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518 results on '"Odde, David J."'

4. Outpatient treatment of COVID-19 and incidence of post-COVID-19 condition over 10 months (COVID-OUT): a multicentre, randomised, quadruple-blind, parallel-group, phase 3 trial

Author

Anderson, Blake, Atwater, Riannon C, Avula, Nandini, Beckman, Kenny B, Belani, Hrishikesh K, Boulware, David R, Bramante, Carolyn T, Brea, Jannis, Broedlow, Courtney A, Buse, John B, Campora, Paula, Challa, Anup, Charles, Jill, Christensen, Grace, Christiansen, Theresa, Cohen, Ken, Connelly, Bo, Datta, Srijani, Deng, Nikita, Dunn, Alex T, Erickson, Spencer M, Fairbairn, Faith M, Fenno, Sarah L, Fraser, Daniel J, Fricton, Regina D, Griffiths, Gwen, Hagen, Aubrey A, Hartman, Katrina M, Hendrickson, Audrey F, Huling, Jared D, Ingraham, Nicholas E, Jeng, Arthur C, Johnson, Darrell M, Karger, Amy B, Klatt, Nichole R, Kuehl, Erik A, LaBar, Derek D, Lee, Samuel, Liebovitz, David M, Lindberg, Sarah, Luke, Darlette G, Machicado, Rosario, Mohamud, Zeinab, Murray, Thomas A, Ngonyama, Rumbidzai, Nicklas, Jacinda M, Odde, David J, Parrens, Elliott, Parra, Daniela, Patel, Barkha, Proper, Jennifer L, Pullen, Matthew F, Puskarich, Michael A, Rao, Via, Reddy, Neha V, Reddy, Naveen, Rypka, Katelyn J, Saveraid, Hanna G, Seloadji, Paula, Shahriar, Arman, Sherwood, Nancy, Siegart, Jamie L, Siegel, Lianne K, Simmons, Lucas, Sinelli, Isabella, Singh, Palak, Snyder, Andrew, Stauffer, Maxwell T, Thompson, Jennifer, Tignanelli, Christopher J, Tople, Tannon L, Tordsen, Walker J, Watson, Ray HB, Wu, Beiqing, Zaman, Adnin, Zolik, Madeline R, Zinkl, Lena, Anderson, Blake J, Thompson, Jennifer L, Pullen, Matthew, Wirtz, Esteban Lemus, Sherwood, Nancy E, Lindberg, Sarah M, Beckman, Kenneth B, Rose, Michael R, Mehta, Tanvi, Griffiths, Gwendolyn, and Bhat, Neeta S

Published
2023
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7. Directed cell migration towards softer environments

Author

Isomursu, Aleksi, Park, Keun-Young, Hou, Jay, Cheng, Bo, Mathieu, Mathilde, Shamsan, Ghaidan A., Fuller, Benjamin, Kasim, Jesse, Mahmoodi, M. Mohsen, Lu, Tian Jian, Genin, Guy M., Xu, Feng, Lin, Min, Distefano, Mark D., Ivaska, Johanna, and Odde, David J.

Published
2022
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12. Integrin-mediated traction force enhances paxillin molecular associations and adhesion dynamics that increase the invasiveness of tumor cells into a three-dimensional extracellular matrix.

Author

Mekhdjian, Armen H, Kai, FuiBoon, Rubashkin, Matthew G, Prahl, Louis S, Przybyla, Laralynne M, McGregor, Alexandra L, Bell, Emily S, Barnes, J Matthew, DuFort, Christopher C, Ou, Guanqing, Chang, Alice C, Cassereau, Luke, Tan, Steven J, Pickup, Michael W, Lakins, Jonathan N, Ye, Xin, Davidson, Michael W, Lammerding, Jan, Odde, David J, Dunn, Alexander R, and Weaver, Valerie M

Subjects
Breast, Cell Line, Tumor, Extracellular Matrix, Humans, Breast Neoplasms, Neoplasm Metastasis, Integrins, Cell Adhesion, Signal Transduction, Phosphorylation, Female, Focal Adhesion Protein-Tyrosine Kinases, Paxillin, Cell Line, Tumor, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Metastasis requires tumor cells to navigate through a stiff stroma and squeeze through confined microenvironments. Whether tumors exploit unique biophysical properties to metastasize remains unclear. Data show that invading mammary tumor cells, when cultured in a stiffened three-dimensional extracellular matrix that recapitulates the primary tumor stroma, adopt a basal-like phenotype. Metastatic tumor cells and basal-like tumor cells exert higher integrin-mediated traction forces at the bulk and molecular levels, consistent with a motor-clutch model in which motors and clutches are both increased. Basal-like nonmalignant mammary epithelial cells also display an altered integrin adhesion molecular organization at the nanoscale and recruit a suite of paxillin-associated proteins implicated in invasion and metastasis. Phosphorylation of paxillin by Src family kinases, which regulates adhesion turnover, is similarly enhanced in the metastatic and basal-like tumor cells, fostered by a stiff matrix, and critical for tumor cell invasion in our assays. Bioinformatics reveals an unappreciated relationship between Src kinases, paxillin, and survival of breast cancer patients. Thus adoption of the basal-like adhesion phenotype may favor the recruitment of molecules that facilitate tumor metastasis to integrin-based adhesions. Analysis of the physical properties of tumor cells and integrin adhesion composition in biopsies may be predictive of patient outcome.

Published
2017

15. Mutual antagonism between CD44 and integrins in glioblastoma cell traction and migration.

Author

Kelly, Marcus D., Pawlak, Matthew R., Zhan, Kevin H., Shamsan, Ghaidan A., Gordon, Wendy R., and Odde, David J.

Subjects
CELL migration, CD44 antigen, EXTRACELLULAR matrix, HYALURONIC acid, CANCER invasiveness
Abstract

Cell migration is the major driver of invasion and metastasis during cancer progression. For cells to migrate, they utilize the actin–myosin cytoskeleton and adhesion molecules, such as integrins and CD44, to generate traction forces in their environment. CD44 primarily binds to hyaluronic acid (HA) and integrins primarily bind to extracellular matrix (ECM) proteins such as collagen. However, the role of CD44 under integrin-mediated conditions and vice versa is not well known. Here, we performed traction force microscopy (TFM) on U251 cells seeded on collagen I-coated polyacrylamide gels to assess the functional mechanical relationship between integrins and CD44. Performing TFM on integrin-mediated adhesion conditions, i.e., collagen, we found that CD44KO U251 cells exerted more traction force than wild-type (WT) U251 cells. Furthermore, untreated WT and CD44-blocked WT exhibited comparable results. Conversely, in CD44-mediated adhesive conditions, integrin-blocked WT cells exerted a higher traction force than untreated WT cells. Our data suggest that CD44 and integrins have a mutually antagonistic relationship where one receptor represses the other's ability to generate traction force on its cognate substrate. [ABSTRACT FROM AUTHOR]

Published
2024
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16. Favorable Antiviral Effect of Metformin on SARS-CoV-2 Viral Load in a Randomized, Placebo-Controlled Clinical Trial of COVID-19.

Author

Bramante, Carolyn T, Beckman, Kenneth B, Mehta, Tanvi, Karger, Amy B, Odde, David J, Tignanelli, Christopher J, Buse, John B, Johnson, Darrell M, Watson, Ray H B, Daniel, Jerry J, Liebovitz, David M, Nicklas, Jacinda M, Cohen, Ken, Puskarich, Michael A, Belani, Hrishikesh K, Siegel, Lianne K, Klatt, Nichole R, Anderson, Blake, Hartman, Katrina M, and Rao, Via

Subjects
MORTALITY prevention, METFORMIN, VIRAL load, EMERGENCY room visits, HOSPITAL care, FLUVOXAMINE, REVERSE transcriptase polymerase chain reaction, DESCRIPTIVE statistics, ANTIVIRAL agents, RACE, ODDS ratio, DRUG efficacy, MACROLIDE antibiotics, CONFIDENCE intervals, COVID-19
Abstract

Background Metformin has antiviral activity against RNA viruses including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The mechanism appears to be suppression of protein translation via targeting the host mechanistic target of rapamycin pathway. In the COVID-OUT randomized trial for outpatient coronavirus disease 2019 (COVID-19), metformin reduced the odds of hospitalizations/death through 28 days by 58%, of emergency department visits/hospitalizations/death through 14 days by 42%, and of long COVID through 10 months by 42%. Methods COVID-OUT was a 2 × 3 randomized, placebo-controlled, double-blind trial that assessed metformin, fluvoxamine, and ivermectin; 999 participants self-collected anterior nasal swabs on day 1 (n = 945), day 5 (n = 871), and day 10 (n = 775). Viral load was quantified using reverse-transcription quantitative polymerase chain reaction. Results The mean SARS-CoV-2 viral load was reduced 3.6-fold with metformin relative to placebo (−0.56 log10 copies/mL; 95% confidence interval [CI], −1.05 to −.06; P =.027). Those who received metformin were less likely to have a detectable viral load than placebo at day 5 or day 10 (odds ratio [OR], 0.72; 95% CI,.55 to.94). Viral rebound, defined as a higher viral load at day 10 than day 5, was less frequent with metformin (3.28%) than placebo (5.95%; OR, 0.68; 95% CI,.36 to 1.29). The metformin effect was consistent across subgroups and increased over time. Neither ivermectin nor fluvoxamine showed effect over placebo. Conclusions In this randomized, placebo-controlled trial of outpatient treatment of SARS-CoV-2, metformin significantly reduced SARS-CoV-2 viral load, which may explain the clinical benefits in this trial. Metformin is pleiotropic with other actions that are relevant to COVID-19 pathophysiology. Clinical Trials Registration NCT04510194. [ABSTRACT FROM AUTHOR]

Published
2024
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19. The OTX2 Gene Induces Tumor Growth and Triggers Leptomeningeal Metastasis by Regulating the mTORC2 Signaling Pathway in Group 3 Medulloblastomas

Author

Ampudia-Mesias, Elisabet, primary, Cameron, Charles S., additional, Yoo, Eunjae, additional, Kelly, Marcus, additional, Anderson, Sarah M., additional, Manning, Riley, additional, Abrahante Lloréns, Juan E., additional, Moertel, Christopher L., additional, Yim, Hyungshin, additional, Odde, David J., additional, Saydam, Nurten, additional, and Saydam, Okay, additional

Published
2024
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21. Myosin IIA suppresses glioblastoma development in a mechanically sensitive manner

Author

Picariello, Hannah S., Kenchappa, Rajappa S., Rai, Vandana, Crish, James F., Dovas, Athanassios, Pogoda, Katarzyna, McMahon, Mariah, Bell, Emily S., Chandrasekharan, Unnikrishnan, Luu, Amanda, West, Rita, Lammerding, Jan, Canoll, Peter, Odde, David J., Janmey, Paul A., Egelhoff, Thomas, and Rosenfeld, Steven S.

Published
2019

25. Minus-End-Directed Kinesin-14 Motors Align Antiparallel Microtubules to Control Metaphase Spindle Length

Author

Hepperla, Austin J, Willey, Patrick T, Coombes, Courtney E, Schuster, Breanna M, Gerami-Nejad, Maryam, McClellan, Mark, Mukherjee, Soumya, Fox, Janet, Winey, Mark, Odde, David J, O’Toole, Eileen, and Gardner, Melissa K

Subjects
Biochemistry and Cell Biology, Biological Sciences, Underpinning research, 1.1 Normal biological development and functioning, Generic health relevance, Kinesins, Microtubule Proteins, Microtubule-Associated Proteins, Microtubules, Models, Biological, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Spindle Apparatus, Kinesin, Medical and Health Sciences, Developmental Biology, Biochemistry and cell biology
Abstract

During cell division, a microtubule-based mitotic spindle mediates the faithful segregation of duplicated chromosomes into daughter cells. Proper length control of the metaphase mitotic spindle is critical to this process and is thought to be achieved through a mechanism in which spindle pole separation forces from plus-end-directed motors are balanced by forces from minus-end-directed motors that pull spindle poles together. However, in contrast to this model, metaphase mitotic spindles with inactive kinesin-14 minus-end-directed motors often have shorter spindle lengths, along with poorly aligned spindle microtubules. A mechanistic explanation for this paradox is unknown. Using computational modeling, in vitro reconstitution, live-cell fluorescence microscopy, and electron microscopy, we now find that the budding yeast kinesin-14 molecular motor Kar3-Cik1 can efficiently align spindle microtubules along the spindle axis. This then allows plus-end-directed kinesin-5 motors to efficiently exert the outward microtubule sliding forces needed for proper spindle bipolarity.

Published
2014

27. Modeling Cell Migration Mechanics

Author

Prahl, Louis S., Odde, David J., COHEN, IRUN R., Series Editor, LAJTHA, ABEL, Series Editor, LAMBRIS, JOHN D., Series Editor, PAOLETTI, RODOLFO, Series Editor, Rezaei, Nima, Series Editor, Dong, Cheng, editor, Zahir, Nastaran, editor, and Konstantopoulos, Konstantinos, editor

Published
2018
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37. Supplementary Figures 4-7 from Sleeping Beauty Insertional Mutagenesis Reveals Important Genetic Drivers of Central Nervous System Embryonal Tumors

Author

Beckmann, Pauline J., primary, Larson, Jon D., primary, Larsson, Alex T., primary, Ostergaard, Jason P., primary, Wagner, Sandra, primary, Rahrmann, Eric P., primary, Shamsan, Ghaidan A., primary, Otto, George M., primary, Williams, Rory L., primary, Wang, Jun, primary, Lee, Catherine, primary, Tschida, Barbara R., primary, Das, Paramita, primary, Dubuc, Adrian M., primary, Moriarity, Branden S., primary, Picard, Daniel, primary, Wu, Xiaochong, primary, Rodriguez, Fausto J., primary, Rosemarie, Quincy, primary, Krebs, Ryan D., primary, Molan, Amy M., primary, Demer, Addison M., primary, Frees, Michelle M., primary, Rizzardi, Anthony E., primary, Schmechel, Stephen C., primary, Eberhart, Charles G., primary, Jenkins, Robert B., primary, Wechsler-Reya, Robert J., primary, Odde, David J., primary, Huang, Annie, primary, Taylor, Michael D., primary, Sarver, Aaron L., primary, and Largaespada, David A., primary

Published
2023
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38. Data from Sleeping Beauty Insertional Mutagenesis Reveals Important Genetic Drivers of Central Nervous System Embryonal Tumors

Author

Beckmann, Pauline J., primary, Larson, Jon D., primary, Larsson, Alex T., primary, Ostergaard, Jason P., primary, Wagner, Sandra, primary, Rahrmann, Eric P., primary, Shamsan, Ghaidan A., primary, Otto, George M., primary, Williams, Rory L., primary, Wang, Jun, primary, Lee, Catherine, primary, Tschida, Barbara R., primary, Das, Paramita, primary, Dubuc, Adrian M., primary, Moriarity, Branden S., primary, Picard, Daniel, primary, Wu, Xiaochong, primary, Rodriguez, Fausto J., primary, Rosemarie, Quincy, primary, Krebs, Ryan D., primary, Molan, Amy M., primary, Demer, Addison M., primary, Frees, Michelle M., primary, Rizzardi, Anthony E., primary, Schmechel, Stephen C., primary, Eberhart, Charles G., primary, Jenkins, Robert B., primary, Wechsler-Reya, Robert J., primary, Odde, David J., primary, Huang, Annie, primary, Taylor, Michael D., primary, Sarver, Aaron L., primary, and Largaespada, David A., primary

Published
2023
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39. Supplementary Tables 1-9 from Sleeping Beauty Insertional Mutagenesis Reveals Important Genetic Drivers of Central Nervous System Embryonal Tumors

Author

Beckmann, Pauline J., primary, Larson, Jon D., primary, Larsson, Alex T., primary, Ostergaard, Jason P., primary, Wagner, Sandra, primary, Rahrmann, Eric P., primary, Shamsan, Ghaidan A., primary, Otto, George M., primary, Williams, Rory L., primary, Wang, Jun, primary, Lee, Catherine, primary, Tschida, Barbara R., primary, Das, Paramita, primary, Dubuc, Adrian M., primary, Moriarity, Branden S., primary, Picard, Daniel, primary, Wu, Xiaochong, primary, Rodriguez, Fausto J., primary, Rosemarie, Quincy, primary, Krebs, Ryan D., primary, Molan, Amy M., primary, Demer, Addison M., primary, Frees, Michelle M., primary, Rizzardi, Anthony E., primary, Schmechel, Stephen C., primary, Eberhart, Charles G., primary, Jenkins, Robert B., primary, Wechsler-Reya, Robert J., primary, Odde, David J., primary, Huang, Annie, primary, Taylor, Michael D., primary, Sarver, Aaron L., primary, and Largaespada, David A., primary

Published
2023
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40. Supplementary Figures 1-3 from Sleeping Beauty Insertional Mutagenesis Reveals Important Genetic Drivers of Central Nervous System Embryonal Tumors

Author

Beckmann, Pauline J., primary, Larson, Jon D., primary, Larsson, Alex T., primary, Ostergaard, Jason P., primary, Wagner, Sandra, primary, Rahrmann, Eric P., primary, Shamsan, Ghaidan A., primary, Otto, George M., primary, Williams, Rory L., primary, Wang, Jun, primary, Lee, Catherine, primary, Tschida, Barbara R., primary, Das, Paramita, primary, Dubuc, Adrian M., primary, Moriarity, Branden S., primary, Picard, Daniel, primary, Wu, Xiaochong, primary, Rodriguez, Fausto J., primary, Rosemarie, Quincy, primary, Krebs, Ryan D., primary, Molan, Amy M., primary, Demer, Addison M., primary, Frees, Michelle M., primary, Rizzardi, Anthony E., primary, Schmechel, Stephen C., primary, Eberhart, Charles G., primary, Jenkins, Robert B., primary, Wechsler-Reya, Robert J., primary, Odde, David J., primary, Huang, Annie, primary, Taylor, Michael D., primary, Sarver, Aaron L., primary, and Largaespada, David A., primary

Published
2023
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46. Main Manuscript for Cell migration simulator-based biomarkers for glioblastoma

Author

Hou, Jay, McMahon, Mariah, Sarkaria, Jann N., Chen, Clark C., and Odde, David J.

Subjects
Article
Abstract

Glioblastoma is the most aggressive malignant brain tumor with poor survival due to its invasive nature driven by cell migration, with unclear linkage to transcriptomic information. Here, we applied a physics-based motor-clutch model, a cell migration simulator (CMS), to parameterize the migration of glioblastoma cells and define physical biomarkers on a patient-by-patient basis. We reduced the 11-dimensional parameter space of the CMS into 3D to identify three principal physical parameters that govern cell migration: motor number – describing myosin II activity, clutch number – describing adhesion level, and F-actin polymerization rate. Experimentally, we found that glioblastoma patient-derived (xenograft) (PD(X)) cell lines across mesenchymal (MES), proneural (PN), classical (CL) subtypes and two institutions (N=13 patients) had optimal motility and traction force on stiffnesses around 9.3kPa, with otherwise heterogeneous and uncorrelated motility, traction, and F-actin flow. By contrast, with the CMS parameterization, we found glioblastoma cells consistently had balanced motor/clutch ratios to enable effective migration, and that MES cells had higher actin polymerization rates resulting in higher motility. The CMS also predicted differential sensitivity to cytoskeletal drugs between patients. Finally, we identified 11 genes that correlated with the physical parameters, suggesting that transcriptomic data alone could potentially predict the mechanics and speed of glioblastoma cell migration. Overall, we describe a general physics-based framework for parameterizing individual glioblastoma patients and connecting to clinical transcriptomic data, that can potentially be used to develop patient-specific anti-migratory therapeutic strategies generally.

Published
2023

48. Outpatient Treatment of COVID-19 and the Development of Long COVID Over 10 Months: A Multi-Center, Quadruple-Blind, Parallel Group Randomized Phase 3 Trial

Author

Bramante, Carolyn, primary, Buse, John B., additional, Liebovitz, David, additional, Nicklas, Jacinda, additional, Puskarich, Michael, additional, Cohen, Kenneth R., additional, Belani, Hrishikesh, additional, Anderson, Blake, additional, Huling, Jared D., additional, Thompson, Jennifer, additional, Pullen, Matthew, additional, Wirtz, Esteban Lemus, additional, Siegel, Lianne, additional, Proper, Jennifer, additional, Odde, David J., additional, Klatt, Nichole, additional, Sherwood, Nancy E., additional, Lindberg, Sarah, additional, Karger, Amy B., additional, Beckman, Kenneth B., additional, Erickson, Spencer, additional, Fenno, Sarah, additional, Hartman, Katrina, additional, Rose, Michael, additional, Mehta, Tanvi, additional, Patel, Barkha, additional, Griffiths, Gwendolyn, additional, Bhat, Neeta, additional, Murray, Thomas A., additional, and Boulware, David R., additional

Published
2023
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49. Outpatient treatment of Covid-19 with metformin, ivermectin, and fluvoxamine and the development of Long Covid over 10-month follow-up

Author

Bramante, Carolyn T., primary, Buse, John B., additional, Liebovitz, David, additional, Nicklas, Jacinda, additional, Puskarich, Michael A., additional, Cohen, Ken, additional, Belani, Hrishikesh, additional, Anderson, Blake, additional, Huling, Jared D., additional, Tignanelli, Christopher, additional, Thompson, Jennifer, additional, Pullen, Matthew, additional, Siegel, Lianne, additional, Proper, Jennifer, additional, Odde, David J., additional, Klatt, Nichole, additional, Sherwood, Nancy, additional, Lindberg, Sarah, additional, Wirtz, Esteban Lemus, additional, Karger, Amy, additional, Beckman, Kenny, additional, Erickson, Spencer, additional, Fenno, Sarah, additional, Hartman, Katrina, additional, Rose, Michael, additional, Patel, Barkha, additional, Griffiths, Gwendolyn, additional, Bhat, Neeta, additional, Murray, Thomas A., additional, and Boulware, David R., additional

Published
2022
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