Search

Your search keyword '"Aifantis, Iannis"' showing total 207 results
Start Over Author "Aifantis, Iannis" Search Limiters Academic (Peer-Reviewed) Journals
207 results on '"Aifantis, Iannis"'

2. Oncogenic drivers dictate immune control of acute myeloid leukemia

Author

Austin, Rebecca J., Straube, Jasmin, Halder, Rohit, Janardhanan, Yashaswini, Bruedigam, Claudia, Witkowski, Matthew, Cooper, Leanne, Porter, Amy, Braun, Matthias, Souza-Fonseca-Guimaraes, Fernando, Minnie, Simone A., Cooper, Emily, Jacquelin, Sebastien, Song, Axia, Bald, Tobias, Nakamura, Kyohei, Hill, Geoffrey R., Aifantis, Iannis, Lane, Steven W., and Bywater, Megan J.

Published
2023
Full Text
View/download PDF

4. An inflammatory state remodels the immune microenvironment and improves risk stratification in acute myeloid leukemia

Author

Lasry, Audrey, Nadorp, Bettina, Fornerod, Maarten, Nicolet, Deedra, Wu, Huiyun, Walker, Christopher J., Sun, Zhengxi, Witkowski, Matthew T., Tikhonova, Anastasia N., Guillamot-Ruano, Maria, Cayanan, Geraldine, Yeaton, Anna, Robbins, Gabriel, Obeng, Esther A., Tsirigos, Aristotelis, Stone, Richard M., Byrd, John C., Pounds, Stanley, Carroll, William L., Gruber, Tanja A., Eisfeld, Ann-Kathrin, and Aifantis, Iannis

Published
2023
Full Text
View/download PDF

5. A membrane-associated MHC-I inhibitory axis for cancer immune evasion

Author

Chen, Xufeng, Lu, Qiao, Zhou, Hua, Liu, Jia, Nadorp, Bettina, Lasry, Audrey, Sun, Zhengxi, Lai, Baoling, Rona, Gergely, Zhang, Jiangyan, Cammer, Michael, Wang, Kun, Al-Santli, Wafa, Ciantra, Zoe, Guo, Qianjin, You, Jia, Sengupta, Debrup, Boukhris, Ahmad, Zhang, Hongbing, Liu, Cheng, Cresswell, Peter, Dahia, Patricia L.M., Pagano, Michele, Aifantis, Iannis, and Wang, Jun

Published
2023
Full Text
View/download PDF

6. A RORγt+ cell instructs gut microbiota-specific Treg cell differentiation

Author

Kedmi, Ranit, Najar, Tariq A., Mesa, Kailin R., Grayson, Allyssa, Kroehling, Lina, Hao, Yuhan, Hao, Stephanie, Pokrovskii, Maria, Xu, Mo, Talbot, Jhimmy, Wang, Jiaxi, Germino, Joe, Lareau, Caleb A., Satpathy, Ansuman T., Anderson, Mark S., Laufer, Terri M., Aifantis, Iannis, Bartleson, Juliet M., Allen, Paul M., Paidassi, Helena, Gardner, James M., Stoeckius, Marlon, and Littman, Dan R.

Published
2022
Full Text
View/download PDF

7. NUDT21 limits CD19 levels through alternative mRNA polyadenylation in B cell acute lymphoblastic leukemia

Author

Witkowski, Matthew T., Lee, Soobeom, Wang, Eric, Lee, Anna K., Talbot, Alexis, Ma, Chao, Tsopoulidis, Nikolaos, Brumbaugh, Justin, Zhao, Yaqi, Roberts, Kathryn G., Hogg, Simon J., Nomikou, Sofia, Ghebrechristos, Yohana E., Thandapani, Palaniraja, Mullighan, Charles G., Hochedlinger, Konrad, Chen, Weiqiang, Abdel-Wahab, Omar, Eyquem, Justin, and Aifantis, Iannis

Published
2022
Full Text
View/download PDF

9. Deep Learning and Pathomics Analyses Reveal Cell Nuclei as Important Features for Mutation Prediction of BRAF-Mutated Melanomas

Author

Kim, Randie H., Nomikou, Sofia, Coudray, Nicolas, Jour, George, Dawood, Zarmeena, Hong, Runyu, Esteva, Eduardo, Sakellaropoulos, Theodore, Donnelly, Douglas, Moran, Una, Hatzimemos, Aristides, Weber, Jeffrey S., Razavian, Narges, Aifantis, Iannis, Fenyo, David, Snuderl, Matija, Shapiro, Richard, Berman, Russell S., Osman, Iman, and Tsirigos, Aristotelis

Published
2022
Full Text
View/download PDF

11. CHD7 and Runx1 interaction provides a braking mechanism for hematopoietic differentiation

Author

Hsu, Jingmei, Huang, Hsuan-Ting, Lee, Chung-Tsai, Choudhuri, Avik, Wilson, Nicola K., Abraham, Brian J., Moignard, Victoria, Kucinski, Iwo, Yu, Shuqian, Hyde, R. Katherine, Tober, Joanna, Cai, Xiongwei, Li, Yan, Guo, Yalin, Yang, Song, Superdock, Michael, Trompouki, Eirini, Calero-Nieto, Fernando J., Ghamari, Alireza, Jiang, Jing, Gao, Peng, Gao, Long, Nguyen, Vy, Robertson, Anne L., Durand, Ellen M., Kathrein, Katie L., Aifantis, Iannis, Gerber, Scott A., Tong, Wei, Tan, Kai, Cantor, Alan B., Zhou, Yi, Liu, P. Paul, Young, Richard A., Göttgens, Berthold, Speck, Nancy A., and Zon, Leonard I.

Published
2020

16. Therapeutic targeting of the E3 ubiquitin ligase SKP2 in T-ALL

Author

Rodriguez, Sonia, Abundis, Christina, Boccalatte, Francesco, Mehrotra, Purvi, Chiang, Mark Y., Yui, Mary A., Wang, Lin, Zhang, Huajia, Zollman, Amy, Bonfim-Silva, Ricardo, Kloetgen, Andreas, Palmer, Joycelynne, Sandusky, George, Wunderlich, Mark, Kaplan, Mark H., Mulloy, James C., Marcucci, Guido, Aifantis, Iannis, Cardoso, Angelo A., and Carlesso, Nadia

Published
2020
Full Text
View/download PDF

17. Three-dimensional chromatin landscapes in T cell acute lymphoblastic leukemia

Author

Kloetgen, Andreas, Thandapani, Palaniraja, Ntziachristos, Panagiotis, Ghebrechristos, Yohana, Nomikou, Sofia, Lazaris, Charalampos, Chen, Xufeng, Hu, Hai, Bakogianni, Sofia, Wang, Jingjing, Fu, Yi, Boccalatte, Francesco, Zhong, Hua, Paietta, Elisabeth, Trimarchi, Thomas, Zhu, Yixing, Van Vlierberghe, Pieter, Inghirami, Giorgio G., Lionnet, Timothee, Aifantis, Iannis, and Tsirigos, Aristotelis

Published
2020
Full Text
View/download PDF

22. Role of Dysregulated Cytokine Signaling and Bacterial Triggers in the Pathogenesis of Cutaneous T-Cell Lymphoma

Author

Fanok, Melania H., Sun, Amy, Fogli, Laura K., Narendran, Vijay, Eckstein, Miriam, Kannan, Kasthuri, Dolgalev, Igor, Lazaris, Charalampos, Heguy, Adriana, Laird, Mary E., Sundrud, Mark S., Liu, Cynthia, Kutok, Jeff, Lacruz, Rodrigo S., Latkowski, Jo-Ann, Aifantis, Iannis, Ødum, Niels, Hymes, Kenneth B., Goel, Swati, and Koralov, Sergei B.

Published
2018
Full Text
View/download PDF

23. The E3 ubiquitin ligase SPOP controls resolution of systemic inflammation by triggering MYD88 degradation

Author

Guillamot, Maria, Ouazia, Dahmane, Dolgalev, Igor, Yeung, Stephen T., Kourtis, Nikos, Dai, Yuling, Corrigan, Kate, Zea-Redondo, Luna, Saraf, Anita, Florens, Laurence, Washburn, Michael P., Tikhonova, Anastasia N., Malumbres, Marina, Gong, Yixiao, Tsirigos, Aristotelis, Park, Christopher, Barbieri, Christopher, Khanna, Kamal M., Busino, Luca, and Aifantis, Iannis

Published
2019
Full Text
View/download PDF

24. The bone marrow microenvironment at single-cell resolution

Author

Tikhonova, Anastasia N., Dolgalev, Igor, Hu, Hai, Sivaraj, Kishor K., Hoxha, Edlira, Cuesta-Domínguez, Álvaro, Pinho, Sandra, Akhmetzyanova, Ilseyar, Gao, Jie, Witkowski, Matthew, Guillamot, Maria, Gutkin, Michael C., Zhang, Yutong, Marier, Christian, Diefenbach, Catherine, Kousteni, Stavroula, Heguy, Adriana, Zhong, Hua, Fooksman, David R., Butler, Jason M., Economides, Aris, Frenette, Paul S., Adams, Ralf H., Satija, Rahul, Tsirigos, Aristotelis, and Aifantis, Iannis

Published
2019
Full Text
View/download PDF

25. The long non-coding RNA HOXB-AS3 regulates ribosomal RNA transcription in NPM1-mutated acute myeloid leukemia

Author

Papaioannou, Dimitrios, Petri, Andreas, Dovey, Oliver M., Terreri, Sara, Wang, Eric, Collins, Frances A., Woodward, Lauren A., Walker, Allison E., Nicolet, Deedra, Pepe, Felice, Kumchala, Prasanthi, Bill, Marius, Walker, Christopher J., Karunasiri, Malith, Mrózek, Krzysztof, Gardner, Miranda L., Camilotto, Virginia, Zitzer, Nina, Cooper, Jonathan L., Cai, Xiongwei, Rong-Mullins, Xiaoqing, Kohlschmidt, Jessica, Archer, Kellie J., Freitas, Michael A., Zheng, Yi, Lee, Robert J., Aifantis, Iannis, Vassiliou, George, Singh, Guramrit, Kauppinen, Sakari, Bloomfield, Clara D., Dorrance, Adrienne M., and Garzon, Ramiro

Published
2019
Full Text
View/download PDF

26. Oncogenic hijacking of the stress response machinery in T cell acute lymphoblastic leukemia

Author

Kourtis, Nikos, Lazaris, Charalampos, Hockemeyer, Kathryn, Balandrán, Juan Carlos, Jimenez, Alejandra R., Mullenders, Jasper, Gong, Yixiao, Trimarchi, Thomas, Bhatt, Kamala, Hu, Hai, Shrestha, Liza, Ambesi-Impiombato, Alberto, Kelliher, Michelle, Paietta, Elisabeth, Chiosis, Gabriela, Guzman, Monica L., Ferrando, Adolfo A., Tsirigos, Aristotelis, and Aifantis, Iannis

Published
2018
Full Text
View/download PDF

34. Pain-sensing neurons mobilize blood stem cells from bone marrow

Author

Tikhonova, Anastasia N. and Aifantis, Iannis

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

Pain-sensing nerve cells can mobilize blood stem cells in mice, with a component of chilli peppers being one stimulus. The finding holds the promise of improving procedures for stem-cell transplantation. Stimulation of nociceptive neurons mobilizes haematopoietic stem cells., Author(s): Anastasia N. Tikhonova, Iannis Aifantis Author Affiliations: Pain-sensing neurons mobilize blood stem cells from bone marrow The cardinal feature of blood stem cells is their ability to regenerate the [...]

Published
2021
Full Text
View/download PDF

36. ASXL1 Mutations Promote Myeloid Transformation through Loss of PRC2-Mediated Gene Repression

Author

Abdel-Wahab, Omar, Adli, Mazhar, LaFave, Lindsay M., Gao, Jie, Hricik, Todd, Shih, Alan H., Pandey, Suveg, Patel, Jay P., Chung, Young Rock, Koche, Richard, Perna, Fabiana, Zhao, Xinyang, Taylor, Jordan E., Park, Christopher Y., Carroll, Martin, Melnick, Ari, Nimer, Stephen D., Jaffe, Jacob D., Aifantis, Iannis, Bernstein, Bradley E., and Levine, Ross L.

Published
2012
Full Text
View/download PDF

38. Contrasting roles of histone 3 lysine 27 demethylases in acute lymphoblastic leukaemia

Author

Ntziachristos, Panagiotis, Tsirigos, Aristotelis, Welstead, G. Grant, Trimarchi, Thomas, Bakogianni, Sofia, Xu, Luyao, Loizou, Evangelia, Holmfeldt, Linda, Strikoudis, Alexandros, King, Bryan, Mullenders, Jasper, Becksfort, Jared, Nedjic, Jelena, Paietta, Elisabeth, Tallman, Martin S., Rowe, Jacob M., Tonon, Giovanni, Satoh, Takashi, Kruidenier, Laurens, Prinjha, Rab, Akira, Shizuo, Van Vlierberghe, Pieter, Ferrando, Adolfo A., Jaenisch, Rudolf, Mullighan, Charles G., and Aifantis, Iannis

Subjects
Lysine -- Genetic aspects -- Health aspects, Histones -- Health aspects -- Genetic aspects, Lymphocytic leukemia -- Genetic aspects, Methyltransferases -- Health aspects -- Genetic aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

T-cell acute lymphoblastic leukaemia (T-ALL) is a haematological malignancy with a dismal overall prognosis, including a relapse rate of up to 25%, mainly because of the lack of non-cytotoxic targeted therapy options. Drugs that target the function of key epigenetic factors have been approved in the context of haematopoietic disorders (1), and mutations that affect chromatin modulators in a variety of leukaemias have recently been identified (2,3); however, 'epigenetic' drugs are not currently used for T-ALL treatment. Recently, we described that the polycomb repressive complex 2 (PRC2) has a tumour-suppressor role in T-ALL4. Here we delineated the role of the histone 3 lysine 27 (H3K27) demethylases JMJD3 and UTX in T-ALL. We show that JMJD3 is essential for the initiation and maintenance of T-ALL, as it controls important oncogenic gene targets by modulating H3K27 methylation. By contrast, we found that UTX functions as a tumour suppressor and is frequently genetically inactivated in T-ALL. Moreover, we demonstrated that the small molecule inhibitor GSKJ4 (ref. 5) affects T-ALL growth, by targeting JMJD3 activity. These findings show that two proteins with a similar enzymatic function can have opposing roles in the context of the same disease, paving the way for treating haematopoietic malignancies with a new category of epigenetic inhibitors., In recent studies, we and other researchers have revealed that PRC2 has a key tumour-suppressor function, catalysing the methylation of H3K27 (refs 2, 4, 6). Since net H3K27me3 levels are [...]

Published
2014

41. Tet2 Loss Leads to Increased Hematopoietic Stem Cell Self-Renewal and Myeloid Transformation

Author

Moran-Crusio, Kelly, Reavie, Linsey, Shih, Alan, Abdel-Wahab, Omar, Ndiaye-Lobry, Delphine, Lobry, Camille, Figueroa, Maria E., Vasanthakumar, Aparna, Patel, Jay, Zhao, Xinyang, Perna, Fabiana, Pandey, Suveg, Madzo, Jozef, Song, Chunxiao, Dai, Qing, He, Chuan, Ibrahim, Sherif, Beran, Miloslav, Zavadil, Jiri, Nimer, Stephen D., Melnick, Ari, Godley, Lucy A., Aifantis, Iannis, and Levine, Ross L.

Published
2011
Full Text
View/download PDF

43. A RORγt+ cell instructs gut microbiota-specific Treg cell differentiation.

Author

Kedmi, Ranit, Najar, Tariq A., Mesa, Kailin R., Grayson, Allyssa, Kroehling, Lina, Hao, Yuhan, Hao, Stephanie, Pokrovskii, Maria, Xu, Mo, Talbot, Jhimmy, Wang, Jiaxi, Germino, Joe, Lareau, Caleb A., Satpathy, Ansuman T., Anderson, Mark S., Laufer, Terri M., Aifantis, Iannis, Bartleson, Juliet M., Allen, Paul M., and Paidassi, Helena

Abstract

The mutualistic relationship of gut-resident microbiota and the host immune system promotes homeostasis that ensures maintenance of the microbial community and of a largely non-aggressive immune cell compartment1,2. The consequences of disturbing this balance include proximal inflammatory conditions, such as Crohn’s disease, and systemic illnesses. This equilibrium is achieved in part through the induction of both effector and suppressor arms of the adaptive immune system. Helicobacter species induce T regulatory (Treg) and T follicular helper (TFH) cells under homeostatic conditions, but induce inflammatory T helper 17 (TH17) cells when induced Treg (iTreg) cells are compromised3,4. How Helicobacter and other gut bacteria direct T cells to adopt distinct functions remains poorly understood. Here we investigated the cells and molecular components required for iTreg cell differentiation. We found that antigen presentation by cells expressing RORγt, rather than by classical dendritic cells, was required and sufficient for induction of Treg cells. These RORγt+ cells—probably type 3 innate lymphoid cells and/or Janus cells5—require the antigen-presentation machinery, the chemokine receptor CCR7 and the TGFβ activator αv integrin. In the absence of any of these factors, there was expansion of pathogenic TH17 cells instead of iTreg cells, induced by CCR7-independent antigen-presenting cells. Thus, intestinal commensal microbes and their products target multiple antigen-presenting cells with pre-determined features suited to directing appropriate T cell differentiation programmes, rather than a common antigen-presenting cell that they endow with appropriate functions.Induction of T regulatory cells by gut microbes is mediated by antigen-presenting RORγt+ cells, unlike that of T follicular helper and T helper 17 cells, which requires different cell types. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

45. The Notch/Hes1 Pathway Sustains NF-κB Activation through CYLD Repression in T Cell Leukemia

Author

Espinosa, Lluis, Cathelin, Severine, D'Altri, Teresa, Trimarchi, Thomas, Statnikov, Alexander, Guiu, Jordi, Rodilla, Veronica, Inglés-Esteve, Julia, Nomdedeu, Josep, Bellosillo, Beatriz, Besses, Carles, Abdel-Wahab, Omar, Kucine, Nicole, Sun, Shao-Cong, Song, Guangchan, Mullighan, Charles C., Levine, Ross L., Rajewsky, Klaus, Aifantis, Iannis, and Bigas, Anna

Published
2010
Full Text
View/download PDF

46. Genetic inactivation of the polycomb repressive complex 2 in T cell acute lymphoblastic leukemia

Author

Ntziachristos, Panagiotis, Tsirigos, Aristotelis, Vlierberghe, Pieter Van, Nedjic, Jelena, Trimarchi, Thomas, Flaherty, Maria Sol, Ferres-Marco, Dolors, Ros, Vanina da, Zuojian, Tang, Siegle, Jasmin, Asp, Patrik, Hadler, Michael, Rigo, Isaura, Keersmaecker, Kim De, Patel, Jay, Huynh, Tien, Utro, Filippo, Poglio, Sandrine, Samon, Jeremy B., Paietta, Elisabeth, Racevskis, Janis, Rowe, Jacob M., Rabadan, Raul, Levine, Ross L., Brown, Stuart, Pflumio, Francoise, Dominguez, Maria, Ferrando, Adolfo, and Aifantis, Iannis

Subjects
T cells -- Genetic aspects, Genetic research, Acute lymphocytic leukemia -- Genetic aspects -- Care and treatment -- Physiological aspects, Biological sciences, Health
Abstract

T cell acute lymphoblastic leukemia (T-ALL) is an immature hematopoietic malignancy driven mainly by oncogenic activation of NOTCH1 signaling (1). In this study we report the presence of loss-of-function mutations [...]

Published
2012
Full Text
View/download PDF

47. A novel tumour-suppressor function for the Notch pathway in myeloid leukaemia

Author

Klinakis, Apostolos, Lobry, Camille, Abdel-Wahab, Omar, Oh, Philmo, Haeno, Hiroshi, Buonamici, Silvia, van DeWalle, Inge, Cathelin, Severine, Trimarchi, Thomas, Araldi, Elisa, Liu, Cynthia, Ibrahim, Sherif, Beran, Miroslav, Zavadil, Jiri, Efstratiadis, Argiris, Taghon, Tom, Michor, Franziska, Levine, Ross L., and Aifantis, Iannis

Subjects
T cells -- Physiological aspects -- Research -- Genetic aspects, Hematopoietic stem cells -- Physiological aspects -- Research, Cellular signal transduction -- Research -- Genetic aspects -- Physiological aspects, Myelocytic leukemia -- Genetic aspects -- Research, Nonlymphoid leukemia -- Genetic aspects -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Notch signalling is a central regulator of differentiation in a variety of organisms and tissue types1. Its activity is controlled by the multi-subunit γ-secretase (γSE) complex (2). Although Notch signalling can play both oncogenic and tumour-suppressor roles in solid tumours, in the haematopoietic system it is exclusively oncogenic, notably in T-cell acute lymphoblastic leukaemia, a disease characterized by Notch1-activating mutations (3). Here we identify novel somatic-inactivating Notch pathway mutations in a fraction of patients with chronic myelomonocytic leukaemia (CMML). Inactivation of Notch signalling in mouse haematopoietic stem cells (HSCs) results in an aberrant accumulation of granulocyte/monocyte progenitors (GMPs), extramedullary haematopoieisis and the induction of CMML-like disease. Transcriptome analysis revealed that Notch signalling regulates an extensive myelomonocytic-specific gene signature, through the direct suppression of gene transcription by the Notch target Hes1. Our studies identify a novel role for Notch signalling during early haematopoietic stem cell differentiation and suggest that the Notch pathway can play both tumour-promoting and -suppressive roles within the same tissue., Notch is essential for the emergence of definitive haematopoiesis (4), controls HSC differentiation to the T-cell lineage (5,6) and is a major oncogene, as most patients with T-cell acute lymphoblastic [...]

Published
2011
Full Text
View/download PDF

48. CCR7 signalling as an essential regulator of CNS infiltration in T-cell leukaemia

Author

Buonamici, Silvia, Trimarchi, Thomas, Ruocco, Maria Grazia, Reavie, Linsey, Cathelin, Severine, Mar, Brenton G., Klinakis, Apostolos, Lukyanov, Yevgeniy, Tseng, Jen-Chieh, Sen, Filiz, Gehrie, Eric, Li, Mengling, Newcomb, Elizabeth, Zavadil, Jiri, Meruelo, Daniel, Lipp, Martin, Ibrahim, Sherif, Efstratiadis, Argiris, Zagzag, David, Bromberg, Jonathan S., Dustin, Michael L., and Aifantis, Iannis

Published
2009
Full Text
View/download PDF

50. [gamma]-secretase inhibitors reverse glucocorticoid resistance in T cell acute lymphoblastic leukemia

Author

Real, Pedro J., Tosello, Valeria, Palomero, Teresa, Castillo, Mireia, Hernando, Eva, de Stanchina, Elisa, Sulis, Maria Luisa, Barnes, Kelly, Sawai, Catherine, Homminga, Irene, Meijerink, Jules, Aifantis, Iannis, Basso, Giuseppe, Cordon-Cardo, Carlos, Ai, Walden, and Ferrando, Adolfo

Subjects
Enzyme inhibitors -- Physiological aspects, Enzyme inhibitors -- Research, Corticosteroids -- Physiological aspects, Corticosteroids -- Research, T cells -- Physiological aspects, T cells -- Genetic aspects, T cells -- Research, Cellular signal transduction -- Research
Abstract

Gamma-secretase inhibitors (GSIs) block the activation of the oncogenic protein Notch homolog-1 (NOTCH 1) in T cell acute lymphoblastic leukemia (T-ALL). However, limited antileukemic cytotoxicity and severe gastrointestinal toxicity have restricted the clinical application of these targeted drugs. Here we show that combination therapy with GSIs plus glucocorticoids can improve the antileukemic effects of GSIs and reduce their gut toxicity in vivo. Inhibition of NOTCH1 signaling in glucocorticoid-resistant T-ALL restored glucocorticoid receptor autoupregulation and induced apoptotic cell death through induction of the gene encoding BCL-2-like apoptosis initiator-11 (BCL2L11). GSI treatment resulted in cell cycle arrest and accumulation of goblet cells in the gut mediated by upregulation of the gene encoding the transcription factor Kruppel-like factor-4 (Klf4), a negative regulator of the cell cycle required for goblet cell differentiation. In contrast, glucocorticoid treatment induced transcriptional upregulation of cyclin D2 (Ccnd2) and protected mice from developing the intestinal goblet cell metaplasia typically induced by inhibition of NOTCH signaling with GSIs. These results support a role for glucocorticoids plus GSIs in the treatment of glucocorticoid-resistant T-ALL., GSIs, which block the presenilin-[gamma]-secretase complex, inhibit the production of amyloidogenic [beta]-amyloid peptides involved in the pathogenesis of Alzheimer's disease and the activation of NOTCH receptors (1,2). The recent identification [...]

Published
2009

Catalog

Books, media, physical & digital resources
See catalog results