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28 results on '"Shen, Tsai-Wei"'

1. Structural variant analysis of a cancer reference cell line sample using multiple sequencing technologies

Author

Talsania, Keyur, Shen, Tsai-wei, Chen, Xiongfong, Jaeger, Erich, Li, Zhipan, Chen, Zhong, Chen, Wanqiu, Tran, Bao, Kusko, Rebecca, Wang, Limin, Pang, Andy Wing Chun, Yang, Zhaowei, Choudhari, Sulbha, Colgan, Michael, Fang, Li Tai, Carroll, Andrew, Shetty, Jyoti, Kriga, Yuliya, German, Oksana, Smirnova, Tatyana, Liu, Tiantain, Li, Jing, Kellman, Ben, Hong, Karl, Hastie, Alex R., Natarajan, Aparna, Moshrefi, Ali, Granat, Anastasiya, Truong, Tiffany, Bombardi, Robin, Mankinen, Veronnica, Meerzaman, Daoud, Mason, Christopher E., Collins, Jack, Stahlberg, Eric, Xiao, Chunlin, Wang, Charles, Xiao, Wenming, and Zhao, Yongmei

Published
2022
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2. Toward best practice in cancer mutation detection with whole-genome and whole-exome sequencing

Author

Xiao, Wenming, Ren, Luyao, Chen, Zhong, Fang, Li Tai, Zhao, Yongmei, Lack, Justin, Guan, Meijian, Zhu, Bin, Jaeger, Erich, Kerrigan, Liz, Blomquist, Thomas M., Hung, Tiffany, Sultan, Marc, Idler, Kenneth, Lu, Charles, Scherer, Andreas, Kusko, Rebecca, Moos, Malcolm, Xiao, Chunlin, Sherry, Stephen T., Abaan, Ogan D., Chen, Wanqiu, Chen, Xin, Nordlund, Jessica, Liljedahl, Ulrika, Maestro, Roberta, Polano, Maurizio, Drabek, Jiri, Vojta, Petr, Kõks, Sulev, Reimann, Ene, Madala, Bindu Swapna, Mercer, Timothy, Miller, Chris, Jacob, Howard, Truong, Tiffany, Moshrefi, Ali, Natarajan, Aparna, Granat, Ana, Schroth, Gary P., Kalamegham, Rasika, Peters, Eric, Petitjean, Virginie, Walton, Ashley, Shen, Tsai-Wei, Talsania, Keyur, Vera, Cristobal Juan, Langenbach, Kurt, de Mars, Maryellen, Hipp, Jennifer A., Willey, James C., Wang, Jing, Shetty, Jyoti, Kriga, Yuliya, Raziuddin, Arati, Tran, Bao, Zheng, Yuanting, Yu, Ying, Cam, Margaret, Jailwala, Parthav, Nguyen, Cu, Meerzaman, Daoud, Chen, Qingrong, Yan, Chunhua, Ernest, Ben, Mehra, Urvashi, Jensen, Roderick V., Jones, Wendell, Li, Jian-Liang, Papas, Brian N., Pirooznia, Mehdi, Chen, Yun-Ching, Seifuddin, Fayaz, Li, Zhipan, Liu, Xuelu, Resch, Wolfgang, Wang, Jingya, Wu, Leihong, Yavas, Gokhan, Miles, Corey, Ning, Baitang, Tong, Weida, Mason, Christopher E., Donaldson, Eric, Lababidi, Samir, Staudt, Louis M., Tezak, Zivana, Hong, Huixiao, Wang, Charles, and Shi, Leming

Published
2021
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3. Targeting purine synthesis in ASS1-expressing tumors enhances the response to immune checkpoint inhibitors

Author

Keshet, Rom, Lee, Joo Sang, Adler, Lital, Iraqi, Muhammed, Ariav, Yarden, Lim, Lisha Qiu Jin, Lerner, Shaul, Rabinovich, Shiran, Oren, Roni, Katzir, Rotem, Weiss Tishler, Hila, Stettner, Noa, Goldman, Omer, Landesman, Hadas, Galai, Sivan, Kuperman, Yael, Kuznetsov, Yuri, Brandis, Alexander, Mehlman, Tevi, Malitsky, Sergey, Itkin, Maxim, Koehler, S. Eleonore, Zhao, Yongmei, Talsania, Keyur, Shen, Tsai-wei, Peled, Nir, Ulitsky, Igor, Porgador, Angel, Ruppin, Eytan, and Erez, Ayelet

Published
2020
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4. Whole genome and exome sequencing reference datasets from a multi-center and cross-platform benchmark study

Author

Zhao, Yongmei, Fang, Li Tai, Shen, Tsai-wei, Choudhari, Sulbha, Talsania, Keyur, Chen, Xiongfong, Shetty, Jyoti, Kriga, Yuliya, Tran, Bao, Zhu, Bin, Chen, Zhong, Chen, Wanqiu, Wang, Charles, Jaeger, Erich, Meerzaman, Daoud, Lu, Charles, Idler, Kenneth, Ren, Luyao, Zheng, Yuanting, Shi, Leming, Petitjean, Virginie, Sultan, Marc, Hung, Tiffany, Peters, Eric, Drabek, Jiri, Vojta, Petr, Maestro, Roberta, Gasparotto, Daniela, Kõks, Sulev, Reimann, Ene, Scherer, Andreas, Nordlund, Jessica, Liljedahl, Ulrika, Foox, Jonathan, Mason, Christopher E., Xiao, Chunlin, Hong, Huixiao, and Xiao, Wenming

Published
2021
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5. Extrachromosomal DNA Amplification Contributes to Small Cell Lung Cancer Heterogeneity and Is Associated with Worse Outcomes

Author

Lőrinc Sándor Pongor, Christopher W. Schultz, Lorenzo Rinaldi, Darawalee Wangsa, Christophe E. Redon, Nobuyuki Takahashi, Gavriel Fialkoff, Parth Desai, Yang Zhang, Sandra Burkett, Nadav Hermoni, Noa Vilk, Jenia Gutin, Rona Gergely, Yongmei Zhao, Samantha Nichols, Rasa Vilimas, Linda Sciuto, Chante Graham, Juan Manuel Caravaca, Sevilay Turan, Shen Tsai-wei, Vinodh N. Rajapakse, Rajesh Kumar, Deep Upadhyay, Suresh Kumar, Yoo Sun Kim, Nitin Roper, Bao Tran, Stephen M. Hewitt, David E. Kleiner, Mirit I. Aladjem, Nir Friedman, Gordon L. Hager, Yves Pommier, Thomas Ried, and Anish Thomas

Subjects
Oncology
Abstract

Small-cell lung cancer (SCLC) is an aggressive neuroendocrine lung cancer. Oncogenic MYC amplifications drive SCLC heterogeneity, but the genetic mechanisms of MYC amplification and phenotypic plasticity, characterized by neuroendocrine and nonneuroendocrine cell states, are not known. Here, we integrate whole-genome sequencing, long-range optical mapping, single-cell DNA sequencing, and fluorescence in situ hybridization to find extrachromosomal DNA (ecDNA) as a primary source of SCLC oncogene amplifications and driver fusions. ecDNAs bring to proximity enhancer elements and oncogenes, creating SCLC transcription-amplifying units, driving exceptionally high MYC gene dosage. We demonstrate that cell-free nucleosome profiling can noninvasively detect ecDNA amplifications in plasma, facilitating its genome-wide interrogation in SCLC and other cancers. Altogether, our work provides the first comprehensive map of SCLC ecDNA and describes a new mechanism that governs MYC-driven SCLC heterogeneity. ecDNA-enabled transcriptional flexibility may explain the significantly worse survival outcomes of SCLC harboring complex ecDNA amplifications. Significance: MYC drives SCLC progression, but the genetic basis of MYC-driven SCLC evolution is unknown. Using SCLC as a paradigm, we report how ecDNA amplifications function as MYC-amplifying units, fostering tumor plasticity and a high degree of tumor heterogeneity. This article is highlighted in the In This Issue feature, p. 799

Published
2023
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6. Tumor Biology and Immune Infiltration Define Primary Liver Cancer Subsets Linked to Overall Survival After Immunotherapy

Author

Budhu, Anuradha, Pehrsson, Erica C, He, Aiwu, Goyal, Lipika, Kelley, Robin Kate, Dang, Hien, Xie, Changqing, Monge, Cecilia, Tandon, Mayank, Ma, Lichun, Revsine, Mahler, Kuhlman, Laura, Zhang, Karen, Baiev, Islam, Lamm, Ryan, Patel, Keyur, Kleiner, David E, Hewitt, Stephen M, Tran, Bao, Shetty, Jyoti, Wu, Xiaolin, Zhao, Yongmei, Shen, Tsai-Wei, Choudhari, Sulbha, Kriga, Yuliya, Ylaya, Kris, Warner, Andrew C, Edmondson, Elijah F, Forgues, Marshonna, Greten, Tim F, Wang, Xin Wei, Budhu, Anuradha, Pehrsson, Erica C, He, Aiwu, Goyal, Lipika, Kelley, Robin Kate, Dang, Hien, Xie, Changqing, Monge, Cecilia, Tandon, Mayank, Ma, Lichun, Revsine, Mahler, Kuhlman, Laura, Zhang, Karen, Baiev, Islam, Lamm, Ryan, Patel, Keyur, Kleiner, David E, Hewitt, Stephen M, Tran, Bao, Shetty, Jyoti, Wu, Xiaolin, Zhao, Yongmei, Shen, Tsai-Wei, Choudhari, Sulbha, Kriga, Yuliya, Ylaya, Kris, Warner, Andrew C, Edmondson, Elijah F, Forgues, Marshonna, Greten, Tim F, and Wang, Xin Wei

Abstract

Primary liver cancer is a rising cause of cancer deaths in the US. Although immunotherapy with immune checkpoint inhibitors induces a potent response in a subset of patients, response rates vary among individuals. Predicting which patients will respond to immune checkpoint inhibitors is of great interest in the field. In a retrospective arm of the National Cancer Institute Cancers of the Liver: Accelerating Research of Immunotherapy by a Transdisciplinary Network (NCI-CLARITY) study, we use archived formalin-fixed, paraffin-embedded samples to profile the transcriptome and genomic alterations among 86 hepatocellular carcinoma and cholangiocarcinoma patients prior to and following immune checkpoint inhibitor treatment. Using supervised and unsupervised approaches, we identify stable molecular subtypes linked to overall survival and distinguished by two axes of aggressive tumor biology and microenvironmental features. Moreover, molecular responses to immune checkpoint inhibitor treatment differ between subtypes. Thus, patients with heterogeneous liver cancer may be stratified by molecular status indicative of treatment response to immune checkpoint inhibitors.

Published
2023

7. Serum microRNA Profiles and Pathways in Hepatitis B-Associated Hepatocellular Carcinoma: A South African Study.

Author

Sartorius, Kurt, Sartorius, Benn, Winkler, Cheryl, Chuturgoon, Anil, Shen, Tsai-Wei, Zhao, Yongmei, and An, Ping

Subjects
GENE expression, HEPATOCELLULAR carcinoma, MICRORNA, HEPATITIS
Abstract

The incidence and mortality of hepatocellular carcinoma (HCC) in Sub-Saharan Africa is projected to increase sharply by 2040 against a backdrop of limited diagnostic and therapeutic options. Two large South African-based case control studies have developed a serum-based miRNome for Hepatitis B-associated hepatocellular carcinoma (HBV-HCC), as well as identifying their gene targets and pathways. Using a combination of RNA sequencing, differential analysis and filters including a unique molecular index count (UMI) ≥ 10 and log fold change (LFC) range > 2: <−0.5 (p < 0.05), 91 dysregulated miRNAs were characterized including 30 that were upregulated and 61 were downregulated. KEGG analysis, a literature review and other bioinformatic tools identified the targeted genes and HBV-HCC pathways of the top 10 most dysregulated miRNAs. The results, which are based on differentiating miRNA expression of cases versus controls, also develop a serum-based miRNA diagnostic panel that indicates 95.9% sensitivity, 91.0% specificity and a Youden Index of 0.869. In conclusion, the results develop a comprehensive African HBV-HCC miRNome that potentially can contribute to RNA-based diagnostic and therapeutic options. [ABSTRACT FROM AUTHOR]

Published
2024
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8. Tumor biology and immune infiltration define primary liver cancer subsets linked to overall survival after immunotherapy

Author

Budhu, Anuradha, primary, Pehrsson, Erica C., additional, He, Aiwu, additional, Goyal, Lipika, additional, Kelley, Robin Kate, additional, Dang, Hien, additional, Xie, Changqing, additional, Monge, Cecilia, additional, Tandon, Mayank, additional, Ma, Lichun, additional, Revsine, Mahler, additional, Kuhlman, Laura, additional, Zhang, Karen, additional, Baiev, Islam, additional, Lamm, Ryan, additional, Patel, Keyur, additional, Kleiner, David E., additional, Hewitt, Stephen M., additional, Tran, Bao, additional, Shetty, Jyoti, additional, Wu, Xiaolin, additional, Zhao, Yongmei, additional, Shen, Tsai-Wei, additional, Choudhari, Sulbha, additional, Kriga, Yuliya, additional, Ylaya, Kris, additional, Warner, Andrew C., additional, Edmondson, Elijah F., additional, Forgues, Marshonna, additional, Greten, Tim F., additional, and Wang, Xin Wei, additional

Published
2023
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9. Data from Extrachromosomal DNA Amplification Contributes to Small Cell Lung Cancer Heterogeneity and Is Associated with Worse Outcomes

Author

Anish Thomas, Thomas Ried, Yves Pommier, Gordon L. Hager, Nir Friedman, Mirit I. Aladjem, David E. Kleiner, Stephen M. Hewitt, Bao Tran, Nitin Roper, Yoo Sun Kim, Suresh Kumar, Deep Upadhyay, Rajesh Kumar, Vinodh N. Rajapakse, Shen Tsai-wei, Sevilay Turan, Juan Manuel Caravaca, Chante Graham, Linda Sciuto, Rasa Vilimas, Samantha Nichols, Yongmei Zhao, Rona Gergely, Jenia Gutin, Noa Vilk, Nadav Hermoni, Sandra Burkett, Yang Zhang, Parth Desai, Gavriel Fialkoff, Nobuyuki Takahashi, Christophe E. Redon, Darawalee Wangsa, Lorenzo Rinaldi, Christopher W. Schultz, and Lőrinc Sándor Pongor

Abstract

Small-cell lung cancer (SCLC) is an aggressive neuroendocrine lung cancer. Oncogenic MYC amplifications drive SCLC heterogeneity, but the genetic mechanisms of MYC amplification and phenotypic plasticity, characterized by neuroendocrine and nonneuroendocrine cell states, are not known. Here, we integrate whole-genome sequencing, long-range optical mapping, single-cell DNA sequencing, and fluorescence in situ hybridization to find extrachromosomal DNA (ecDNA) as a primary source of SCLC oncogene amplifications and driver fusions. ecDNAs bring to proximity enhancer elements and oncogenes, creating SCLC transcription-amplifying units, driving exceptionally high MYC gene dosage. We demonstrate that cell-free nucleosome profiling can noninvasively detect ecDNA amplifications in plasma, facilitating its genome-wide interrogation in SCLC and other cancers. Altogether, our work provides the first comprehensive map of SCLC ecDNA and describes a new mechanism that governs MYC-driven SCLC heterogeneity. ecDNA-enabled transcriptional flexibility may explain the significantly worse survival outcomes of SCLC harboring complex ecDNA amplifications.Significance:MYC drives SCLC progression, but the genetic basis of MYC-driven SCLC evolution is unknown. Using SCLC as a paradigm, we report how ecDNA amplifications function as MYC-amplifying units, fostering tumor plasticity and a high degree of tumor heterogeneity.This article is highlighted in the In This Issue feature, p. 799

Published
2023
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10. Table S4 from Extrachromosomal DNA Amplification Contributes to Small Cell Lung Cancer Heterogeneity and Is Associated with Worse Outcomes

Author

Anish Thomas, Thomas Ried, Yves Pommier, Gordon L. Hager, Nir Friedman, Mirit I. Aladjem, David E. Kleiner, Stephen M. Hewitt, Bao Tran, Nitin Roper, Yoo Sun Kim, Suresh Kumar, Deep Upadhyay, Rajesh Kumar, Vinodh N. Rajapakse, Shen Tsai-wei, Sevilay Turan, Juan Manuel Caravaca, Chante Graham, Linda Sciuto, Rasa Vilimas, Samantha Nichols, Yongmei Zhao, Rona Gergely, Jenia Gutin, Noa Vilk, Nadav Hermoni, Sandra Burkett, Yang Zhang, Parth Desai, Gavriel Fialkoff, Nobuyuki Takahashi, Christophe E. Redon, Darawalee Wangsa, Lorenzo Rinaldi, Christopher W. Schultz, and Lőrinc Sándor Pongor

Abstract

Fusion analysis results calculated with STARfusion and summary of RLF exon1 and exon2 expression for the CCLE cohort. Table summarizes the RLF-MYCL expression qPCR results.

Published
2023
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11. Figure S1 from Extrachromosomal DNA Amplification Contributes to Small Cell Lung Cancer Heterogeneity and Is Associated with Worse Outcomes

Author

Anish Thomas, Thomas Ried, Yves Pommier, Gordon L. Hager, Nir Friedman, Mirit I. Aladjem, David E. Kleiner, Stephen M. Hewitt, Bao Tran, Nitin Roper, Yoo Sun Kim, Suresh Kumar, Deep Upadhyay, Rajesh Kumar, Vinodh N. Rajapakse, Shen Tsai-wei, Sevilay Turan, Juan Manuel Caravaca, Chante Graham, Linda Sciuto, Rasa Vilimas, Samantha Nichols, Yongmei Zhao, Rona Gergely, Jenia Gutin, Noa Vilk, Nadav Hermoni, Sandra Burkett, Yang Zhang, Parth Desai, Gavriel Fialkoff, Nobuyuki Takahashi, Christophe E. Redon, Darawalee Wangsa, Lorenzo Rinaldi, Christopher W. Schultz, and Lőrinc Sándor Pongor

Abstract

ecDNA in SCLC, related to Figure 1

Published
2023
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12. Figure 2 extended data from Extrachromosomal DNA Amplification Contributes to Small Cell Lung Cancer Heterogeneity and Is Associated with Worse Outcomes

Author

Anish Thomas, Thomas Ried, Yves Pommier, Gordon L. Hager, Nir Friedman, Mirit I. Aladjem, David E. Kleiner, Stephen M. Hewitt, Bao Tran, Nitin Roper, Yoo Sun Kim, Suresh Kumar, Deep Upadhyay, Rajesh Kumar, Vinodh N. Rajapakse, Shen Tsai-wei, Sevilay Turan, Juan Manuel Caravaca, Chante Graham, Linda Sciuto, Rasa Vilimas, Samantha Nichols, Yongmei Zhao, Rona Gergely, Jenia Gutin, Noa Vilk, Nadav Hermoni, Sandra Burkett, Yang Zhang, Parth Desai, Gavriel Fialkoff, Nobuyuki Takahashi, Christophe E. Redon, Darawalee Wangsa, Lorenzo Rinaldi, Christopher W. Schultz, and Lőrinc Sándor Pongor

Abstract

Cell line AmpliconArchitect assemblies, related to figure 1 and Figure 2

Published
2023
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13. Extrachromosomal DNA Amplification Contributes to Small Cell Lung Cancer Heterogeneity and is Associated with Worse Outcomes

Author

Pongor, Lorinc Sandor., primary, Schultz, Christopher W., additional, Rinaldi, Lorenzo, additional, Wangsa, Darawalee, additional, Redon, Christophe E., additional, Takahashi, Nobuyuki, additional, Fialkoff, Gavriel, additional, Desai, Parth, additional, Zhang, Yang, additional, Burkett, Sandra, additional, Hermoni, Nadav, additional, Vilk, Noa, additional, Gutin, Jenia, additional, Rona, Gergely, additional, Zhao, Yongmei, additional, Nichols, Samantha, additional, Vilimas, Rasa, additional, Sciuto, Linda, additional, Graham, Chante, additional, Caravaca, Juan Manuel, additional, Turan, Sevilay, additional, Shen, Tsai-Wei, additional, Rajapakse, Vinodh N., additional, Kumar, Rajesh, additional, Upadhyay, Deep, additional, Kumar, Suresh, additional, Kim, Yoo Sun, additional, Roper, Nitin, additional, Tran, Bao, additional, Hewitt, Stephen M., additional, Kleiner, David E., additional, Aladjem, Mirit I., additional, Friedman, Nir, additional, Hager, Gordon L., additional, Pommier, Yves, additional, Ried, Thomas, additional, and Thomas, Anish, additional

Published
2023
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14. An Evolutionary Approach with Pharmacophore-Based Scoring Functions for Virtual Database Screening

Author

Yang, Jinn-Moon, Shen, Tsai-Wei, Chen, Yen-Fu, Chiu, Yi-Yuan, Kanade, Takeo, editor, Kittler, Josef, editor, Kleinberg, Jon M., editor, Mattern, Friedemann, editor, Mitchell, John C., editor, Naor, Moni, editor, Nierstrasz, Oscar, editor, Pandu Rangan, C., editor, Steffen, Bernhard, editor, Sudan, Madhu, editor, Terzopoulos, Demetri, editor, Tygar, Dough, editor, Vardi, Moshe Y., editor, Weikum, Gerhard, editor, and Deb, Kalyanmoy, editor

Published
2004
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15. Abstract 3044: C. albicans infection mediates upper gastrointestinal tract malignancy independently of Il17a in an APECED-like mouse model

Author

Zhu, Feng, primary, Phan, Quynh T., additional, Ferre, Elise M., additional, Willette-Brown, Jami, additional, Salcedo, Rosalba, additional, Shen, Tsai-Wei, additional, Fan, Yu, additional, Zhao, Yongmei, additional, Mehta, Monika, additional, Meerzaman, Daoud, additional, Tran, Bao, additional, Trinchieri, Giorgio, additional, Lionakis, Michail S., additional, Filler, Scott G., additional, and Hu, Yinling, additional

Published
2022
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16. The tumour microenvironment shapes innate lymphoid cells in patients with hepatocellular carcinoma

Author

Heinrich, Bernd, primary, Gertz, E Michael, additional, Schäffer, Alejandro A, additional, Craig, Amanda, additional, Ruf, Benjamin, additional, Subramanyam, Varun, additional, McVey, John C, additional, Diggs, Laurence P, additional, Heinrich, Sophia, additional, Rosato, Umberto, additional, Ma, Chi, additional, Yan, Chunhua, additional, Hu, Ying, additional, Zhao, Yongmei, additional, Shen, Tsai-Wei, additional, Kapoor, Veena, additional, Telford, William, additional, Kleiner, David E, additional, Stovroff, Merril K, additional, Dhani, Harmeet S, additional, Kang, Jiman, additional, Fishbein, Thomas, additional, Wang, Xin Wei, additional, Ruppin, E, additional, Kroemer, Alexander, additional, Greten, Tim F, additional, and Korangy, Firouzeh, additional

Published
2021
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17. Establishing community reference samples, data and call sets for benchmarking cancer mutation detection using whole-genome sequencing

Author

Fang, Li Tai, Zhu, Bin, Zhao, Yongmei, Chen, Wanqiu, Yang, Zhaowei, Kerrigan, Liz, Langenbach, Kurt, de Mars, Maryellen, Lu, Charles, Idler, Kenneth, Jacob, Howard, Zheng, Yuanting, Ren, Luyao, Yu, Ying, Jaeger, Erich, Schroth, Gary P., Abaan, Ogan D., Talsania, Keyur, Lack, Justin, Shen, Tsai-Wei, Chen, Zhong, Stanbouly, Seta, Tran, Bao, Shetty, Jyoti, Kriga, Yuliya, Meerzaman, Daoud, Nguyen, Cu, Petitjean, Virginie, Sultan, Marc, Cam, Margaret, Mehta, Monika, Hung, Tiffany, Peters, Eric, Kalamegham, Rasika, Sahraeian, Sayed Mohammad Ebrahim, Mohiyuddin, Marghoob, Guo, Yunfei, Yao, Lijing, Song, Lei, Lam, Hugo Y. K., Drabek, Jiri, Vojta, Petr, Maestro, Roberta, Gasparotto, Daniela, Koks, Sulev, Reimann, Ene, Scherer, Andreas, Nordlund, Jessica, Liljedahl, Ulrika, Jensen, Roderick, V, Pirooznia, Mehdi, Li, Zhipan, Xiao, Chunlin, Sherry, Stephen T., Kusko, Rebecca, Moos, Malcolm, Donaldson, Eric, Tezak, Zivana, Ning, Baitang, Tong, Weida, Li, Jing, Duerken-Hughes, Penelope, Catalanotti, Claudia, Maheshwari, Shamoni, Shuga, Joe, Liang, Winnie S., Keats, Jonathan, Adkins, Jonathan, Tassone, Erica, Zismann, Victoria, McDaniel, Timothy, Trent, Jeffrey, Foox, Jonathan, Butler, Daniel, Mason, Christopher E., Hong, Huixiao, Shi, Leming, Wang, Charles, Xiao, Wenming, Fang, Li Tai, Zhu, Bin, Zhao, Yongmei, Chen, Wanqiu, Yang, Zhaowei, Kerrigan, Liz, Langenbach, Kurt, de Mars, Maryellen, Lu, Charles, Idler, Kenneth, Jacob, Howard, Zheng, Yuanting, Ren, Luyao, Yu, Ying, Jaeger, Erich, Schroth, Gary P., Abaan, Ogan D., Talsania, Keyur, Lack, Justin, Shen, Tsai-Wei, Chen, Zhong, Stanbouly, Seta, Tran, Bao, Shetty, Jyoti, Kriga, Yuliya, Meerzaman, Daoud, Nguyen, Cu, Petitjean, Virginie, Sultan, Marc, Cam, Margaret, Mehta, Monika, Hung, Tiffany, Peters, Eric, Kalamegham, Rasika, Sahraeian, Sayed Mohammad Ebrahim, Mohiyuddin, Marghoob, Guo, Yunfei, Yao, Lijing, Song, Lei, Lam, Hugo Y. K., Drabek, Jiri, Vojta, Petr, Maestro, Roberta, Gasparotto, Daniela, Koks, Sulev, Reimann, Ene, Scherer, Andreas, Nordlund, Jessica, Liljedahl, Ulrika, Jensen, Roderick, V, Pirooznia, Mehdi, Li, Zhipan, Xiao, Chunlin, Sherry, Stephen T., Kusko, Rebecca, Moos, Malcolm, Donaldson, Eric, Tezak, Zivana, Ning, Baitang, Tong, Weida, Li, Jing, Duerken-Hughes, Penelope, Catalanotti, Claudia, Maheshwari, Shamoni, Shuga, Joe, Liang, Winnie S., Keats, Jonathan, Adkins, Jonathan, Tassone, Erica, Zismann, Victoria, McDaniel, Timothy, Trent, Jeffrey, Foox, Jonathan, Butler, Daniel, Mason, Christopher E., Hong, Huixiao, Shi, Leming, Wang, Charles, and Xiao, Wenming

Abstract

Tumor-normal paired DNA samples from a breast cancer cell line and a matched lymphoblastoid cell line enable calibration of clinical sequencing pipelines and benchmarking 'tumor-only' or 'matched tumor-normal' analyses. The lack of samples for generating standardized DNA datasets for setting up a sequencing pipeline or benchmarking the performance of different algorithms limits the implementation and uptake of cancer genomics. Here, we describe reference call sets obtained from paired tumor-normal genomic DNA (gDNA) samples derived from a breast cancer cell line-which is highly heterogeneous, with an aneuploid genome, and enriched in somatic alterations-and a matched lymphoblastoid cell line. We partially validated both somatic mutations and germline variants in these call sets via whole-exome sequencing (WES) with different sequencing platforms and targeted sequencing with >2,000-fold coverage, spanning 82% of genomic regions with high confidence. Although the gDNA reference samples are not representative of primary cancer cells from a clinical sample, when setting up a sequencing pipeline, they not only minimize potential biases from technologies, assays and informatics but also provide a unique resource for benchmarking 'tumor-only' or 'matched tumor-normal' analyses.

Published
2021
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18. Whole Genome and Exome Sequencing Reference Datasets from A Multi-center and Cross-platform Benchmark Study

Author

Zhao, Yongmei, primary, Fang, Li Tai, additional, Shen, Tsai-wei, additional, Choudhari, Sulbha, additional, Talsania, Keyur, additional, Chen, Xiongfong, additional, Shetty, Jyoti, additional, Kriga, Yuliya, additional, Tran, Bao, additional, Zhu, Bin, additional, Chen, Zhong, additional, Chen, Wangqiu, additional, Wang, Charles, additional, Jaeger, Erich, additional, Meerzaman, Daoud, additional, Lu, Charles, additional, Idler, Kenneth, additional, Zheng, Yuanting, additional, Shi, Leming, additional, Petitjean, Virginie, additional, Sultan, Marc, additional, Hung, Tiffany, additional, Peters, Eric, additional, Drabek, Jiri, additional, Vojta, Petr, additional, Maestro, Roberta, additional, Gasparotto, Daniela, additional, Kõks, Sulev, additional, Reimann, Ene, additional, Scherer, Andreas, additional, Nordlund, Jessica, additional, Liljedahl, Ulrika, additional, Foox, Jonathan, additional, Mason, Christopher, additional, Xiao, Chunlin, additional, and Xiao, Wenming, additional

Published
2021
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19. Abstract 224: Evaluation of next generation sequencing of DNA and RNA from archival formalin-fixed, paraffin-embedded pancreatic cancer tissue: A pilot study of the SEER-linked virtual tissue repository

Author

Yuan, Yao, primary, Van Dyke, Alison, additional, Petkov, Valentina, additional, Tuan, Alyssa, additional, Singhi, Aatur, additional, Matrisian, Lynn, additional, Rahib, Lola, additional, Pearson, John, additional, Nones, Katia, additional, Waddell, Nicola, additional, Zhao, Yongmei, additional, Shen, Tsai-wei, additional, Tran, Bao, additional, Shetty, Jyoti, additional, Gillanders, Elizabeth, additional, Carrick, Danielle, additional, Cress, Rosemary, additional, Mueller, Lloyd, additional, Hernandez, Brenda, additional, Lynch, Charles, additional, Tucker, Thomas, additional, Wu, Xiao-Cheng, additional, and Penberthy, Lynne, additional

Published
2020
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22. The tumour microenvironment shapes innate lymphoid cells in patients with hepatocellular carcinoma.

Author

Heinrich, Bernd, Gertz, E. Michael, Schäffer, Alejandro A., Craig, Amanda, Ruf, Benjamin, Subramanyam, Varun, McVey, John C., Diggs, Laurence P., Heinrich, Sophia, Rosato, Umberto, Chi Ma, Chunhua Yan, Ying Hu, Yongmei Zhao, Tsai-Wei Shen, Tsai-Wei, Kapoor, Veena, Telford, William, Kleiner, David E., Stovroff, Merril K., and Dhani, Harmeet S.

Subjects
INNATE lymphoid cells, TUMOR microenvironment, HEPATOCELLULAR carcinoma, TUMOR-infiltrating immune cells
Published
2022
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24. Smooth Muscle Cell Genome Browser: Enabling the Identification of Novel Serum Response Factor Target Genes

Author

Lee, Moon Young, primary, Park, Chanjae, additional, Berent, Robyn M., additional, Park, Paul J., additional, Fuchs, Robert, additional, Syn, Hannah, additional, Chin, Albert, additional, Townsend, Jared, additional, Benson, Craig C., additional, Redelman, Doug, additional, Shen, Tsai-wei, additional, Park, Jong Kun, additional, Miano, Joseph M., additional, Sanders, Kenton M., additional, and Ro, Seungil, additional

Published
2015
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28. BiophysicalCharacteristics of Cholera Toxin and Escherichia coliHeat-Labile Enterotoxin Structure and Chemistry Lead to DifferentialToxicity.

Author

Craft, John W., Shen, Tsai-wei, Brier, Lindsey M., and Briggs, James M.

Subjects
*CHOLERA toxin, *PHYSICAL biochemistry, *TOXICITY testing, *ESCHERICHIA coli, *ENTEROTOXINS, *MOLECULAR structure
Abstract

Thebiophysical chemistry of macromolecular complexes confer their functionalcharacteristics. We investigate the mechanisms that make the AB5 holotoxinof Vibrio cholerae(CT) a significantlymore pathogenic molecule than the enterotoxin of Escherichiacoli(LT) with which it shares 88% similarity andwhose structure is homologous with a backbone RMSD of 0.84 Åand imposes its deleterious effects though the same process to constitutivelyADP-ribosylate adenylate cyclase. We present computational data thatcharacterizes the impact of amino acid variations in the A2 tail,which helps to explain experimental data that demonstrate CT’shigher toxicity. A hydrophobic patch on the B pentamer interface andits interactions with the A subdomain are partially disrupted by thesubstitution of an aspartic acid (LT) for glycine in CT. CT’sholotoxin has less solvent accessible surface area (94 Å2vs 54 Å2) and higher contact area (280 Å2vs 241 Å2) with S228, which is a gatekeeper,partially controlling the diffusion of water into the pore. CT excludeswater from the top of the central pore whereas LT allows much morewater to interact. These biophysical properties of the toxins leadto their differential toxicity and resulting impact to human health. [ABSTRACT FROM AUTHOR]

Published
2015
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