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14 results on '"Erdogan, Fettah"'

2. Structural and functional consequences of the STAT5BN642H driver mutation

Author

de Araujo, Elvin D., Erdogan, Fettah, Neubauer, Heidi A., Meneksedag-Erol, Deniz, Manaswiyoungkul, Pimyupa, Eram, Mohammad S., Seo, Hyuk-Soo, Qadree, Abdul K., Israelian, Johan, Orlova, Anna, Suske, Tobias, Pham, Ha T. T., Boersma, Auke, Tangermann, Simone, Kenner, Lukas, Rülicke, Thomas, Dong, Aiping, Ravichandran, Manimekalai, Brown, Peter J., Audette, Gerald F., Rauscher, Sarah, Dhe-Paganon, Sirano, Moriggl, Richard, and Gunning, Patrick T.

Published
2019
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3. High Efficacy and Drug Synergy of HDAC6-Selective Inhibitor NN-429 in Natural Killer (NK)/T-Cell Lymphoma

Author

Garcha, Harsimran Kaur, Gunning, Patrick T., Moriggl, Richard, de Araujo, Elvin D., Herling, Marco, Mustjoki, Satu M, Neubauer, Heidi A., Dhe-Paganon, Sirano, Pölöske, Daniel, Schönefeldt, Susann, Seo, Hyuk-Soo, Manaswiyoungkul, Pimyupa, Sedighi, Abootaleb, Aung, Myint Myat Khine, Erdogan, Fettah, Nawar, Nabanita, and Sorger, Helena

Subjects
Drug Discovery, Pharmaceutical Science, Molecular Medicine, T-Cell Lymphoma, Histone Deacetylase Inhibitor, Refinement, Therapy, Tubulin, Cancer, Hdac6, Features, Assay, NKTCL, HDAC6, synergy, combination treatment, small molecule inhibitor
Abstract

NK/T-cell lymphoma (NKTCL) and γδ T-cell non-Hodgkin lymphomas (γδ T-NHL) are highly aggressive lymphomas that lack rationally designed therapies and rely on repurposed chemotherapeutics from other hematological cancers. Histone deacetylases (HDACs) have been targeted in a range of malignancies, including T-cell lymphomas. This study represents exploratory findings of HDAC6 inhibition in NKTCL and γδ T-NHL through a second-generation inhibitor NN-429. With nanomolar in vitro HDAC6 potency and high in vitro and in cellulo selectivity for HDAC6, NN-429 also exhibited long residence time and improved pharmacokinetic properties in contrast to older generation inhibitors. Following unique selective cytotoxicity towards γδ T-NHL and NKTCL, NN-429 demonstrated a synergistic relationship with the clinical agent etoposide and potential synergies with doxorubicin, cytarabine, and SNS-032 in these disease models, opening an avenue for combination treatment strategies.

Published
2022
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4. JAK‐STAT core cancer pathway: An integrative cancer interactome analysis

Author

Erdogan, Fettah, primary, Radu, Tudor Bogdan, additional, Orlova, Anna, additional, Qadree, Abdul Khawazak, additional, de Araujo, Elvin Dominic, additional, Israelian, Johan, additional, Valent, Peter, additional, Mustjoki, Satu M., additional, Herling, Marco, additional, Moriggl, Richard, additional, and Gunning, Patrick Thomas, additional

Published
2022
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5. Structural and utational nalysis of ember-pecific STAT unctions

Author

Erdogan, Fettah, primary, Qadree, Abdul K., additional, Radu, Tudor B., additional, Orlova, Anna, additional, de Araujo, Elvin D., additional, Israelian, Johan, additional, Valent, Peter, additional, Mustjoki, Satu M., additional, Herling, Marco, additional, Moriggl, Richard, additional, and Gunning, Patrick T., additional

Published
2022
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6. JAK-STAT core cancer pathway: An integrative cancer interactome analysis

Author

Erdogan, Fettah, Gunning, Patrick Thomas, Moriggl, Richard, Herling, Marco, Mustjoki, Satu M, Valent, Peter, Israelian, Johan, de Araujo, Elvin Dominic, Qadree, Abdul Khawazak, Radu, Tudor Bogdan, Orlova, Anna, HUS Comprehensive Cancer Center, Department of Clinical Chemistry and Hematology, Clinicum, Digital Precision Cancer Medicine (iCAN), TRIMM - Translational Immunology Research Program, and Hematologian yksikkö

Subjects
liver cancers, MUTATIONS, blood cancer, EGFR, protein-protein interactions, INHIBITION, DISEASE GENES, TUMORS, JAK, COLORECTAL-CANCER, APOPTOSIS, ACTIVATION, lung cancer, breast cancer, STAT pathway in cancers, CELLS, 1182 Biochemistry, cell and molecular biology, 3111 Biomedicine, systems medicine, Cytokinesmetabolism, ErbB Receptorsmetabolism, Humans, Neoplasmsgenetics, STAT Transcription Factorsgeneticsmetabolism, colorectal cancers, HUMAN BREAST
Abstract

Through a comprehensive review and in silico analysis of reported data on STAT-linked diseases, we analysed the communication pathways and interactome of the seven STATs in major cancer categories and proposed rational targeting approaches for therapeutic intervention to disrupt critical pathways and addictions to hyperactive JAK/STAT in neoplastic states. Although all STATs follow a similar molecular activation pathway, STAT1, STAT2, STAT4 and STAT6 exert specific biological profiles associated with a more restricted pattern of activation by cytokines. STAT3 and STAT5A as well as STAT5B have pleiotropic roles in the body and can act as critical oncogenes that promote many processes involved in cancer development. STAT1, STAT3 and STAT5 also possess tumour suppressive action in certain mutational and cancer type context. Here, we demonstrated member-specific STAT activity in major cancer types. Through systems biology approaches, we found surprising roles for EGFR family members, sex steroid hormone receptor ESR1 interplay with oncogenic STAT function and proposed new drug targeting approaches of oncogenic STAT pathway addiction.

Published
2022

7. Unique Molecular Interaction with the Histone Deacetylase 6 Catalytic Tunnel: Crystallographic and Biological Characterization of a Model Chemotype

Author

Olaoye, Olasunkanmi O., primary, Watson, Paris R., additional, Nawar, Nabanita, additional, Geletu, Mulu, additional, Sedighi, Abootaleb, additional, Bukhari, Shazreh, additional, Raouf, Yasir S., additional, Manaswiyoungkul, Pimyupa, additional, Erdogan, Fettah, additional, Abdeldayem, Ayah, additional, Cabral, Aaron D., additional, Hassan, Muhammad Murtaza, additional, Toutah, Krimo, additional, Shouksmith, Andrew E., additional, Gawel, Justyna M., additional, Israelian, Johan, additional, Radu, Tudor B., additional, Kachhiyapatel, Niyati, additional, de Araujo, Elvin D., additional, Christianson, David W., additional, and Gunning, Patrick T., additional

Published
2021
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8. Characterization of Conformationally Constrained Benzanilide Scaffolds for Potent and Selective HDAC8 Targeting

Author

Hassan, Muhammad Murtaza, primary, Israelian, Johan, additional, Nawar, Nabanita, additional, Ganda, Giovanni, additional, Manaswiyoungkul, Pimyupa, additional, Raouf, Yasir S., additional, Armstrong, David, additional, Sedighi, Abootaleb, additional, Olaoye, Olasunkanmi O., additional, Erdogan, Fettah, additional, Cabral, Aaron D., additional, Angeles, Fabrizio, additional, Altintas, Rabia, additional, de Araujo, Elvin D., additional, and Gunning, Patrick T., additional

Published
2020
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14. Structural and functional consequences of the STAT5BN642H driver mutation.

Author

de Araujo, Elvin D., Erdogan, Fettah, Neubauer, Heidi A., Meneksedag-Erol, Deniz, Manaswiyoungkul, Pimyupa, Eram, Mohammad S., Seo, Hyuk-Soo, Qadree, Abdul K., Israelian, Johan, Orlova, Anna, Suske, Tobias, Pham, Ha T. T., Boersma, Auke, Tangermann, Simone, Kenner, Lukas, Rülicke, Thomas, Dong, Aiping, Ravichandran, Manimekalai, Brown, Peter J., and Audette, Gerald F.

Abstract

Hyper-activated STAT5B variants are high value oncology targets for pharmacologic intervention. STAT5BN642H, a frequently-occurring oncogenic driver mutation, promotes aggressive T-cell leukemia/lymphoma in patient carriers, although the molecular origins remain unclear. Herein, we emphasize the aggressive nature of STAT5BN642H in driving T-cell neoplasia upon hematopoietic expression in transgenic mice, revealing evidence of multiple T-cell subset organ infiltration. Notably, we demonstrate STAT5BN642H-driven transformation of γδ T-cells in in vivo syngeneic transplant models, comparable to STAT5BN642H patient γδ T-cell entities. Importantly, we present human STAT5B and STAT5BN642H crystal structures, which propose alternative mutation-mediated SH2 domain conformations. Our biophysical data suggests STAT5BN642H can adopt a hyper-activated and hyper-inactivated state with resistance to dephosphorylation. MD simulations support sustained interchain cross-domain interactions in STAT5BN642H, conferring kinetic stability to the mutant anti-parallel dimer. This study provides a molecular explanation for the STAT5BN642H activating potential, and insights into pre-clinical models for targeted intervention of hyper-activated STAT5B. Hyper-activated STAT5B and its disease-causing variants are of interest as cancer drug targets. Here the authors combine cell based studies, X-ray crystallography, biophysical experiments and MD simulations to structurally and functionally characterize the STAT5BN642H mutant found in aggressive T-cell leukemia and lymphomas and find that it has an increased affinity for self-dimerization. [ABSTRACT FROM AUTHOR]

Published
2019
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