, Song, Minsun, Momozawa, Yukihide, Kamatani, Yoichiro, Kobayashi, Masashi, Okubo, Kenichi, Honda, Takayuki, Hosgood, Dean H, Kunitoh, Hideo, Patel, Harsh, Watanabe, Shun-Ichi, Miyagi, Yohei, Nakayama, Haruhiko, Matsumoto, Shingo, Horinouchi, Hidehito, Tsuboi, Masahiro, Hamamoto, Ryuji, Goto, Koichi, Ohe, Yuichiro, Takahashi, Atsushi, Goto, Akiteru, Minamiya, Yoshihiro, Hara, Megumi, Nishida, Yuichiro, Takeuchi, Kenji, Wakai, Kenji, Matsuda, Koichi, Murakami, Yoshinori, Shimizu, Kimihiro, Suzuki, Hiroyuki, Saito, Motonobu, Ohtaki, Yoichi, Tanaka, Kazumi, Wu, Tangchun, Wei, Fusheng, Dai, Hongji, Machiela, Mitchell J, Su, Jian, Kim, Yeul Hong, Oh, In-Jae, Lee, Victor Ho Fun, Chang, Gee-Chen, Tsai, Ying-Huang, Chen, Kuan-Yu, Huang, Ming-Shyan, Su, Wu-Chou, Chen, Yuh-Min, Seow, Adeline, Park, Jae Yong, Kweon, Sun-Seog, Chen, Kun-Chieh, Gao, Yu-Tang, Qian, Biyun, Wu, Chen, Lu, Daru, Liu, Jianjun, Schwartz, Ann G, Houlston, Richard, Spitz, Margaret R, Gorlov, Ivan P, Wu, Xifeng, Yang, Ping, Lam, Stephen, Tardon, Adonina, Chen, Chu, Bojesen, Stig E, Johansson, Mattias, Risch, Angela, Bickeböller, Heike, Ji, Bu-Tian, Wichmann, H-Erich, Christiani, David C, Rennert, Gadi, Arnold, Susanne, Brennan, Paul, McKay, James, Field, John K, Shete, Sanjay S, Le Marchand, Loic, Liu, Geoffrey, Andrew, Angeline, Kiemeney, Lambertus A, Zienolddiny-Narui, Shan, Grankvist, Kjell, Johansson, Mikael, Cox, Angela, Taylor, Fiona, Yuan, Jian-Min, Lazarus, Philip, Schabath, Matthew B, Aldrich, Melinda C, Jeon, Hyo-Sung, Jiang, Shih Sheng, Sung, Jae Sook, Chen, Chung-Hsing, Hsiao, Chin-Fu, Jung, Yoo Jin, Guo, Huan, Hu, Zhibin, Burdett, Laurie, Yeager, Meredith, Hutchinson, Amy, Hicks, Belynda, Liu, Jia, Zhu, Bin, Berndt, Sonja I, Wu, Wei, Wang, Junwen, Li, Yuqing, Choi, Jin Eun, Park, Kyong Hwa, Sung, Sook Whan, Liu, Li, Kang, Chang Hyun, Wang, Wen-Chang, Xu, Jun, Guan, Peng, Tan, Wen, Yu, Chong-Jen, Yang, Gong, Sihoe, Alan Dart Loon, Chen, Ying, Choi, Yi Young, Kim, Jun Suk, Yoon, Ho-Il, Park, In Kyu, Xu, Ping, He, Qincheng, Wang, Chih-Liang, Hung, Hsiao-Han, Vermeulen, Roel C H, Cheng, Iona, Wu, Junjie, Lim, Wei-Yen, Tsai, Fang-Yu, Chan, John K C, Li, Jihua, Chen, Hongyan, Lin, Hsien-Chih, Jin, Li, Liu, Jie, Sawada, Norie, Yamaji, Taiki, Wyatt, Kathleen, Li, Shengchao A, Ma, Hongxia, Zhu, Meng, Wang, Zhehai, Cheng, Sensen, Li, Xuelian, Ren, Yangwu, Chao, Ann, Iwasaki, Motoki, Zhu, Junjie, Jiang, Gening, Fei, Ke, Wu, Guoping, Chen, Chih-Yi, Chen, Chien-Jen, Yang, Pan-Chyr, Yu, Jinming, Stevens, Victoria L, Fraumeni, Joseph F, Chatterjee, Nilanjan, Gorlova, Olga Y, Hsiung, Chao Agnes, Amos, Christopher I, Shen, Hongbing, Chanock, Stephen J, Rothman, Nathaniel, Kohno, Takashi, Lan, Qing

المساهمون: IRAS OH Epidemiology Chemical Agents

مصطلحات موضوعية: Humans, Genome-Wide Association Study, Genetic Predisposition to Disease, Adenocarcinoma of Lung/genetics, Asia, Eastern/epidemiology, Lung Neoplasms/epidemiology, Polymorphism, Single Nucleotide

الوصف: Lung adenocarcinoma is the most common type of lung cancer. Known risk variants explain only a small fraction of lung adenocarcinoma heritability. Here, we conducted a two-stage genome-wide association study of lung adenocarcinoma of East Asian ancestry (21,658 cases and 150,676 controls; 54.5% never-smokers) and identified 12 novel susceptibility variants, bringing the total number to 28 at 25 independent loci. Transcriptome-wide association analyses together with colocalization studies using a Taiwanese lung expression quantitative trait loci dataset (n = 115) identified novel candidate genes, including FADS1 at 11q12 and ELF5 at 11p13. In a multi-ancestry meta-analysis of East Asian and European studies, four loci were identified at 2p11, 4q32, 16q23, and 18q12. At the same time, most of our findings in East Asian populations showed no evidence of association in European populations. In our studies drawn from East Asian populations, a polygenic risk score based on the 25 loci had a stronger association in never-smokers vs. individuals with a history of smoking (P interaction = 0.0058). These findings provide new insights into the etiology of lung adenocarcinoma in individuals from East Asian populations, which could be important in developing translational applications.

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العلاقة: https://dspace.library.uu.nl/handle/1874/429550Test

الإتاحة: https://dspace.library.uu.nl/handle/1874/429550Test

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النص الكامل

5

دورية أكاديمية

PM2.5 promotes lung cancer progression through activation of the AhR‐TMPRSS2‐IL18 pathway

المؤلفون: Wang, Tong‐Hong, Huang, Kuo‐Yen, Chen, Chin‐Chuan, Chang, Ya‐Hsuan, Chen, Hsuan‐Yu, Hsueh, Chuen, Liu, Yi‐Tsen, Yang, Shuenn‐Chen, Yang, Pan‐Chyr, Chen, Chi‐Yuan

المساهمون: Chang Gung Memorial Hospital

المصدر: EMBO Molecular Medicine ; volume 15, issue 6 ; ISSN 1757-4676 1757-4684

مصطلحات موضوعية: Molecular Medicine

الوصف: Particulate matter 2.5 (PM2.5) is a risk factor for lung cancer. In this study, we investigated the molecular mechanisms of PM2.5 exposure on lung cancer progression. We found that short‐term exposure to PM2.5 for 24 h activated the EGFR pathway in lung cancer cells (EGFR wild‐type and mutant), while long‐term exposure of lung cancer cells to PM2.5 for 90 days persistently promoted EGFR activation, cell proliferation, anchorage‐independent growth, and tumor growth in a xenograft mouse model in EGFR‐driven H1975 cancer cells. We showed that PM2.5 activated AhR to translocate into the nucleus and promoted EGFR activation. AhR further interacted with the promoter of TMPRSS2, thereby upregulating TMPRSS2 and IL18 expression to promote cancer progression. Depletion of TMPRSS2 in lung cancer cells suppressed anchorage‐independent growth and xenograft tumor growth in mice. The expression levels of TMPRSS2 were found to correlate with nuclear AhR expression and with cancer stage in lung cancer patient tissue. Long‐term exposure to PM2.5 could promote tumor progression in lung cancer through activation of EGFR and AhR to enhance the TMPRSS2‐IL18 pathway.

الإتاحة: https://doi.org/10.15252/emmm.202217014Test

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6

دورية أكاديمية

Exosomal long noncoding RNA MLETA1 promotes tumor progression and metastasis by regulating the miR-186-5p/EGFR and miR-497-5p/IGF1R axes in non-small cell lung cancer

المؤلفون: Hsu, Xiu-Rui, Wu, Jia-En, Wu, Yi-Ying, Hsiao, Sheng-Yen, Liang, Jui-Lin, Wu, Ya-Ju, Tung, Chia-Hao, Huang, Meng-Fan, Lin, Ming-Shiu, Yang, Pan-Chyr, Chen, Yuh-Ling, Hong, Tse-Ming

المساهمون: Ministry of Science and Technology, Taiwan

المصدر: Journal of Experimental & Clinical Cancer Research ; volume 42, issue 1 ; ISSN 1756-9966

مصطلحات موضوعية: Cancer Research, Oncology

الوصف: Background Lung cancer is the most common and deadliest cancer worldwide, and approximately 90% of all lung cancer deaths are caused by tumor metastasis. Tumor-derived exosomes could potentially promote tumor metastasis through the delivery of metastasis-related molecules. However, the function and underlying mechanism of exosomal long noncoding RNA (lncRNA) in lung cancer metastasis remain largely unclear. Methods Cell exosomes were purified from conditioned media by differential ultracentrifugation and observed using transmission electron microscopy, and the size distributions were determined by nanoparticle tracking analysis. Exosomal lncRNA sequencing (lncRNA-seq) was used to identify long noncoding RNAs. Cell migration and invasion were determined by wound-healing assays, two-chamber transwell invasion assays and cell mobility tracking. Mice orthotopically and subcutaneously xenografted with human cancer cells were used to evaluate tumor metastasis in vivo. Western blot, qRT‒PCR, RNA-seq, and dual-luciferase reporter assays were performed to investigate the potential mechanism. The level of exosomal lncRNA in plasma was examined by qRT‒PCR. MS2-tagged RNA affinity purification (MS2-TRAP) assays were performed to verify lncRNA-bound miRNAs. Results Exosomes derived from highly metastatic lung cancer cells promoted the migration and invasion of lung cancer cells with low metastatic potential. Using lncRNA-seq, we found that a novel lncRNA, lnc-MLETA1, was upregulated in highly metastatic cells and their secreted exosomes. Overexpression of lnc-MLETA1 augmented cell migration and invasion of lung cancer. Conversely, knockdown of lnc-MLETA1 attenuated the motility and metastasis of lung cancer cells. Interestingly, exosome-transmitted lnc-MLETA1 promoted cell motility and metastasis of lung cancer. Reciprocally, targeting lnc-MLETA1 with an LNA suppressed exosome-induced lung cancer cell motility. Mechanistically, lnc-MLETA1 regulated the expression of EGFR and IGF1R by sponging miR-186-5p and ...

الإتاحة: https://doi.org/10.1186/s13046-023-02859-yTest

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