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6. Normal hematopoiesis and neurofibromin-deficient myeloproliferative disease require Erk

Author

Staser, Karl, Park, Su-Jung, Rhodes, Steven D., Zeng, Yi, He, Yong Zheng, Shew, Matthew A., Gehlhausen, Jeffrey R., Cerabona, Donna, Menon, Keshav, Chen, Shi, Sun, Zejin, Yuan, Jin, Ingram, David A., Nalepa, Grzegorz, Yang, eng-Chun, and Clapp, D. Wade

Subjects
Hematopoiesis -- Physiological aspects -- Research, Myeloproliferative disorders -- Complications and side effects -- Prevention -- Risk factors -- Research -- Genetic aspects, Protein kinases -- Genetic aspects -- Research -- Physiological aspects, Health care industry
Abstract

Neurofibromatosis type 1 (NF1) predisposes individuals to the development of juvenile myelomonocytic leukemia (JMML), a fatal myeloproliferative disease (MPD). In genetically engineered murine models, nullizygosity of Nf1, a tumor suppressor [...]

Published
2013
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7. A murine model of neurofibromatosis type 2 that accurately phenocopies human schwannoma formation

Author

Gehlhausen, Jeffrey R., Park, Su-Jung, Hickox, Ann E., Shew, Matthew, Staser, Karl, Rhodes, Steven D., Menon, Keshav, Lajiness, Jacquelyn D., Mwanthi, Muithi, Yang, Xianlin, Yuan, Jin, Territo, Paul, Hutchins, Gary, Nalepa, Grzegorz, Yang, Feng-Chun, Conway, Simon J., Heinz, Michael G., Stemmer-Rachamimov, Anat, Yates, Charles W., and Wade Clapp, D.

Published
2015
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8. Contributors

Author

Abdallah, M. Abdel Rahim, Abdallah, Mahmoud M.A., Abdallah, Marwa, Adler, Brandon L., Adusumilli, Nagasai C., Akaike, Tomoko, Alavi, Afsaneh, Amagai, Masayuki, Ambros-Rudolph, Priv.-Doz. Dr. Christina M., Rox Anderson, R., Antaya, Richard J., Ardigò, Marco, Argenyi, Zsolt B., Argenziano, Giuseppe, Avram, Marc R., Avram, Mathew M., Baker, Christopher, Barete, Stéphane, Barnhill, Raymond L., Baselga, Eulalia, Baugh, Erica G., Bayliss, Susan J., Beck, Lisa A., Bergqvist, Christina, Bernhard, Jeffrey D., Blanton, Lucas S., Bodemer, Apple, Bolognia, Jean L., Borradori, Luca, Dominik Braun, Andreas, Bravo, Francisco G., Brodland, David G., Brownell, Isaac, Bruckner, Anna L., Bruckner-Tuderman, Leena, Burkhart, Craig G., Burkhart, Craig N., Burrows, Nigel P., Callen, Jeffrey P., Camacho, Francisco M., Cameli Carley, Alexandra, Carruthers, Alastair, Carruthers, Jean, Cartee, Todd V., Cerroni, Lorenzo, Chan, Roy K.W., Wu Chang, Mary, Chio, Martin T.W., Chosidow, Olivier, Christiano, Angela M., Clayton, Anna S., Cockerell MD MBA JD, Clay J., Cohen, Bernard A., Cohen, David E., Coleman, Kyle M., Coleman, William P., Kari Connolly, M., Cooper, Susan M., Corey, Kristen, Cowen, Edward W., Cribier, Bernard, Darling, Thomas N., Davis, Mark D.P., de Berker, David, De Leo, Vincent A., Detmar, Michael, Diana Draelos, Zoe, Duncan, Karynne O., Elewski, Boni E., Elias, Peter M., Elston, Dirk M., Eming, Sabine A., España, Agustín, Fairley, Janet A., Feingold, Kenneth R., Fine, Jo-David, Flowers, Franklin P., Fox, Matthew, Fraitag, Sylvie, Franceschini, Chiara, Frank, Jorge, French, Lars E., Fried, Isabella, Frieden, Ilona J., Garzon, Maria C., Gasslitter, Irina, Gattorno, Marco, Gehlhausen, Jeffrey R., Ghoreschi, Kamran, Goldman, Mitchel P., Goldsmith, Charya B., Gollnick, Harald P., Grattan, Clive E.H., Groves, Richard W., Guillén-Navarro, Encarna, Haemel, Anna K., Hafner, Ariela, Haggstrom, Anita N., Hand, Jennifer L., Hannam, Sarah, Hausauer, Amelia K., Hay, Roderick J., Helfrich, Yolanda R., Hernández-Martín, Ángela, Hertl, Michael, Heymann, Warren R., High, Whitney A., Hirakawa, Satoshi, Hivnor, Chad M., Hohl, Prof. Dr. med. Daniel M., Hönigsmann, Herbert, Hötzenecker, Wolfram, Howard, Josie, Howard, Renee M., Hruza, George J., Hrynewycz, Katherine, Hsiao, Jennifer L., Huang, Jennifer T., Hughey, Lauren C., Hull, Christopher M., Marchiony Hunt, Katherine, Ingen-Housz-Oro, Saskia, Irvine, Alan D., Iversen, Lars, Mark Jackson, J., Jackson, Scott M., Jacobe, Heidi T., Jebain, Joseph, Jessri, Maryam, Jones, Derek H., Jorizzo, Joseph L., Kaddu, Steven, Kalia, Sunil, Kang, Sewon, Kelly, Kristen M., Kelly, Robert, Kempf, Werner, Kim, Brian, Kirnbauer, Reinhard, Kirsner, Robert S., Kittler, Nicole W., Knowles BSc Phm, Sandra R., Ko, Christine J., Kocatürk, Emek, Koch, Priv.-Doz. Dr. Lukas, Koch, Peter J., Koh, Hong Yi, Koo, John Y.M., Koss, Tamara, Koster, Maranke I., Kroshinsky, Daniela, G. Kumar, Monique, Kutzner, Heinz H., Kwong, Bernice Y., Lalor, Leah E.B., Lam, Charlene, Latheef, Faheem, Lee, Lela A., Lenormand, Cédric, Lenz, Petra, Lesher, Jack L., Jr., Leslie, Kieron S., Lev-Tov, Hadar, Liegl-Atzwanger, Bernadette, Lim, Henry W., Hua Liang Lim, Joel, Linos, Eleni, Lio, Peter, Lipsker, Dan, Loomis, Cynthia A., Lui, Harvey, Luo, Su, Maari, Catherine, Machan, Salma, Madigan, Lauren M., Maguiness, Sheilagh M., Maiberger, Mary P., Mancini, Anthony J., Marchitto, Mark, Marks Jr, James G., Martínez-Menchón, Teresa, Mascaró, José M., Jr., Trent Massengale, William, Massone, Cesare, Mauro, Theodora M., Mc Aleer, Maeve A., Mc Calmont, Timothy H., Carol Mc Connell, R., Mc Govern, Thomas W., Matthew Mc Larney, R., Mc Meniman, Erin K., Mc Murray, Stacy L., Mc Namara, Kristin K., Mc Niff, Jennifer M., Mellerio, Jemima E., Menon, Gopinathan K., Metze, Dieter, Meyer, Jason, Micheletti, Robert G., Milam, Emily C., Millard-Garcia, Ashley N., Miller, Jami L., Mizukawa, Yoshiko, Molho-Pessach, Vered, Molina-Ruiz, Ana María, Monheit, Gary D., Morrell, Dean S., Mowad, Christen M., Mahindra Nayyar, Priya, Nelson, Amanda M., Nghiem, Paul, Ní Raghallaigh, Síona, Nixon AM, Rosemary L., Noguera-Morel, Lucero, North, Paula E., Nunley, Julia R., Nyström, Alexander, Teresa Ochoa, Maria, Oji, Vinzenz, Olbricht, Suzanne, Orlow, Seth J., Ortega-Loayza, Alex G., Ortonne, Jean-Paul, Oschmann, Anna, Paller, Amy S., Pasquali, Paola, Passeron, Thierry, Patterson, James W., P. Pereira, Manuel, Pfisterer, Karin, Piette, Warren W., Pincus, Laura B., Maria Piraccini, Bianca, Pittelkow, Mark R., Plewig, Gerd, Pollack, Sheldon V., Powell, Julie, Prausnitz, Mark R., Quist, Jennifer E., Quist, Sven R., Qureshi, Abrar A., Raimer, Ben G., Raimer, Sharon S., Raimer-Goodman, Lauren, Ramachandran, Sarika, Ramos-e-Silva, Marcia, Rapini, Ronald P., Ratner, Désirée, Reboli, Annette C., Reider, Norbert, Reizner, George T., Requena, Celia, Requena, Luis, Reynolds, Rachel, Cristina Ribeiro de Castro, Maria, Rich, Phoebe, Richard, Gabriele, Richards, Shawn W., Richert, Bertrand, Ringpfeil, Franziska, Röcken, Martin, Rogers MD FAAD, Nicole E., Rohrer, Thomas E., Rongioletti, Franco, Rosen, Cheryl F., Rosenbach, Misha A., Rudnicka, Lidia, Rünger, Thomas M., Saggini, Andrea, Saini, Sarbjit S., Sakamoto, Fernanda H., Saurat, Jean-Hilaire, Schadt, Courtney R., Ann Mc Leish, Stephanie, Schaffer, Julie V., Schaller, Martin, Schmuth, Matthias, Schwarz, Thomas, Schwarzenberger, Kathryn, Seneschal, Julien, Shani-Adir, Ayelet, Shapiro, Lori E., Shear, Neil H., Shi, Vivian Y., Shields, Bridget E., Shiohara, Tetsuo, Sidbury, Robert, Siller, Alfredo, Jr., Sivamani, Raja, Smith, Gideon P., Smith, Michael L., Smoller, Bruce R., Sommer, Lacy L., Sontheimer, Richard D., Sorg, Olivier, Peter Soyer, H., Sprecher, Eli, Ständer, Sonja, Stary, Angelika, Stary, Georg, Steadmon, Matthew, Stefanato, Catherine M., Seabury Stone, Mary, Stratman, Erik J., Süßmuth, Kira, Swetter, Susan M., Sybert, Virginia P., Hoon Tan, Suat, Tanzi, Elizabeth, Liang Tey, Hong, Tharp, Michael D., Tomasini, Carlo F., Torrelo, Antonio, Tosti, Antonella, Travelute, Christie R., Treister, Nathaniel, Trindade de Almeida, Ada Regina, Tsao, Hensin, Tschandl, Philipp, Tüting, Thomas, Tyring, Stephen K., Uitto, Jouni, van de Kerkhof, Peter C.M., Vandergriff, Travis W., Veness, Michael J., Verhave, Brendon, Vidimos, Allison T., Virós, Amaya, Ann Vleugels, Ruth, Walker, David H., Wanat, Karolyn A., Wang, Etienne C.E., Wang, Jennifer Y., Watsky, Kalman L., Weber, Benedikt, Weiss, Robert A., Weisshaar, Elke, Weninger, Wolfgang, Werth, Victoria P., Wesley, Naissan O., Weston, Gillian K., Whittaker, Sean, Wiesner, Thomas, Mark Wilkinson, S., Willemze, Rein, Winfield, Harry L., Wolf, Ingrid H., Wolf, Peter, Wolverton, Stephen E., Wood, Gary S., Yancey, Kim B., Yang, Eric J., Yang, Yul W., Yosipovitch, Gil, Rasar Young, Melissa, Zaba, Lisa C., Zachary, Christopher B., Zaenglein, Andrea L., Zalaudek, Iris, and Zone, John J.

Published
2025
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10. VEXAS Syndrome: Histiocytoid Cells With Feathery Cytoplasm as a Clue to the Diagnosis.

Author

Ko, Christine J., Odell, Ian, Gehlhausen, Jeffrey R., Leventhal, Jonathan, McNiff, Jennifer M., and Zubek, Amanda

Subjects
*SWEET'S syndrome, *CYTOPLASM, *DIAGNOSIS, *SYNDROMES, *ENZYMES
Abstract

ABSTRACT VEXAS (Vacuoles, E1‐ubiquitin activating enzyme UBA1 variant, X‐linked, Autoinflammatory, Somatic) syndrome was initially described as having mature neutrophil‐predominant infiltrates. More recent reports suggest that infiltrates can be composed of variable cell types. We report three cases of VEXAS syndrome with seven total biopsies having in common histiocytoid cells with feathery cytoplasm; these cells may be a potential clue to the diagnosis. [ABSTRACT FROM AUTHOR]

Published
2024
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11. Contributors

Author

Adams, David R., Adams, Stewart, Amin, Mina, Avashia-Khemka, Nidhi, Beck, Kristen M., Bhatia, Bhavnit K., Bhatia, Sravya Mallam, Bhutani, Tina, Braue, Jonathan A., Brodell, Robert T., Brodland, David G., Broussard-Steinberg, Candace, Callen, Jeffrey P., Camisa, Charles, Chehade, Ahmad, Chima, Margot, Clark, Richard A., Cline, Abigail, Cordoro, Kelly M., Cruz Ramón, Julio C., Davis, Loretta S., Feld, Salma de la, M.C. DeKlotz, Cynthia, Duprat, Gabrielle-Eugenie, Eaglstein, William H., Elston, Carly A., Elston, Dirk M., Emerson, Ashley N., Fabbro, Stephanie K., Feldman, Steven R., Ferris, Laura K., Foley, Kelly A., Forman, Seth B., Garofola, Craig, Gehlhausen, Jeffrey R., Gelfand, Joel M., Girardi, Michael, Goerge, Tobias, Gordon, Kenneth B., Greiling, Teri M., Grinich, Erin E., Grove, Daniel, Gupta, Aditya K., Haggstrom, Anita, Haley, Christopher T., Hall, Russell P., III, Hamzavi, Iltefat, Heffernan, Michael P., Helfrich, Yolanda R., Hessel, Adam B., Higgins, Shauna, High, Whitney A., Hrynewycz, Katherine, Hsu, Sylvia, Huether, Michael J., Isaacs, Michael J., Kaminer, Michael S., Kandula, Prasanthi, Kandula, Swetha, Kang, Sewon, Kapp, Marshall B., Kim, Hee Jin, Kim, Sa Rang, Kingsley, Melanie, Knowles, Sandra R., Koo, John Y.M., Kulp-Shorten, Carol L., Landis, Megan N., Lebwohl, Mark G., Lee, Erica B., Lee, Katherine B., Lewis, Amy B., Lim, Geoffrey F.S., Lim, Henry W., Lockshin, Benjamin N., Luger, Thomas A., Majerowski, Jacquelyn, Mark, Lawrence A., Marshall, Dana, Martell, David, Mays, Rachel R., McElhiney, Linda F., Mirowski, Ginat W., Mori, Shoko, Motaparthi, Kiran, Mui, Uyen Ngoc, Murray, Christian, Nielson, Colton, Noe, Megan H., Okoye, Ginette A., Owen, Cindy England, Patton, Timothy, Piette, Warren W., Rahnama-Moghadam, Sahand, Ramachandran, Sarika Manoj, Rancour, Elizabeth A., Rao, Jaggi, Rosenbach, Misha, Roy, Katherine, Sachs, Dana L., Sami, Naveed, Sawaya, Marty E., Schadt, Courtney R., Schaffenburg, William, Schlosser, Bethanee J., Sekhon, Sahil, Shah, Vidhi V., Shapiro, Lori E., Shear, Neil H., Sheehan, Michael, Simpson, Eric L., Snodgrass, Alexandra, Solish, Nowell, Somani, Ally-Khan, Somani, Najwa, Strober, Bruce, Sulk, Mathias, Suozzi, Kathleen C., Tharp, Michael D., Tomayko, Mary M., Tyring, Stephen K., Vogt-Schiavo, Kaitlin, Vuppalanchi, Raj, Wang, Steve Q., Weston, Gillian, Wolverton, Stephen E., Wu, Jashin J., Wysong, Ashley, Zic, John, and Zwerner, Jeffrey P.

Published
2021
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13. Toxoplasmosis: The Heart of the Diagnosis.

Author

England, James H, Bailin, Samuel S, Gehlhausen, Jeffrey R, and Rubin, Donald H

Abstract

Toxoplasma gondii is a common parasite that infects warm-blooded animals, including humans, and is a foodborne pathogen. We report a case of acute toxoplasmosis in a 76-year-old man after ingestion of the undercooked heart of a white-tailed deer (Odocoileus virginianus) in Tennessee. The patient's adult grandson, who also consumed part of the heart, became ill with nearly identical symptoms, though he did not seek medical care. This case highlights important public health concerns about deer-to-human transmission of Toxoplasma. [ABSTRACT FROM AUTHOR]

Published
2019
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14. Ketotifen Modulates Mast Cell Chemotaxis to Kit-Ligand, but Does Not Impact Mast Cell Numbers, Degranulation, or Tumor Behavior in Neurofibromas of Nf1 -Deficient Mice.

Author

Burks CA, Rhodes SD, Bessler WK, Chen S, Smith A, Gehlhausen JR, Hawley ET, Jiang L, Li X, Yuan J, Lu Q, Jacobsen M, Sandusky GE, Jones DR, Clapp DW, and Blakeley JO

Subjects
Animals, Histamine H1 Antagonists pharmacology, Ketotifen pharmacology, Mice, Stem Cell Factor, Chemotaxis physiology, Histamine H1 Antagonists therapeutic use, Ketotifen therapeutic use, Mast Cells drug effects, Neurofibroma genetics, Neurofibromin 1 deficiency
Abstract

Neurofibromatosis Type 1 (NF1) is one of the most common genetic tumor predisposition syndromes in humans. Mutant NF1 results in dysregulated RAS allowing neoplasms throughout the neuroaxis. Plexiform neurofibromas (pNF) afflict up to 50% of patients with NF1. They are complex tumors of the peripheral nerve that cause major morbidity via nerve dysregulation and mortality via conversion to malignant sarcoma. Genetically engineered mouse models (GEMM) of NF1 provide valuable insights for the identification of therapies that have utility in people with pNF. Preclinical studies in GEMMs implicate mast cells and the c-Kit/Kit ligand pathway in pNF tumorigenesis. Kit ligand is a potent chemokine secreted by tumorigenic, Nf1 -deficient Schwann cells. Ketotifen is an FDA-approved drug for the treatment of allergic conjunctivitis and asthma that promotes mast cell stabilization and has been used in prior case studies to treat or prevent pNFs. This study investigated the effect of ketotifen on mast cell infiltration and degranulation in the presence and absence of Kit ligand provocation and the effect of ketotifen on shrinking or preventing pNF formation in the Nf1 flox/flox ; PostnCre + GEMM. Ketotifen decreased mast cell infiltration in response to exogenous Kit ligand administration, but did not affect mast cell degranulation. Importantly, ketotifen did not reduce mast cells numbers or activity in pNF and did not prevent pNF formation or decrease the volume of established pNF despite administration of pharmacologically active doses. These findings suggest that ketotifen has limited use as monotherapy to prevent or reduce pNF burden in the setting of Nf1 mutations., (©2019 American Association for Cancer Research.)

Published
2019
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15. A proteasome-resistant fragment of NIK mediates oncogenic NF-κB signaling in schwannomas.

Author

Gehlhausen JR, Hawley E, Wahle BM, He Y, Edwards D, Rhodes SD, Lajiness JD, Staser K, Chen S, Yang X, Yuan J, Li X, Jiang L, Smith A, Bessler W, Sandusky G, Stemmer-Rachamimov A, Stuhlmiller TJ, Angus SP, Johnson GL, Nalepa G, Yates CW, Wade Clapp D, and Park SJ

Subjects
Animals, Autocrine Communication genetics, Carcinogenesis genetics, Caspase 1 genetics, Cell Proliferation genetics, Disease Models, Animal, Gene Expression Regulation, Neoplastic, Hepatocyte Growth Factor genetics, Humans, Mice, Molecular Targeted Therapy, NF-kappa B genetics, Neurilemmoma complications, Neurilemmoma drug therapy, Neurilemmoma pathology, Neurofibromatosis 2 complications, Neurofibromatosis 2 drug therapy, Neurofibromatosis 2 pathology, Proteasome Endopeptidase Complex genetics, Proto-Oncogene Mas, Proto-Oncogene Proteins c-met genetics, Schwann Cells, Signal Transduction genetics, NF-kappaB-Inducing Kinase, Neurilemmoma genetics, Neurofibromatosis 2 genetics, Neurofibromin 2 genetics, Protein Serine-Threonine Kinases genetics
Abstract

Schwannomas are common, highly morbid and medically untreatable tumors that can arise in patients with germ line as well as somatic mutations in neurofibromatosis type 2 (NF2). These mutations most commonly result in the loss of function of the NF2-encoded protein, Merlin. Little is known about how Merlin functions endogenously as a tumor suppressor and how its loss leads to oncogenic transformation in Schwann cells (SCs). Here, we identify nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)-inducing kinase (NIK) as a potential drug target driving NF-κB signaling and Merlin-deficient schwannoma genesis. Using a genomic approach to profile aberrant tumor signaling pathways, we describe multiple upregulated NF-κB signaling elements in human and murine schwannomas, leading us to identify a caspase-cleaved, proteasome-resistant NIK kinase domain fragment that amplifies pathogenic NF-κB signaling. Lentiviral-mediated transduction of this NIK fragment into normal SCs promotes proliferation, survival, and adhesion while inducing schwannoma formation in a novel in vivo orthotopic transplant model. Furthermore, we describe an NF-κB-potentiated hepatocyte growth factor (HGF) to MET proto-oncogene receptor tyrosine kinase (c-Met) autocrine feed-forward loop promoting SC proliferation. These innovative studies identify a novel signaling axis underlying schwannoma formation, revealing new and potentially druggable schwannoma vulnerabilities with future therapeutic potential.

Published
2019
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16. Chemopreventative celecoxib fails to prevent schwannoma formation or sensorineural hearing loss in genetically engineered murine model of neurofibromatosis type 2.

Author

Wahle BM, Hawley ET, He Y, Smith AE, Yuan J, Masters AR, Jones DR, Gehlhausen JR, Park SJ, Conway SJ, Clapp DW, and Yates CW

Abstract

Mutations in the tumor suppressor gene NF2 lead to Neurofibromatosis type 2 (NF2), a tumor predisposition syndrome characterized by the development of schwannomas, including bilateral vestibular schwannomas with complete penetrance. Recent work has implicated the importance of COX-2 in schwannoma growth. Using a genetically engineered murine model of NF2, we demonstrate that selective inhibition of COX-2 with celecoxib fails to prevent the spontaneous development of schwannomas or sensorineural hearing loss in vivo , despite elevated expression levels of COX-2 in Nf2 -deficient tumor tissue. These results suggest that COX-2 is nonessential to schwannomagenesis and that the proposed tumor suppressive effects of NSAIDs on schwannomas may occur through COX-2 independent mechanisms., Competing Interests: CONFLICTS OF INTEREST The authors declare no potential conflicts of interest.

Published
2017
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