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1. An enhanced label‐free proteomics approach for deep‐diving into equine plasma proteome, including the discovery of protein biomarkers for strenuous exercise.

Author

Cheung, Hiu Wing, Wong, Kin‐Sing, To, Ning Sum, Wan, Terence S. M., and Ho, Emmie N. M.

Abstract

Plasma proteins have been a valuable source of biomarkers for clinical uses and for monitoring of the illicit use of prohibited substances or practices in equine sports. We have previously reported the first use of label‐free proteomics in profiling equine plasma proteome. This study aimed to refine the method by systematically evaluating various plasma fractionation methods and the use of narrower precursor mass ranges in data‐independent acquisition (DIA) mass spectrometry (MS). Tandem fractionations of equine plasma with octanoic acid precipitation followed by solid‐phase extraction (SPE) with C4 cartridges provided the largest increase in the number of new proteins identified. The use of two narrow precursor mass ranges of m/z 400–600 and 600–800 in DIA not only identified most proteins detectable by using a single mass range of m/z 350–1500 but also identified ~27% more proteins. The improved method was applied to analyse the plasma proteome of 'postrace' samples which, unlike other samples, had been collected from racehorses soon after racing. Multivariate data analysis has identified upregulation of 14 proteins and downregulation of six proteins in postrace plasma compared with the non‐postrace plasma samples. Literature review of these proteins has provided evidence of exercise‐induced haemolysis and changes in antioxidant enzyme activities, kinin system, insulin signalling and energy metabolism after strenuous exercise. The improved method has enabled a deeper profiling of the equine plasma proteome and identified the proteins associated with normal physiological changes after racing which are potential confounding factors in the development of a biomarker approach for doping control. [ABSTRACT FROM AUTHOR]

Published
2024
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5. Screening and confirmation of recombinant human follistatin in equine plasma for doping control purposes.

Author

Wong, Kin‐Sing, Cheung, Hiu Wing, Choi, Yung‐Ching, To, Ning‐Sum, Wan, Terence S. M., and Ho, Emmie N. M.

Abstract

Recombinant human follistatin (rhFST) is a potential performance‐enhancing agent owing to its stimulating effect on muscle growth. Administration of rhFST to athletes is prohibited in human sports by the World Anti‐Doping Agency (WADA) and in horseracing according to Article 6 of the International Agreement on Breeding, Racing and Wagering published by the International Federation of Horseracing Authorities (IFHA). For effective control of the potential misuse of rhFST in flat racing, methods for screening and confirmatory analysis are required. This paper describes the development and validation of a complete solution for detecting rhFST and confirming its presence in plasma samples collected from racehorses. A high‐throughput analysis of rhFST with a commercially available enzyme‐linked immunosorbent assay (ELISA) was evaluated for the screening of equine plasma samples. Any suspicious finding would then be subjected to a confirmatory analysis using immunocapture, followed by nano‐liquid chromatography/high‐resolution tandem mass spectrometry (nanoLC‐MS/HRMS). The confirmation of rhFST by nanoLC‐MS/HRMS was achieved by comparing the retention times and relative abundances of three characteristic product‐ions with those from the reference standard in accordance with the industry criteria published by the Association of Official Racing Chemists. The two methods achieved comparable limit of detection (~2.5–5 ng/mL) and limit of confirmation (2.5 ng/mL or below), as well as adequate specificity, precision and reproducibility. To our knowledge, this is the first report of the screening and confirmation methods for rhFST in equine samples. [ABSTRACT FROM AUTHOR]

Published
2024
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7. Data from Systematic Interrogation of 3q26 Identifies TLOC1 and SKIL as Cancer Drivers

Author

Hagerstrand, Daniel, primary, Tong, Alexander, primary, Schumacher, Steven E., primary, Ilic, Nina, primary, Shen, Rhine R., primary, Cheung, Hiu Wing, primary, Vazquez, Francisca, primary, Shrestha, Yashaswi, primary, Kim, So Young, primary, Giacomelli, Andrew O., primary, Rosenbluh, Joseph, primary, Schinzel, Anna C., primary, Spardy, Nicole A., primary, Barbie, David A., primary, Mermel, Craig H., primary, Weir, Barbara A., primary, Garraway, Levi A., primary, Tamayo, Pablo, primary, Mesirov, Jill P., primary, Beroukhim, Rameen, primary, and Hahn, William C., primary

Published
2023
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8. Supplementary Table S3 from Systematic Interrogation of 3q26 Identifies TLOC1 and SKIL as Cancer Drivers

Author

Hagerstrand, Daniel, primary, Tong, Alexander, primary, Schumacher, Steven E., primary, Ilic, Nina, primary, Shen, Rhine R., primary, Cheung, Hiu Wing, primary, Vazquez, Francisca, primary, Shrestha, Yashaswi, primary, Kim, So Young, primary, Giacomelli, Andrew O., primary, Rosenbluh, Joseph, primary, Schinzel, Anna C., primary, Spardy, Nicole A., primary, Barbie, David A., primary, Mermel, Craig H., primary, Weir, Barbara A., primary, Garraway, Levi A., primary, Tamayo, Pablo, primary, Mesirov, Jill P., primary, Beroukhim, Rameen, primary, and Hahn, William C., primary

Published
2023
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9. Supplementary Figures 1-9 from Amplification of CRKL Induces Transformation and Epidermal Growth Factor Receptor Inhibitor Resistance in Human Non–Small Cell Lung Cancers

Author

Cheung, Hiu Wing, primary, Du, Jinyan, primary, Boehm, Jesse S., primary, He, Frank, primary, Weir, Barbara A., primary, Wang, Xiaoxing, primary, Butaney, Mohit, primary, Sequist, Lecia V., primary, Luo, Biao, primary, Engelman, Jeffrey A., primary, Root, David E., primary, Meyerson, Matthew, primary, Golub, Todd R., primary, Jänne, Pasi A., primary, and Hahn, William C., primary

Published
2023
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10. Supplementary Figure 1 from Systematic Interrogation of 3q26 Identifies TLOC1 and SKIL as Cancer Drivers

Author

Hagerstrand, Daniel, primary, Tong, Alexander, primary, Schumacher, Steven E., primary, Ilic, Nina, primary, Shen, Rhine R., primary, Cheung, Hiu Wing, primary, Vazquez, Francisca, primary, Shrestha, Yashaswi, primary, Kim, So Young, primary, Giacomelli, Andrew O., primary, Rosenbluh, Joseph, primary, Schinzel, Anna C., primary, Spardy, Nicole A., primary, Barbie, David A., primary, Mermel, Craig H., primary, Weir, Barbara A., primary, Garraway, Levi A., primary, Tamayo, Pablo, primary, Mesirov, Jill P., primary, Beroukhim, Rameen, primary, and Hahn, William C., primary

Published
2023
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12. Data from Amplification of CRKL Induces Transformation and Epidermal Growth Factor Receptor Inhibitor Resistance in Human Non–Small Cell Lung Cancers

Author

Cheung, Hiu Wing, primary, Du, Jinyan, primary, Boehm, Jesse S., primary, He, Frank, primary, Weir, Barbara A., primary, Wang, Xiaoxing, primary, Butaney, Mohit, primary, Sequist, Lecia V., primary, Luo, Biao, primary, Engelman, Jeffrey A., primary, Root, David E., primary, Meyerson, Matthew, primary, Golub, Todd R., primary, Jänne, Pasi A., primary, and Hahn, William C., primary

Published
2023
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13. Supplementary Figure 3 from Systematic Interrogation of 3q26 Identifies TLOC1 and SKIL as Cancer Drivers

Author

Hagerstrand, Daniel, primary, Tong, Alexander, primary, Schumacher, Steven E., primary, Ilic, Nina, primary, Shen, Rhine R., primary, Cheung, Hiu Wing, primary, Vazquez, Francisca, primary, Shrestha, Yashaswi, primary, Kim, So Young, primary, Giacomelli, Andrew O., primary, Rosenbluh, Joseph, primary, Schinzel, Anna C., primary, Spardy, Nicole A., primary, Barbie, David A., primary, Mermel, Craig H., primary, Weir, Barbara A., primary, Garraway, Levi A., primary, Tamayo, Pablo, primary, Mesirov, Jill P., primary, Beroukhim, Rameen, primary, and Hahn, William C., primary

Published
2023
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14. Supplementary Legends from Systematic Interrogation of 3q26 Identifies TLOC1 and SKIL as Cancer Drivers

Author

Hagerstrand, Daniel, primary, Tong, Alexander, primary, Schumacher, Steven E., primary, Ilic, Nina, primary, Shen, Rhine R., primary, Cheung, Hiu Wing, primary, Vazquez, Francisca, primary, Shrestha, Yashaswi, primary, Kim, So Young, primary, Giacomelli, Andrew O., primary, Rosenbluh, Joseph, primary, Schinzel, Anna C., primary, Spardy, Nicole A., primary, Barbie, David A., primary, Mermel, Craig H., primary, Weir, Barbara A., primary, Garraway, Levi A., primary, Tamayo, Pablo, primary, Mesirov, Jill P., primary, Beroukhim, Rameen, primary, and Hahn, William C., primary

Published
2023
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15. Supplementary Figure 2 from Systematic Interrogation of 3q26 Identifies TLOC1 and SKIL as Cancer Drivers

Author

Hagerstrand, Daniel, primary, Tong, Alexander, primary, Schumacher, Steven E., primary, Ilic, Nina, primary, Shen, Rhine R., primary, Cheung, Hiu Wing, primary, Vazquez, Francisca, primary, Shrestha, Yashaswi, primary, Kim, So Young, primary, Giacomelli, Andrew O., primary, Rosenbluh, Joseph, primary, Schinzel, Anna C., primary, Spardy, Nicole A., primary, Barbie, David A., primary, Mermel, Craig H., primary, Weir, Barbara A., primary, Garraway, Levi A., primary, Tamayo, Pablo, primary, Mesirov, Jill P., primary, Beroukhim, Rameen, primary, and Hahn, William C., primary

Published
2023
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25. Systematic investigation of genetic vulnerabilities across cancer cell lines reveals lineage-specific dependencies in ovarian cancer

Author

Cheung, Hiu Wing, Cowley, Glenn S., Weir, Barbara A., Boehm, Jesse S., Rusin, Scott, Scott, Justine A., East, Alexandra, Ali, Levi D., Lizotte, Patrick H., Wong, Terence C., Jiang, Guozhi, Hsiao, Jessica, Mermel, Craig H., Getz, Gad, Barretina, Jordi, Gopal, Shuba, Tamayo, Pablo, Gould, Joshua, Tsherniak, Aviad, Stransky, Nicolas, Luo, Biao, Ren, Yin, Drapkin, Ronny, Bhatia, Sangeeta N., Mesirov, Jill P., Garraway, Levi A., Meyerson, Matthew, Lander, Eric S., Root, David E., and Hahn, William C.

Published
2011

26. Highly Parallel Identification of Essential Genes in Cancer Cells

Author

Luo, Biao, Cheung, Hiu Wing, Subramanian, Aravind, Sharifnia, Tanaz, Okamoto, Michael, Yang, Xiaoping, Hinkle, Greg, Boehm, Jesse S., Beroukhim, Rameen, Weir, Barbara A., Mermel, Craig, Barbie, David A., Awad, Tarif, Zhou, Xiaochuan, Nguyen, Tuyen, Piqani, Bruno, Li, Cheng, Golub, Todd R., Meyerson, Matthew, Hacohen, Nir, Hahn, William C., Lander, Eric S., Sabatini, David M., and Root, David E.

Published
2008
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36. A duplex qPCR assay for human erythropoietin (EPO) transgene to control gene doping in horses.

Author

Cheung, Hiu Wing, Wong, Kin‐Sing, Lin, Venus Y.C., Wan, Terence S.M., and Ho, Emmie N.M.

Abstract

The misuse of genetic manipulation technology to enhance athletic performance is termed gene doping which is prohibited in human sports, horseracing, and equestrian sports. Although many qPCR assays have been developed, most assays employ genomic DNA (gDNA) from humans, non‐human primates, and mice as a background and they may not be applicable for testing horse samples. This study aimed to develop a qPCR assay for the detection of human erythropoietin (hEPO) transgene in horse blood cells where the viral vectors used in gene therapy can reside for months. For the detection of hEPO transgene, the performance of three sets of primers and a hydrolysis probe for hEPO were compared. One set showed adequate specificity, sensitivity, amplification efficiency, and a dynamic range of detection in the presence of horse gDNA. The assay was duplexed with the detection of horse tubulin α 4A (TUBA4A) gene as an endogenous internal control in order to prevent false‐negative results due to poor recovery and storage of extracted DNA and/or qPCR experimental variation. For the extraction of hEPO‐plasmid, the QIAGEN Gentra Puregene blood kit was shown to recover the majority (62%) of hEPO‐plasmid from spiked horse blood cells. The specificity and limit of detection (LOD) of the duplex qPCR assay were determined in accordance with MIQE guidelines. These findings supported the application of this duplex qPCR assay to the detection of hEPO transgene in horse blood cells. [ABSTRACT FROM AUTHOR]

Published
2021
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41. Amplification of CRKL induces transformation and EGFR inhibitor resistance in human non small cell lung cancers

Author

Cheung, Hiu Wing, Du, Jinyan, Boehm, Jesse S., He, Frank, Weir, Barbara A., Wang, Xiaoxing, Butaney, Mohit, Sequist, Lecia V., Luo, Biao, Engelman, Jeffrey A., Root, David E., Meyerson, Matthew, Golub, Todd R., Jänne, Pasi A., and Hahn, William C.

Subjects
ErbB Receptors, Lung Neoplasms, Humans, Nuclear Proteins, Adenocarcinoma of Lung, Adenocarcinoma, Article, respiratory tract diseases, Adaptor Proteins, Signal Transducing
Abstract

We previously identified a region of recurrent amplification on chromosome 22q11.21 in a subset of primary lung adenocarcinomas. Here we show that CRKL, encoding for an adaptor protein, is amplified and overexpressed in non-small cell lung cancer (NSCLC) cells that harbor 22q11.21 amplifications. Overexpression of CRKL in immortalized human airway epithelial cells promoted anchorage independent growth and tumorigenicity. Oncogenic CRKL activates SOS1-RAS-RAF-ERK and SRC-C3G-RAP1 pathways. Suppression of CRKL in NSCLC cells that harbor CRKL amplifications induced cell death. Overexpression of CRKL in EGFR mutant cells induces resistance to gefitinib by activating ERK and AKT signaling. We identified CRKL amplification in an EGFR inhibitor treated lung adenocarcinoma that was not present prior to treatment. These observations show that CRKL overexpression induces cell transformation, credential CRKL as a therapeutic target for a subset of NSCLC that harbor CRKL amplifications and implicate CRKL as an additional mechanism of resistance to EGFR-directed therapy.

Published
2011

44. Targeted Tumor-Penetrating siRNA Nanocomplexes for Credentialing the Ovarian Cancer Target ID4

Author

Whitaker College of Health Sciences and Technology, Massachusetts Institute of Technology. Department of Electrical Engineering and Computer Science, Koch Institute for Integrative Cancer Research at MIT, Ren, Yin, von Maltzhan, Geoffrey, Agrawal, Amit, Mesirov, Jill P., Lo, Justin H., Bhatia, Sangeeta N., Cheung, Hiu Wing, Cowley, Glenn S., Weir, Barbara A., Boehm, Jesse S., Tamayo, Pablo, Karst, Alison M., Liu, Joyce F., Hirsch, Michelle S., Drapkin, Ronny, Root, David E., Fogal, Valentina, Ruoslahti, Erkki, Hahn, William C., Bhatia, Sangeeta N, Whitaker College of Health Sciences and Technology, Massachusetts Institute of Technology. Department of Electrical Engineering and Computer Science, Koch Institute for Integrative Cancer Research at MIT, Ren, Yin, von Maltzhan, Geoffrey, Agrawal, Amit, Mesirov, Jill P., Lo, Justin H., Bhatia, Sangeeta N., Cheung, Hiu Wing, Cowley, Glenn S., Weir, Barbara A., Boehm, Jesse S., Tamayo, Pablo, Karst, Alison M., Liu, Joyce F., Hirsch, Michelle S., Drapkin, Ronny, Root, David E., Fogal, Valentina, Ruoslahti, Erkki, Hahn, William C., and Bhatia, Sangeeta N

Abstract

The comprehensive characterization of a large number of cancer genomes will eventually lead to a compendium of genetic alterations in specific cancers. Unfortunately, the number and complexity of identified alterations complicate endeavors to identify biologically relevant mutations critical for tumor maintenance because many of these targets are not amenable to manipulation by small molecules or antibodies. RNA interference provides a direct way to study putative cancer targets; however, specific delivery of therapeutics to the tumor parenchyma remains an intractable problem. We describe a platform for the discovery and initial validation of cancer targets, composed of a systematic effort to identify amplified and essential genes in human cancer cell lines and tumors partnered with a novel modular delivery technology. We developed a tumor-penetrating nanocomplex (TPN) that comprised small interfering RNA (siRNA) complexed with a tandem tumor-penetrating and membrane-translocating peptide, which enabled the specific delivery of siRNA deep into the tumor parenchyma. We used TPN in vivo to evaluate inhibitor of DNA binding 4 (ID4) as a novel oncogene. Treatment of ovarian tumor–bearing mice with ID4-specific TPN suppressed growth of established tumors and significantly improved survival. These observations not only credential ID4 as an oncogene in 32% of high-grade ovarian cancers but also provide a framework for the identification, validation, and understanding of potential therapeutic cancer targets., Howard Hughes Medical Institute, National Cancer Institute (U.S.) (Grant U54 CA119349), National Cancer Institute (U.S.) (Grant CA119335), National Cancer Institute (U.S.) (Grant R01 CA124427), Starr Cancer Consortium, Marie D. and Pierre Casimir-Lambert Fund, National Cancer Institute (U.S.) (Cancer Center Support Core Grant P30 CA14051)

Published
2014

45. Systematic investigation of genetic vulnerabilities across cancer cell lines reveals lineage-specific dependencies in ovarian cancer

Author

Harvard University--MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology. Department of Electrical Engineering and Computer Science, Koch Institute for Integrative Cancer Research at MIT, Lander, Eric Steven, Ren, Yin, Bhatia, Sangeeta N., Meyerson, Matthew L., Drapkin, Ronny, Cheung, Hiu Wing, Cowley, Glenn S., Weir, Barbara A., Boehm, Jesse S., Rusin, Scott, Scott, Justine A., East, Alexandra, Ali, Levi D., Lizotte, Patrick H., Wong, Terence C., Jiang, Guozhi, Hsiao, Jessica, Mermel, Craig H., Getz, Gad, Barretina, Jordi, Gopal, Shuba, Tamayo, Pablo, Gould, Joshua, Tsherniak, Aviad, Stransky, Nicolas, Luo, Biao, Mesirov, Jill P., Garraway, Levi A., Lander, Eric S., Root, David E., Hahn, William C., Bhatia, Sangeeta N, Harvard University--MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology. Department of Electrical Engineering and Computer Science, Koch Institute for Integrative Cancer Research at MIT, Lander, Eric Steven, Ren, Yin, Bhatia, Sangeeta N., Meyerson, Matthew L., Drapkin, Ronny, Cheung, Hiu Wing, Cowley, Glenn S., Weir, Barbara A., Boehm, Jesse S., Rusin, Scott, Scott, Justine A., East, Alexandra, Ali, Levi D., Lizotte, Patrick H., Wong, Terence C., Jiang, Guozhi, Hsiao, Jessica, Mermel, Craig H., Getz, Gad, Barretina, Jordi, Gopal, Shuba, Tamayo, Pablo, Gould, Joshua, Tsherniak, Aviad, Stransky, Nicolas, Luo, Biao, Mesirov, Jill P., Garraway, Levi A., Lander, Eric S., Root, David E., Hahn, William C., and Bhatia, Sangeeta N

Abstract

A comprehensive understanding of the molecular vulnerabilities of every type of cancer will provide a powerful roadmap to guide therapeutic approaches. Efforts such as The Cancer Genome Atlas Project will identify genes with aberrant copy number, sequence, or expression in various cancer types, providing a survey of the genes that may have a causal role in cancer. A complementary approach is to perform systematic loss-of-function studies to identify essential genes in particular cancer cell types. We have begun a systematic effort, termed Project Achilles, aimed at identifying genetic vulnerabilities across large numbers of cancer cell lines. Here, we report the assessment of the essentiality of 11,194 genes in 102 human cancer cell lines. We show that the integration of these functional data with information derived from surveying cancer genomes pinpoints known and previously undescribed lineage-specific dependencies across a wide spectrum of cancers. In particular, we found 54 genes that are specifically essential for the proliferation and viability of ovarian cancer cells and also amplified in primary tumors or differentially overexpressed in ovarian cancer cell lines. One such gene, PAX8, is focally amplified in 16% of high-grade serous ovarian cancers and expressed at higher levels in ovarian tumors. Suppression of PAX8 selectively induces apoptotic cell death of ovarian cancer cells. These results identify PAX8 as an ovarian lineage-specific dependency. More generally, these observations demonstrate that the integration of genome-scale functional and structural studies provides an efficient path to identify dependencies of specific cancer types on particular genes and pathways., National Institutes of Health (U.S.) (R33 CA128625), National Institutes of Health (U.S.) (U54 CA112962), National Institutes of Health (U.S.) (RC2 CA148268), Novartis Pharmaceuticals Corporation, Richard Hunt, H. L. Snyder Foundation

Published
2012

48. Systematic Interrogation of 3q26 Identifies TLOC1 and SKIL as Cancer Drivers

Author

Hagerstrand, Daniel, primary, Tong, Alexander, additional, Schumacher, Steven E., additional, Ilic, Nina, additional, Shen, Rhine R., additional, Cheung, Hiu Wing, additional, Vazquez, Francisca, additional, Shrestha, Yashaswi, additional, Kim, So Young, additional, Giacomelli, Andrew O., additional, Rosenbluh, Joseph, additional, Schinzel, Anna C., additional, Spardy, Nicole A., additional, Barbie, David A., additional, Mermel, Craig H., additional, Weir, Barbara A., additional, Garraway, Levi A., additional, Tamayo, Pablo, additional, Mesirov, Jill P., additional, Beroukhim, Rameen, additional, and Hahn, William C., additional

Published
2013
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