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2. Unifying mechanism for different fibrotic diseases

Author

Wernig, Gerlinde, Chen, Shih-Yu, Cui, Lu, Van Neste, Camille, Tsai, Jonathan M., Kambham, Neeraja, Vogel, Hannes, Natkunam, Yaso, Gilliland, D. Gary, Nolan, Garry, and Weissman, Irving L.

Published
2017

3. P115: Distinct signaling pathways and checkpoint molecule expression across histological subtypes of nodular lymphocyte-predominant Hodgkin lymphoma

Author

Kalashnikov, Ilja, primary, Kositsky, Rachel, additional, Karjalainen-Lindsberg, Marja-Liisa, additional, Dunkel, Johannes, additional, Pasanen, Annika, additional, Love, Cassandra, additional, Parker, Clay, additional, Ondrejka, Sarah, additional, Hsi, Eric, additional, Juskevicius, Ridas, additional, Evans, Andrew, additional, Evans, Andrew G., additional, Czader, Magdalena, additional, Wang, Lin, additional, Xu, Mina, additional, Paulson, Nathan, additional, Pedersen, Mette ølgod, additional, Ortved Gang, Anne, additional, Koff, Jean, additional, Mccal, Chad, additional, Natkunam, Yaso, additional, Louissaint, Abner, additional, Shin Yeu, Ong, additional, Pillai, Raju, additional, Chapman, Jennifer, additional, Amador, Catalina, additional, Chadburn, Amy, additional, Goswami, Rashmi, additional, Behdad, Amir, additional, Sojitra, Payal, additional, Tse, Eric, additional, Kikkeri, Naresh, additional, Nasresh, Kikkeri N., additional, Fedoriw, Yuri, additional, Dave, Sandeep, additional, and Leppä, Sirpa, additional

Published
2022
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4. Conditional expression of HGAL leads to the development of diffuse large B-cell lymphoma in mice

Author

Raboso-Gallego, Javier, primary, Casado-García, Ana, additional, Jiang, Xiaoyu, additional, Isidro-Hernández, Marta, additional, Gentles, Andrew J., additional, Zhao, Shuchun, additional, Natkunam, Yaso, additional, Blanco, Oscar, additional, Domínguez, Verónica, additional, Pintado, Belén, additional, Alonso-López, Diego, additional, De Las Rivas, Javier, additional, Vicente-Dueñas, Carolina, additional, Lossos, Izidore S., additional, and Sanchez-Garcia, Isidro, additional

Published
2021
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8. Prognostic Significance of MYC Rearrangement and Translocation Partner in Diffuse Large B-Cell Lymphoma: A Study by the Lunenburg Lymphoma Biomarker Consortium

Author

Rosenwald, Andreas, primary, Bens, Susanne, additional, Advani, Ranjana, additional, Barrans, Sharon, additional, Copie-Bergman, Christiane, additional, Elsensohn, Mad-Helenie, additional, Natkunam, Yaso, additional, Calaminici, Maria, additional, Sander, Birgitta, additional, Baia, Maryse, additional, Smith, Alexandra, additional, Painter, Daniel, additional, Pham, Luu, additional, Zhao, Shuchun, additional, Ziepert, Marita, additional, Jordanova, Ekaterina S., additional, Molina, Thierry J., additional, Kersten, Marie José, additional, Kimby, Eva, additional, Klapper, Wolfram, additional, Raemaekers, John, additional, Schmitz, Norbert, additional, Jardin, Fabrice, additional, Stevens, Wendy B.C., additional, Hoster, Eva, additional, Hagenbeek, Anton, additional, Gribben, John G., additional, Siebert, Reiner, additional, Gascoyne, Randy D., additional, Scott, David W., additional, Gaulard, Philippe, additional, Salles, Gilles, additional, Burton, Catherine, additional, de Jong, Daphne, additional, Sehn, Laurie H., additional, and Maucort-Boulch, Delphine, additional

Published
2019
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9. Abstract LB-102: Extranodal natural killer/T cell lymphoma (ENKTL) exhibits an unprecedented degree of global DNA hypermethylation, providing a potent targeted therapy in vivo

Author

Weigel, Christoph, primary, Mundy-Bosse, Bethany L., additional, Wu, Yue-Zhong, additional, McConnell, Kathleen, additional, Mishra, Anjali, additional, Caligiuri, Michael A., additional, Baiocchi, Robert A., additional, Natkunam, Yaso, additional, Porcu, Pierluigi, additional, Brammer, Jonathan, additional, Freud, Aharon G., additional, and Oakes, Christopher C., additional

Published
2019
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10. Prognostic Significance of Rearrangement and Translocation Partner in Diffuse Large B-Cell Lymphoma: A Study by the Lunenburg Lymphoma Biomarker Consortium.

Author

Rosenwald, Andreas, Bens, Susanne, Advani, Ranjana, Barrans, Sharon, Copie-Bergman, Christiane, Elsensohn, Mad-Helenie, Natkunam, Yaso, Calaminici, Maria, Sander, Birgitta, Baia, Maryse, Smith, Alexandra, Painter, Daniel, Pham, Luu, Zhao, Shuchun, Ziepert, Marita, Jordanova, Ekaterina S., Molina, Thierry J., Kersten, Marie José, Kimby, Eva, and Klapper, Wolfram

Published
2019
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11. Putting the ‘Activate’ in Activated B Cell-like Diffuse Large B Cell Lymphoma: A Role for the Noncanonical NF-κB Pathway

Author

Koff, Jean L., primary, Guo, Xiangxue, additional, Ramachandiran, Sampath, additional, Switchenko, Jeffrey M., additional, Mosunjac, Marina B., additional, Neill, Stewart G., additional, Mann, Karen, additional, Bagirov, Mahir, additional, Flowers, Christopher R., additional, Lossos, Izidore S., additional, Natkunam, Yaso, additional, Kowalski, Jeanne, additional, and Bernal-Mizrachi, Leon, additional

Published
2014
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12. Unifying mechanism for different fibrotic diseases.

Author

Tsai, Jonathan M., Wernig, Gerlinde, Weissman, Irving L., Lu Cui, Van Neste, Camille, Kambham, Neeraja, Vogel, Hannes, Natkunam, Yaso, Shih-Yu Chen, Nolan, Garry, and Gilliland, D. Gary

Subjects
FIBROSIS, IDIOPATHIC pulmonary fibrosis, PROGNOSIS, GENETICS, DIAGNOSIS
Abstract

Fibrotic diseases are not well-understood. They represent a number of different diseases that are characterized by the development of severe organ fibrosis without any obvious cause, such as the devastating diseases idiopathic pulmonary fibrosis (IPF) and scleroderma. These diseases have a poor prognosis comparable with endstage cancer and are uncurable. Given the phenotypic differences, it was assumed that the different fibrotic diseases also have different pathomechanisms. Here, we demonstrate that many endstage fibrotic diseases, including IPF; scleroderma; myelofibrosis; kidney-, pancreas-, and heart-fibrosis; and nonalcoholic steatohepatosis converge in the activation of the AP1 transcription factor c-JUN in the pathologic fibroblasts. Expression of the related AP1 transcription factor FRA2 was restricted to pulmonary artery hypertension. Induction of c-Jun in mice was sufficient to induce severe fibrosis in multiple organs and steatohepatosis, which was dependent on sustained c-Jun expression. Single cell mass cytometry revealed that c-Jun activates multiple signaling pathways in mice, including pAkt and CD47, which were also induced in human disease. αCD47 antibody treatment and VEGF or PI3K inhibition reversed various organ c-Jun-mediated fibroses in vivo. These data suggest that c-JUN is a central molecular mediator of most fibrotic conditions. [ABSTRACT FROM AUTHOR]

Published
2017
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20. Rapamycin inhibits the interleukin 10 signal transduction pathway and the growth of Epstein Barr virus B-cell lymphomas.

Author

Nepomuceno RR, Balatoni CE, Natkunam Y, Snow AL, Krams SM, and Martinez OM

Subjects
Animals, Cell Division drug effects, DNA-Binding Proteins metabolism, Enzyme Activation drug effects, Epstein-Barr Virus Infections etiology, Epstein-Barr Virus Infections metabolism, Epstein-Barr Virus Infections prevention & control, Herpesvirus 4, Human, Humans, Immunosuppressive Agents pharmacology, Interleukin-10 biosynthesis, Interleukin-10 metabolism, Interleukin-10 physiology, Janus Kinase 1, Lymphoma, B-Cell metabolism, Lymphoma, B-Cell prevention & control, Male, Mice, Protein-Tyrosine Kinases metabolism, STAT3 Transcription Factor, Signal Transduction drug effects, Trans-Activators metabolism, Transplantation adverse effects, Xenograft Model Antitumor Assays, Antibiotics, Antineoplastic pharmacology, Epstein-Barr Virus Infections drug therapy, Interleukin-10 antagonists & inhibitors, Lymphoma, B-Cell drug therapy, Lymphoma, B-Cell virology, Sirolimus pharmacology
Abstract

EBV-infected B-cell lymphomas are a potentially life-threatening complication in bone marrow and solid organ transplant recipients. Immunosuppressive drugs required to prevent allograft rejection also impair anti-EBV T-cell immunity, thereby increasing the risk of EBV-associated disease. Here we demonstrate that the immunosuppressant rapamycin (RAPA) has a strong antiproliferative effect in vitro on B-cell lines derived from organ transplant recipients with EBV-associated posttransplant lymphoproliferative disorder (PTLD). Furthermore, RAPA significantly inhibits or delays the growth of solid tumors established from EBV-infected B-cell lines in a xenogeneic mouse model of PTLD. RAPA acts via cell cycle arrest, induction of apoptosis, and, most importantly, inhibition of interleukin 10 secretion, a necessary autocrine growth factor. The reduced interleukin 10 production is accompanied by corresponding decreases in the constitutive activation of the growth-promoting transcription factors signal transducer and activator of transcription 1 and 3. Thus, RAPA can limit B-cell lymphoma growth while simultaneously providing immunosuppression to prevent graft rejection in patients who are otherwise at risk for EBV-associated PTLD. Moreover, these findings may have application to other EBV-associated malignancies.

Published
2003

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