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220 results on '"Loncarek, Jadranka"'

6. Direct molecular dissection of tumor parenchyma from tumor stroma in tumor xenograft using mass spectrometry-based glycoproteomics

Author

Ye, Xiaoying, Luke, Brian T, Wei, Bih-Rong, Kaczmarczyk, Jan A, Loncarek, Jadranka, Dwyer, Jennifer E, Johann, Donald J, Saul, Richard G, Nissley, Dwight V, McCormick, Frank, Whiteley, Gordon R, and Blonder, Josip

Subjects
Lung, Rare Diseases, Lung Cancer, Biotechnology, Cancer, lung cancer, tumor microenvironment, Oncology and Carcinogenesis
Abstract

The most widely used cancer animal model is the human-murine tumor xenograft. Unbiased molecular dissection of tumor parenchyma versus stroma in human-murine xenografts is critical for elucidating dysregulated protein networks/pathways and developing therapeutics that may target these two functionally codependent compartments. Although antibody-reliant technologies (e.g., immunohistochemistry, imaging mass cytometry) are capable of distinguishing tumor-proper versus stromal proteins, the breadth or extent of targets is limited. Here, we report an antibody-free targeted cross-species glycoproteomic (TCSG) approach that enables direct dissection of human tumor parenchyma from murine tumor stroma at the molecular/protein level in tumor xenografts at a selectivity rate presently unattainable by other means. This approach was used to segment/dissect and obtain the protein complement phenotype of the tumor stroma and parenchyma of the metastatic human lung adenocarcinoma A549 xenograft, with no need for tissue microdissection prior to mass-spectrometry analysis. An extensive molecular map of the tumor proper and the associated microenvironment was generated along with the top functional N-glycosylated protein networks enriched in each compartment. Importantly, immunohistochemistry-based cross-validation of selected parenchymal and stromal targets applied on human tissue samples of lung adenocarcinoma and normal adjacent tissue is indicative of a noteworthy translational capacity for this unique approach that may facilitate identifications of novel targets for next generation antibody therapies and development of real time preclinical tumor models.

Published
2018

7. Endogenous EWSR1 Exists in Two Visual Modalities That Reflect Its Associations with Nucleic Acids and Concentration at Sites of Active Transcription

Author

Sundara Rajan, Soumya, primary, Ebegboni, Vernon J., additional, Pichling, Patricio, additional, Ludwig, Katelyn R., additional, Jones, Tamara L., additional, Chari, Raj, additional, Tran, Andy, additional, Kruhlak, Michael J., additional, Loncarek, Jadranka, additional, and Caplen, Natasha J., additional

Published
2024
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8. Comparative proteomics of a model MCF10A-KRas G12V cell line reveals a distinct molecular signature of the KRas G12V cell surface

Author

Ye, Xiaoying, Chan, King C, Waters, Andrew M, Bess, Matthew, Harned, Adam, Wei, Bih-Rong, Loncarek, Jadranka, Luke, Brian T, Orsburn, Benjamin C, Hollinger, Bradley D, Stephens, Robert M, Bagni, Rachel, Martinko, Alex, Wells, James A, Nissley, Dwight V, McCormick, Frank, Whiteley, Gordon, and Blonder, Josip

Subjects
Cancer, Biotechnology, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Aetiology, 2.1 Biological and endogenous factors, Antigens, CD, Antigens, Neoplasm, Basigin, Cell Adhesion Molecules, Cell Line, Tumor, Cell Movement, Computational Biology, Epithelial-Mesenchymal Transition, Glycoproteins, Humans, Mass Spectrometry, Membrane Proteins, Microscopy, Electron, Scanning, Mutant Proteins, Neoplasm Proteins, Proteomics, Proto-Oncogene Proteins p21(ras), KRas(G12V), cell surface proteome, drug targets, proteomics, mass spectrometry, KRasG12V, Oncology and Carcinogenesis
Abstract

Oncogenic Ras mutants play a major role in the etiology of most aggressive and deadly carcinomas in humans. In spite of continuous efforts, effective pharmacological treatments targeting oncogenic Ras isoforms have not been developed. Cell-surface proteins represent top therapeutic targets primarily due to their accessibility and susceptibility to different modes of cancer therapy. To expand the treatment options of cancers driven by oncogenic Ras, new targets need to be identified and characterized at the surface of cancer cells expressing oncogenic Ras mutants. Here, we describe a mass spectrometry-based method for molecular profiling of the cell surface using KRasG12V transfected MCF10A (MCF10A-KRasG12V) as a model cell line of constitutively activated KRas and native MCF10A cells transduced with an empty vector (EV) as control. An extensive molecular map of the KRas surface was achieved by applying, in parallel, targeted hydrazide-based cell-surface capturing technology and global shotgun membrane proteomics to identify the proteins on the KRasG12V surface. This method allowed for integrated proteomic analysis that identified more than 500 cell-surface proteins found unique or upregulated on the surface of MCF10A-KRasG12V cells. Multistep bioinformatic processing was employed to elucidate and prioritize targets for cross-validation. Scanning electron microscopy and phenotypic cancer cell assays revealed changes at the cell surface consistent with malignant epithelial-to-mesenchymal transformation secondary to KRasG12V activation. Taken together, this dataset significantly expands the map of the KRasG12V surface and uncovers potential targets involved primarily in cell motility, cellular protrusion formation, and metastasis.

Published
2016

9. Comparative proteomics of a model MCF10A-KRasG12V cell line reveals a distinct molecular signature of the KRasG12V cell surface.

Author

Ye, Xiaoying, Chan, King C, Waters, Andrew M, Bess, Matthew, Harned, Adam, Wei, Bih-Rong, Loncarek, Jadranka, Luke, Brian T, Orsburn, Benjamin C, Hollinger, Bradley D, Stephens, Robert M, Bagni, Rachel, Martinko, Alex, Wells, James A, Nissley, Dwight V, McCormick, Frank, Whiteley, Gordon, and Blonder, Josip

Subjects
Cell Line, Tumor, Humans, Glycoproteins, Cell Adhesion Molecules, Membrane Proteins, Neoplasm Proteins, Antigens, CD, Microscopy, Electron, Scanning, Proteomics, Computational Biology, Cell Movement, Proto-Oncogene Proteins p21(ras), Mutant Proteins, Mass Spectrometry, Epithelial-Mesenchymal Transition, Basigin, KRasG12V, cell surface proteome, drug targets, mass spectrometry, proteomics, Antigens, Neoplasm, KRas(G12V), Antigens, CD, Neoplasm, Cell Line, Tumor, Microscopy, Electron, Scanning, Oncology and Carcinogenesis
Abstract

Oncogenic Ras mutants play a major role in the etiology of most aggressive and deadly carcinomas in humans. In spite of continuous efforts, effective pharmacological treatments targeting oncogenic Ras isoforms have not been developed. Cell-surface proteins represent top therapeutic targets primarily due to their accessibility and susceptibility to different modes of cancer therapy. To expand the treatment options of cancers driven by oncogenic Ras, new targets need to be identified and characterized at the surface of cancer cells expressing oncogenic Ras mutants. Here, we describe a mass spectrometry-based method for molecular profiling of the cell surface using KRasG12V transfected MCF10A (MCF10A-KRasG12V) as a model cell line of constitutively activated KRas and native MCF10A cells transduced with an empty vector (EV) as control. An extensive molecular map of the KRas surface was achieved by applying, in parallel, targeted hydrazide-based cell-surface capturing technology and global shotgun membrane proteomics to identify the proteins on the KRasG12V surface. This method allowed for integrated proteomic analysis that identified more than 500 cell-surface proteins found unique or upregulated on the surface of MCF10A-KRasG12V cells. Multistep bioinformatic processing was employed to elucidate and prioritize targets for cross-validation. Scanning electron microscopy and phenotypic cancer cell assays revealed changes at the cell surface consistent with malignant epithelial-to-mesenchymal transformation secondary to KRasG12V activation. Taken together, this dataset significantly expands the map of the KRasG12V surface and uncovers potential targets involved primarily in cell motility, cellular protrusion formation, and metastasis.

Published
2016

13. Catalytically Inactive Human Cathepsin D Triggers Fibroblast Invasive Growth

Author

Laurent-Matha, Valérie, Maruani-Herrmann, Sharon, Prébois, Christine, Beaujouin, Mélanie, Glondu, Murielle, Noël, Agnès, Alvarez-Gonzalez, Marie Luz, Blacher, Sylvia, Coopman, Peter, Baghdiguian, Stephen, Gilles, Christine, Loncarek, Jadranka, Freiss, Gilles, Vignon, FranÇoise, and Liaudet-Coopman, Emmanuelle

Published
2005

16. Supplementary Figure 3 from CLPTM1L Promotes Growth and Enhances Aneuploidy in Pancreatic Cancer Cells

Author

Jia, Jinping, primary, Bosley, Allen D., primary, Thompson, Abbey, primary, Hoskins, Jason W., primary, Cheuk, Adam, primary, Collins, Irene, primary, Parikh, Hemang, primary, Xiao, Zhen, primary, Ylaya, Kris, primary, Dzyadyk, Marta, primary, Cozen, Wendy, primary, Hernandez, Brenda Y., primary, Lynch, Charles F., primary, Loncarek, Jadranka, primary, Altekruse, Sean F., primary, Zhang, Lizhi, primary, Westlake, Christopher J., primary, Factor, Valentina M., primary, Thorgeirsson, Snorri, primary, Bamlet, William R., primary, Hewitt, Stephen M., primary, Petersen, Gloria M., primary, Andresson, Thorkell, primary, and Amundadottir, Laufey T., primary

Published
2023
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17. Data from CLPTM1L Promotes Growth and Enhances Aneuploidy in Pancreatic Cancer Cells

Author

Jia, Jinping, primary, Bosley, Allen D., primary, Thompson, Abbey, primary, Hoskins, Jason W., primary, Cheuk, Adam, primary, Collins, Irene, primary, Parikh, Hemang, primary, Xiao, Zhen, primary, Ylaya, Kris, primary, Dzyadyk, Marta, primary, Cozen, Wendy, primary, Hernandez, Brenda Y., primary, Lynch, Charles F., primary, Loncarek, Jadranka, primary, Altekruse, Sean F., primary, Zhang, Lizhi, primary, Westlake, Christopher J., primary, Factor, Valentina M., primary, Thorgeirsson, Snorri, primary, Bamlet, William R., primary, Hewitt, Stephen M., primary, Petersen, Gloria M., primary, Andresson, Thorkell, primary, and Amundadottir, Laufey T., primary

Published
2023
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18. Supplementary Figure Legends from CLPTM1L Promotes Growth and Enhances Aneuploidy in Pancreatic Cancer Cells

Author

Jia, Jinping, primary, Bosley, Allen D., primary, Thompson, Abbey, primary, Hoskins, Jason W., primary, Cheuk, Adam, primary, Collins, Irene, primary, Parikh, Hemang, primary, Xiao, Zhen, primary, Ylaya, Kris, primary, Dzyadyk, Marta, primary, Cozen, Wendy, primary, Hernandez, Brenda Y., primary, Lynch, Charles F., primary, Loncarek, Jadranka, primary, Altekruse, Sean F., primary, Zhang, Lizhi, primary, Westlake, Christopher J., primary, Factor, Valentina M., primary, Thorgeirsson, Snorri, primary, Bamlet, William R., primary, Hewitt, Stephen M., primary, Petersen, Gloria M., primary, Andresson, Thorkell, primary, and Amundadottir, Laufey T., primary

Published
2023
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19. Supplementary Table 1 from CLPTM1L Promotes Growth and Enhances Aneuploidy in Pancreatic Cancer Cells

Author

Jia, Jinping, primary, Bosley, Allen D., primary, Thompson, Abbey, primary, Hoskins, Jason W., primary, Cheuk, Adam, primary, Collins, Irene, primary, Parikh, Hemang, primary, Xiao, Zhen, primary, Ylaya, Kris, primary, Dzyadyk, Marta, primary, Cozen, Wendy, primary, Hernandez, Brenda Y., primary, Lynch, Charles F., primary, Loncarek, Jadranka, primary, Altekruse, Sean F., primary, Zhang, Lizhi, primary, Westlake, Christopher J., primary, Factor, Valentina M., primary, Thorgeirsson, Snorri, primary, Bamlet, William R., primary, Hewitt, Stephen M., primary, Petersen, Gloria M., primary, Andresson, Thorkell, primary, and Amundadottir, Laufey T., primary

Published
2023
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20. Supplementary Figure 2 from CLPTM1L Promotes Growth and Enhances Aneuploidy in Pancreatic Cancer Cells

Author

Jia, Jinping, primary, Bosley, Allen D., primary, Thompson, Abbey, primary, Hoskins, Jason W., primary, Cheuk, Adam, primary, Collins, Irene, primary, Parikh, Hemang, primary, Xiao, Zhen, primary, Ylaya, Kris, primary, Dzyadyk, Marta, primary, Cozen, Wendy, primary, Hernandez, Brenda Y., primary, Lynch, Charles F., primary, Loncarek, Jadranka, primary, Altekruse, Sean F., primary, Zhang, Lizhi, primary, Westlake, Christopher J., primary, Factor, Valentina M., primary, Thorgeirsson, Snorri, primary, Bamlet, William R., primary, Hewitt, Stephen M., primary, Petersen, Gloria M., primary, Andresson, Thorkell, primary, and Amundadottir, Laufey T., primary

Published
2023
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21. Supplementary Figure 6 from CLPTM1L Promotes Growth and Enhances Aneuploidy in Pancreatic Cancer Cells

Author

Jia, Jinping, primary, Bosley, Allen D., primary, Thompson, Abbey, primary, Hoskins, Jason W., primary, Cheuk, Adam, primary, Collins, Irene, primary, Parikh, Hemang, primary, Xiao, Zhen, primary, Ylaya, Kris, primary, Dzyadyk, Marta, primary, Cozen, Wendy, primary, Hernandez, Brenda Y., primary, Lynch, Charles F., primary, Loncarek, Jadranka, primary, Altekruse, Sean F., primary, Zhang, Lizhi, primary, Westlake, Christopher J., primary, Factor, Valentina M., primary, Thorgeirsson, Snorri, primary, Bamlet, William R., primary, Hewitt, Stephen M., primary, Petersen, Gloria M., primary, Andresson, Thorkell, primary, and Amundadottir, Laufey T., primary

Published
2023
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22. Supplementary Figure 4 from CLPTM1L Promotes Growth and Enhances Aneuploidy in Pancreatic Cancer Cells

Author

Jia, Jinping, primary, Bosley, Allen D., primary, Thompson, Abbey, primary, Hoskins, Jason W., primary, Cheuk, Adam, primary, Collins, Irene, primary, Parikh, Hemang, primary, Xiao, Zhen, primary, Ylaya, Kris, primary, Dzyadyk, Marta, primary, Cozen, Wendy, primary, Hernandez, Brenda Y., primary, Lynch, Charles F., primary, Loncarek, Jadranka, primary, Altekruse, Sean F., primary, Zhang, Lizhi, primary, Westlake, Christopher J., primary, Factor, Valentina M., primary, Thorgeirsson, Snorri, primary, Bamlet, William R., primary, Hewitt, Stephen M., primary, Petersen, Gloria M., primary, Andresson, Thorkell, primary, and Amundadottir, Laufey T., primary

Published
2023
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23. Supplementary Figure 1 from CLPTM1L Promotes Growth and Enhances Aneuploidy in Pancreatic Cancer Cells

Author

Jia, Jinping, primary, Bosley, Allen D., primary, Thompson, Abbey, primary, Hoskins, Jason W., primary, Cheuk, Adam, primary, Collins, Irene, primary, Parikh, Hemang, primary, Xiao, Zhen, primary, Ylaya, Kris, primary, Dzyadyk, Marta, primary, Cozen, Wendy, primary, Hernandez, Brenda Y., primary, Lynch, Charles F., primary, Loncarek, Jadranka, primary, Altekruse, Sean F., primary, Zhang, Lizhi, primary, Westlake, Christopher J., primary, Factor, Valentina M., primary, Thorgeirsson, Snorri, primary, Bamlet, William R., primary, Hewitt, Stephen M., primary, Petersen, Gloria M., primary, Andresson, Thorkell, primary, and Amundadottir, Laufey T., primary

Published
2023
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24. Supplementary Figure 5 from CLPTM1L Promotes Growth and Enhances Aneuploidy in Pancreatic Cancer Cells

Author

Jia, Jinping, primary, Bosley, Allen D., primary, Thompson, Abbey, primary, Hoskins, Jason W., primary, Cheuk, Adam, primary, Collins, Irene, primary, Parikh, Hemang, primary, Xiao, Zhen, primary, Ylaya, Kris, primary, Dzyadyk, Marta, primary, Cozen, Wendy, primary, Hernandez, Brenda Y., primary, Lynch, Charles F., primary, Loncarek, Jadranka, primary, Altekruse, Sean F., primary, Zhang, Lizhi, primary, Westlake, Christopher J., primary, Factor, Valentina M., primary, Thorgeirsson, Snorri, primary, Bamlet, William R., primary, Hewitt, Stephen M., primary, Petersen, Gloria M., primary, Andresson, Thorkell, primary, and Amundadottir, Laufey T., primary

Published
2023
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36. The centromere geometry essential for keeping mitosis error free is controlled by spindle forces

Author

Loncarek, Jadranka, Kisurina-Evgenieva, Olga, Vinogradova, Tatiana, Hergert, Polla, La Terra, Sabrina, Kapoor, Tarun M., and Khodjakov, Alexey

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Accurate segregation of chromosomes, essential for the stability of the genome, depends on 'bi-orientation'--simultaneous attachment of each individual chromosome to both poles of the mitotic spindle'. On bi-oriented chromosomes, kinetochores [...]

Published
2007

47. Single-Cell Analysis Reveals that Chronic Silver Nanoparticle Exposure Induces Cell Division Defects in Human Epithelial Cells

Author

Garcia, Ellen B., Alms, Cynthia, Hinman, Albert W., Kelly, Conor, Smith, Adam, Vance, Marina, Loncarek, Jadranka, Marr, Linsey C., Cimini, Daniela, Garcia, Ellen B., Alms, Cynthia, Hinman, Albert W., Kelly, Conor, Smith, Adam, Vance, Marina, Loncarek, Jadranka, Marr, Linsey C., and Cimini, Daniela

Abstract

Multiple organizations have urged a paradigm shift from traditional, whole animal, chemical safety testing to alternative methods. Although these forward-looking methods exist for risk assessment and predication, animal testing is still the preferred method and will remain so until more robust cellular and computational methods are established. To meet this need, we aimed to develop a new, cell division-focused approach based on the idea that defective cell division may be a better predictor of risk than traditional measurements. To develop such an approach, we investigated the toxicity of silver nanoparticles (AgNPs) on human epithelial cells. AgNPs are the type of nanoparticle most widely employed in consumer and medical products, yet toxicity reports are still confounding. Cells were exposed to a range of AgNP doses for both short- and-long term exposure times. The analysis of treated cell populations identified an effect on cell division and the emergence of abnormal nuclear morphologies, including micronuclei and binucleated cells. Overall, our results indicate that AgNPs impair cell division, not only further confirming toxicity to human cells, but also highlighting the propagation of adverse phenotypes within the cell population. Furthermore, this work illustrates that cell division-based analysis will be an important addition to future toxicology studies.

Published
2019
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48. Single-Cell Analysis Reveals that Chronic Silver Nanoparticle Exposure Induces Cell Division Defects in Human Epithelial Cells

Author

Civil and Environmental Engineering, Biological Sciences, Fralin Life Sciences Institute, Garcia, Ellen B., Alms, Cynthia, Hinman, Albert W., Kelly, Conor, Smith, Adam, Vance, Marina, Loncarek, Jadranka, Marr, Linsey C., Cimini, Daniela, Civil and Environmental Engineering, Biological Sciences, Fralin Life Sciences Institute, Garcia, Ellen B., Alms, Cynthia, Hinman, Albert W., Kelly, Conor, Smith, Adam, Vance, Marina, Loncarek, Jadranka, Marr, Linsey C., and Cimini, Daniela

Abstract

Multiple organizations have urged a paradigm shift from traditional, whole animal, chemical safety testing to alternative methods. Although these forward-looking methods exist for risk assessment and predication, animal testing is still the preferred method and will remain so until more robust cellular and computational methods are established. To meet this need, we aimed to develop a new, cell division-focused approach based on the idea that defective cell division may be a better predictor of risk than traditional measurements. To develop such an approach, we investigated the toxicity of silver nanoparticles (AgNPs) on human epithelial cells. AgNPs are the type of nanoparticle most widely employed in consumer and medical products, yet toxicity reports are still confounding. Cells were exposed to a range of AgNP doses for both short- and-long term exposure times. The analysis of treated cell populations identified an effect on cell division and the emergence of abnormal nuclear morphologies, including micronuclei and binucleated cells. Overall, our results indicate that AgNPs impair cell division, not only further confirming toxicity to human cells, but also highlighting the propagation of adverse phenotypes within the cell population. Furthermore, this work illustrates that cell division-based analysis will be an important addition to future toxicology studies.

Published
2019

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