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26 results on '"Cohen, Jeffrey"'

1. The International Consensus Classification of Mature Lymphoid Neoplasms: a report from the Clinical Advisory Committee

Author

Campo, Elias, Jaffe, Elaine S., Cook, James R., Quintanilla-Martinez, Leticia, Swerdlow, Steven H., Anderson, Kenneth C., Brousset, Pierre, Cerroni, Lorenzo, de Leval, Laurence, Dirnhofer, Stefan, Dogan, Ahmet, Feldman, Andrew L., Fend, Falko, Friedberg, Jonathan W., Gaulard, Philippe, Ghia, Paolo, Horwitz, Steven M., King, Rebecca L., Salles, Gilles, San-Miguel, Jesus, Seymour, John F., Treon, Steven P., Vose, Julie M., Zucca, Emanuele, Advani, Ranjana, Ansell, Stephen, Au, Wing-Yan, Barrionuevo, Carlos, Bergsagel, Leif, Chan, Wing C., Cohen, Jeffrey I., d'Amore, Francesco, Davies, Andrew, Falini, Brunangelo, Ghobrial, Irene M., Goodlad, John R., Gribben, John G., Hsi, Eric D., Kahl, Brad S., Kim, Won-Seog, Kumar, Shaji, LaCasce, Ann S., Laurent, Camille, Lenz, Georg, Leonard, John P., Link, Michael P., Lopez-Guillermo, Armando, Mateos, Maria Victoria, Macintyre, Elizabeth, Melnick, Ari M., Morschhauser, Franck, Nakamura, Shigeo, Narbaitz, Marina, Pavlovsky, Astrid, Pileri, Stefano A., Piris, Miguel, Pro, Barbara, Rajkumar, Vincent, Rosen, Steven T., Sander, Birgitta, Sehn, Laurie, Shipp, Margaret A., Smith, Sonali M., Staudt, Louis M., Thieblemont, Catherine, Tousseyn, Thomas, Wilson, Wyndham H., Yoshino, Tadashi, Zinzani, Pier-Luigi, Dreyling, Martin, Scott, David W., Winter, Jane N., and Zelenetz, Andrew D.

Published
2022
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2. SARS-CoV-2–specific T cells are rapidly expanded for therapeutic use and target conserved regions of the membrane protein

Author

Keller, Michael D., Harris, Katherine M., Jensen-Wachspress, Mariah A., Kankate, Vaishnavi V., Lang, Haili, Lazarski, Christopher A., Durkee-Shock, Jessica, Lee, Ping-Hsien, Chaudhry, Kajal, Webber, Kathleen, Datar, Anushree, Terpilowski, Madeline, Reynolds, Emily K., Stevenson, Eva M., Val, Stephanie, Shancer, Zoe, Zhang, Nan, Ulrey, Robert, Ekanem, Uduak, Stanojevic, Maja, Geiger, Ashley, Liang, Hua, Hoq, Fahmida, Abraham, Allistair A., Hanley, Patrick J., Cruz, C. Russell, Ferrer, Kathleen, Dropulic, Lesia, Gangler, Krista, Burbelo, Peter D., Jones, R. Brad, Cohen, Jeffrey I., and Bollard, Catherine M.

Published
2020
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5. Characterization and treatment of chronic active Epstein-Barr virus disease: a 28-year experience in the United States

Author

Cohen, Jeffrey I., Jaffe, Elaine S., Dale, Janet K., Pittaluga, Stefania, Heslop, Helen E., Rooney, Cliona M., Gottschalk, Stephen, Bollard, Catherine M., Rao, V. Koneti, Marques, Adriana, Burbelo, Peter D., Turk, Siu-Ping, Fulton, Rachael, Wayne, Alan S., Little, Richard F., Cairo, Mitchell S., El-Mallawany, Nader K., Fowler, Daniel, Sportes, Claude, Bishop, Michael R., Wilson, Wyndham, and Straus, Stephen E.

Published
2011
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8. Effect of Bruton Tyrosine Kinase Inhibitor on Serologic and Cellular Immune Responses to Recombinant Zoster Vaccine

Author

Pleyer, Christopher, primary, Laing, Kerry J, additional, Ali, Mir, additional, McClurkan, Christopher L, additional, Soto, Susan, additional, Ahn, Inhye E., additional, Nierman, Pia, additional, Maddux, Emeline, additional, Lotter, Jennifer, additional, Superata, Jeanine, additional, Tian, Xin, additional, Gaglione, Erika M, additional, Wiestner, Adrian, additional, Cohen, Jeffrey, additional, Koelle, David M, additional, and Sun, Clare, additional

Published
2021
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10. Impaired Sars-Cov-2 Specific Antibody Responses in Patients Treated with Anti-CD20 Antibodies

Author

Sottini, Alessandra, primary, Imberti, Luisa, additional, Paghera, Simone, additional, Previcini, Vanessa, additional, Cattaneo, Chiara, additional, Quiros-Roldan, Eugenia, additional, Capra, Ruggero, additional, Rossi, Giuseppe, additional, Dobbs, Kerry, additional, Shaw, Elana, additional, Notarangelo, Luigi D., additional, Burbelo, Peter, additional, and Cohen, Jeffrey, additional

Published
2020
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13. Response to the Shingrix Varicella Zoster Virus (VZV) Vaccine in Patients with Chronic Lymphocytic Leukemia (CLL) That Are Treatment Naive or Treated with a Bruton's Tyrosine Kinase Inhibitor (BTK-I)

Author

Pleyer, Christopher, primary, Cohen, Jeffrey, additional, Soto, Susan, additional, Ali, Mir, additional, Ahn, Inhye E, additional, Nierman, Pia, additional, Valdez, Janet, additional, Lotter, Jennifer, additional, Superata, Jeanine, additional, Tian, Xin, additional, Wiestner, Adrian, additional, and Sun, Clare, additional

Published
2019
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14. Hydroa vacciniforme–like lymphoproliferative disorder: an EBV disease with a low risk of systemic illness in whites

Author

Cohen, Jeffrey I., primary, Manoli, Irini, additional, Dowdell, Kennichi, additional, Krogmann, Tammy A., additional, Tamura, Deborah, additional, Radecki, Pierce, additional, Bu, Wei, additional, Turk, Siu-Ping, additional, Liepshutz, Kelly, additional, Hornung, Ronald L., additional, Fassihi, Hiva, additional, Sarkany, Robert P., additional, Bonnycastle, Lori L., additional, Chines, Peter S., additional, Swift, Amy J., additional, Myers, Timothy G., additional, Levoska, Melissa A., additional, DiGiovanna, John J., additional, Collins, Francis S., additional, Kraemer, Kenneth H., additional, Pittaluga, Stefania, additional, and Jaffe, Elaine S., additional

Published
2019
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16. Chronic active Epstein-Barr virus infection: a novel cause of lymphocytic variant hypereosinophilic syndrome

Author

Klion, Amy D., Mejia, Rojelio, Cowen, Edward W., Dowdell, Kennichi C., Dunleavy, Kieron, Fahle, Gary A., Holland-Thomas, Nicole, Maric, Irina, Pittaluga, Stefania, Raffeld, Mark, Santos, Carlo, Stetler-Stevenson, Maryalice, Krogmann, Tammy, Shatzer, Amber N., Turk, Siu-Ping, Yin, Yuzhi, Xi, Liqiang, Prussin, Calman, and Cohen, Jeffrey I.

Published
2013
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17. Nivolumab in Lymphomatoid Granulomatosis (LYG) and Other Epstein-Barr Virus (EBV)-Positive Lymphoproliferative Disorders (LPDs) and Non-Hodgkin Lymphomas (NHLs) with Systemic and/or CNS Involvement: Preliminary Analysis of Efficacy and Safety from an Ongoing Phase II Study

Author

Dalela, Disha, Lakhotia, Rahul, Pittaluga, Stefania, Muppidi, Jagan R., Phelan, James D, Pradhan, Amynah, Evans, Sarah, Morrison, Candis, Tadese, Atekelt, Steinberg, Seth M., Cohen, Jeffrey, Jaffe, Elaine S., Wilson, Wyndham H, Roschewski, Mark, and Melani, Christopher

Abstract

Background:Programmed cell death protein-1 (PD-1) is a signaling molecule on the surface of T-cells that suppresses the cytotoxic effects of T-cells on tumor cells. We previously demonstrated increased PD-1 expression on CD8+ T-cells compared to healthy controls in pts with LYG, which could be reversed with immunotherapy using interferon alpha-2b (Melani et al. Lancet Haematol. 2023). Additionally, elevated expression of programmed death-ligand 1 (PD-L1) has been observed in other EBV-LPDs and NHLs as well as in chronic viral infections, such as EBV. Given this likely shared disease pathobiology, we hypothesized that treatment with the anti-PD-1 antibody, nivolumab, may reverse T-cell exhaustion and result in anti-tumor responses in pts with LYG and other EBV-LPDs and NHLs, including those with systemic and/or CNS involvement.

Published
2023
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18. Immune Characteristics Associated with Lymphomatoid Granulomatosis and Outcome Following Treatment with Interferon-Alpha

Author

Dunleavy, Kieron, primary, Chattopadhyay, Pratip, additional, Kawada, Junichi, additional, Calattini, Sara, additional, Gostick, Emma, additional, Price, David, additional, Roderer, Mario, additional, Cohen, Jeffrey, additional, Grant, Nicole, additional, Pittaluga, Stefania, additional, Janik, John E, additional, Jaffe, Elaine S, additional, and Wilson, Wyndham H., additional

Published
2010
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19. Somatic Fas Mutations Account for Nearly One Third of Autoimmune Lymphoproliferative Syndrome (ALPS) Cases with Previously Unknown Genetic Mutations.

Author

Dowdell, Kennichi, primary, Niemela, Julie, additional, Price, Susan, additional, Davis, Joie, additional, Perkins, Katie, additional, Dale, Janet, additional, Puck, Jennifer M., additional, Oliveira, Joao Bosco, additional, Cohen, Jeffrey, additional, Fleisher, Thomas, additional, and Rao, V. Koneti, additional

Published
2009
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20. Dermatofibrosarcoma Protuberans in 3 Patients with ADA-SCID

Author

Kesserwan, Chimene, primary, Sokolic, Robert A., primary, Heselmeyer, Kerstin, primary, Ortiz-Melendez, Clarymar, primary, Cohen, Jeffrey, primary, Jagadeesh, Jaya, primary, Garabedian, Elizabeth, primary, Baird, Kristin, primary, Wayne, Alan S., primary, Cowen, Edward W., primary, Pittaluga, Stefania, primary, Lee, Chyi-Chia Richard, primary, Sherry, Richard, primary, Bridge, Julia, primary, Finlayson, Laura, primary, Walsh, Noreen, primary, Issekutz, Andrew, primary, and Candotti, Fabio, primary

Published
2008
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22. Mutations in GATA2cause human NK cell deficiency with specific loss of the CD56brightsubset

Author

Mace, Emily M., Hsu, Amy P., Monaco-Shawver, Linda, Makedonas, George, Rosen, Joshua B., Dropulic, Lesia, Cohen, Jeffrey I., Frenkel, Eugene P., Bagwell, John C., Sullivan, John L., Biron, Christine A., Spalding, Christine, Zerbe, Christa S., Uzel, Gulbu, Holland, Steven M., and Orange, Jordan S.

Abstract

Mutations in the transcription factor GATA2 underlie the syndrome of monocytopenia and B- and natural killer (NK)-cell lymphopenia associated with opportunistic infections and cancers. In addition, patients have recurrent and severe viral infections. NK cells play a critical role in mediating antiviral immunity. Human NK cells are thought to mature in a linear fashion, with the CD56brightstage preceding terminal maturation to the CD56dimstage, considered the most enabled for cytotoxicity. Here we report an NK cell functional defect in GATA2-deficient patients and extend this genetic lesion to what is considered to be the original NK cell-deficient patient. In most cases, GATA2 deficiency is accompanied by a severe reduction in peripheral blood NK cells and marked functional impairment. The NK cells detected in peripheral blood of some GATA2-deficient patients are exclusively of the CD56dimsubset, which is recapitulated on in vitro NK cell differentiation. In vivo, interferon α treatment increased NK cell number and partially restored function but did not correct the paucity of CD56brightcells. Thus, GATA2 is required for the maturation of human NK cells and the maintenance of the CD56brightpool in the periphery. Defects in GATA2 are a novel cause of profound NK cell dysfunction.

Published
2013
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23. Somatic FASmutations are common in patients with genetically undefined autoimmune lymphoproliferative syndrome

Author

Dowdell, Kennichi C., Niemela, Julie E., Price, Susan, Davis, Joie, Hornung, Ronald L., Oliveira, João Bosco, Puck, Jennifer M., Jaffe, Elaine S., Pittaluga, Stefania, Cohen, Jeffrey I., Fleisher, Thomas A., and Rao, V. Koneti

Abstract

Autoimmune lymphoproliferative syndrome (ALPS) is characterized by childhood onset of lymphadenopathy, hepatosplenomegaly, autoimmune cytopenias, elevated numbers of double-negative T (DNT) cells, and increased risk of lymphoma. Most cases of ALPS are associated with germline mutations of the FASgene (type Ia), whereas some cases have been noted to have a somatic mutation of FAS primarily in their DNT cells. We sought to determine the proportion of patients with somatic FASmutations among a group of our ALPS patients with no detectable germline mutation and to further characterize them. We found more than one-third (12 of 31) of the patients tested had somatic FASmutations, primarily involving the intracellular domain of FAS resulting in loss of normal FAS signaling. Similar to ALPS type Ia patients, the somatic ALPS patients had increased DNT cell numbers and elevated levels of serum vitamin B12, interleukin-10, and sFAS-L. These data support testing for somatic FASmutations in DNT cells from ALPS patients with no detectable germline mutation and a similar clinical and laboratory phenotype to that of ALPS type Ia. These findings also highlight the potential role for somatic mutations in the pathogenesis of nonmalignant and/or autoimmune hematologic conditions in adults and children.

Published
2010
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24. Distinct EBV and CMV reactivation patterns following antibody-based immunosuppressive regimens in patients with severe aplastic anemia

Author

Scheinberg, Phillip, Fischer, Steven H., Li, Li, Nunez, Olga, Wu, Colin O., Sloand, Elaine M., Cohen, Jeffrey I., Young, Neal S., and John Barrett, A.

Abstract

The natural history of EBV and CMV reactivation and the potential for serious complications following antibody-based immunosuppressive treatment for bone marrow failure syndromes in the absence of transplantation is not known. We monitored blood for EBV and CMV reactivation by polymerase chain reaction (PCR) weekly in 78 consecutive patients (total of 99 immunosuppressive courses) with aplastic anemia. Four regimens were studied: (1) HC, horse ATG/cyclosporine; (2) HCS, horse ATG/CsA/sirolimus; (3) RC, rabbit ATG/CsA; and (4) CP, alemtuzumab. There were no cases of EBV or CMV disease, but EBV reactivation occurred in 82 (87%) of 94 and CMV reactivation in 19 (33%) of 57 seropositive patients after starting immunosuppression. The median peak EBV copies were higher in the RC group when compared with HC, HCS, and alemtuzumab (P < .001). The median duration of PCR positivity for EBV was higher in the RC group compared with HC, HCS, and alemtuzumab (P = .001). Subclinical reactivation of both EBV and CMV is common and nearly always self-limited in patients with bone marrow failure receiving immunosuppression; different regimens are associated with different intensity of immunosuppression as measured by viral load and lymphocyte count; and viral reactivation patterns differ according to immunosuppressive regimens.

Published
2007
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25. Mutations in GATA2 cause human NK cell deficiency with specific loss of the CD56bright subset.

Author

Mace, Emily M., Hsu, Amy P., Monaco-Shawver, Linda, Makedonas, George, Rosen, Joshua B., Dropulic, Lesia, Cohen, Jeffrey I., Frenkel, Eugene P., Bagwell, John C., Sullivan, John L., Biron, Christine A., Spalding, Christine, Zerbe, Christa S., Uzel, Gulbu, Holland, Steven M., and Orange, Jordan S.

Subjects
*KILLER cells, *LYMPHOPENIA, *ANTIVIRAL agents, *IMMUNITY, *PERIPHERAL circulation, *CELL physiology
Abstract

Mutations in the transcription factor GATA2 underlie the syndrome of monocytopenia and B- and natural killer (NK)-cell lymphopenia associated with opportunistic infections and cancers. In addition, patients have recurrent and severe viral infections. NK cells play a critical role in mediating antiviral immunity. Human NK cells are thought to mature in a linear fashion, with the CD56bright stage preceding terminal maturation to the CD56dim stage, considered the most enabled for cytotoxicity. Here we report an NK cell functional defect in GATA2-deficient patients and extend this genetic lesion to what is considered to be the original NK cell-deficient patient. In most cases, GATA2 deficiency is accompanied by a severe reduction in peripheral blood NK cells and marked functional impairment. The NK cells detected in peripheral blood of some GATA2-deficient patients are exclusively of the CD56dim subset, which is recapitulated on in vitro NK cell differentiation. In vivo, interferon α treatment increased NK cell number and partially restored function but did not correót the paucity of CD56bright cells. Thus, GATA2 is required for the maturation of human NK cells and the maintenance of the CD56bright pool in the periphery. Defects in GATA2 are a novel cause of profound NK cell dysfunction. [ABSTRACT FROM AUTHOR]

Published
2013
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26. Chronic active Epstein-Barr virus infection: a novel cause of lymphocytic variant hypereosinophilic syndrome.

Author

Kilon, Amy D., Melia, Rojelio, Cowen, Edward W., Dowdell, Kennichi C., Dunleavy, Kieron, Fahie, Gary A., Holland-Thomas, Nicole, Maric, Irina, Pittaluga, Stefania, Raffeld, Mark, Santos, Carlo, Stetler-Stevenson, Maryalice, Krogmann, Tammy, Shatzer, Amber N., Turk, Siu-Ping, Yuzhi Yin, Liqiang Xi, Prussin, Calman, and Cohen, Jeffrey I.

Subjects
*EPSTEIN-Barr virus diseases, *HYPEREOSINOPHILIC syndrome, *PATIENTS
Abstract

A letter to the editor is presented regarding a case of lymphocytic variant hypereosinophilic syndrome (LHES) in a patient with chronic active Epstein-Barr virus (CAEBV) infection.

Published
2013

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