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Ibrutinib: From Molecule to Medicine

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dc.authorscopusid6701810655
dc.authorscopusid7005094713
dc.authorscopusid57203104682
dc.authorscopusid35459001500
dc.authorscopusid7005816382
dc.authorscopusid25639501700
dc.authorscopusid59850044200
dc.contributor.authorAyyildiz, O.
dc.contributor.authorDemirkan, F.
dc.contributor.authorGöker, H.
dc.contributor.authorHaznedarogˇlu, I.C.
dc.contributor.authorÍlhan, O.
dc.contributor.authorKaynar, L.G.
dc.contributor.authorÖzdemir, E.
dc.date.accessioned2020-06-21T14:04:08Z
dc.date.available2020-06-21T14:04:08Z
dc.date.issued2014
dc.departmentOndokuz Mayıs Üniversitesien_US
dc.department-temp[Ayyildiz] Orhan, Department of Internal Medicine, Dicle University, Faculty of Medicine, Diyarbakir, Turkey; [Demirkan] Fatih, Department of Hematology, Dokuz Eylül Üniversitesi, Izmir, Turkey; [Göker] Hakan, Department of Hematology, Hacettepe Üniversitesi, Ankara, Turkey; [Haznedarogˇlu] Ibrahim Celalettin, Department of Hematology, Hacettepe Üniversitesi, Ankara, Turkey; [Ílhan] Osman, Department of Internal Medicine, Ankara Üniversitesi, Ankara, Turkey; [Kaynar] L., Department of Hematology, Erciyes University, Faculty of Medicine, Kayseri, Turkey; [Özdemir] Evren, Department of Oncology, Hacettepe Üniversitesi, Ankara, Turkey; [Saydam] Güray, Department of Hematology, Ege University Medical School, Izmir, Turkey; [Sayinalp] Nilgün M., Department of Hematology, Hacettepe Üniversitesi, Ankara, Turkey; [Şahin] Fahri, Department of Hematology, Ege University Medical School, Izmir, Turkey; [Turgut] Mehmet, Department of Hematology, Ondokuz Mayis University, Medical School, Samsun, Turkey; [Unal] Ali, Department of Hematology, Erciyes University, Faculty of Medicine, Kayseri, Turkey; [Vural] Filiz, Department of Hematology, Ege University Medical School, Izmir, Turkeyen_US
dc.description.abstractBruton’s tyrosine kinase (BTK) inhibitor Ibrutinib (PCI-32765) is a novel targeted-therapeutic agent modulating BCR, which serves as a covalent irreversible inhibitor of BTK. Ibrutinib significantly alters the composition of the tumor microenvironment in CLL, affecting soluble as well as cellular molecular elements without myelosupression. Ibrutinib is clinically developed as an orally administered anti-cancer agent with lead indications in relapse/refractory and in treatment-naïve patients with B-cell malignancies as a single agent. The clinical activities of Ibrutinib as a drug were shown in the B-cell malignancies, especially in patients with CLL, mantle cell lymphoma (MCL), and Waldenstrom’s macroglobulinemia (WM). Ibrutinib has generated the most extensive results so far in patients with CLL, predominately refractory or relapsed CLL where durable disease control as well as improved progression-free survival (PFS) and overall survival (OS) has been observed. The aim of this review is to outline the pharmacophysiological basis of Ibrutinib treatment as well as the current clinical experience based on the trials. The treatment algorithms of B-lymphoproliferative diseases will continue to be revised to a more personalized approach to treat with improved efficacy devoid of unnecessary toxicity. © 2014, UHOD - Uluslararasi Hematoloji Onkoloji Dergisi. All rights reserved.en_US
dc.identifier.doi10.4999/uhod.14601
dc.identifier.endpage14en_US
dc.identifier.issue3en_US
dc.identifier.scopus2-s2.0-85172173638
dc.identifier.startpage4en_US
dc.identifier.urihttps://doi.org/10.4999/uhod.14601
dc.identifier.volume24en_US
dc.identifier.wosWOS:000342544800002
dc.language.isoenen_US
dc.publisherUHOD - Uluslararası Hematoloji Onkoloji Dergisien_US
dc.relation.ispartofUHOD - Uluslararasi Hematoloji-Onkoloji Dergisien_US
dc.relation.journalUhod-Uluslararasi Hematoloji-Onkoloji Dergisien_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectBCRen_US
dc.subjectBTKen_US
dc.subjectCLLen_US
dc.subjectIbrutiniben_US
dc.titleIbrutinib: From Molecule to Medicineen_US
dc.title.alternativeİbrutinib: Molekülden İlaçaen_US
dc.typeArticleen_US
dspace.entity.typePublication

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