Yazar "Kaynar, Leyla G." seçeneğine göre listele

Listeleniyor 1 - 2 / 2
  • Küçük Resim Yok
    Öğe
    Ibrutinib: From Molecule to Medicine
    (Akad Doktorlar Yayinevi, 2014) Ayyildiz, Orhan; Demirkan, Fatih; Goker, Hakan; Haznedaroglu, Ibrahim C.; Ilhan, Osman; Kaynar, Leyla G.; Ozdemir, Evren; Saydam, Güray; Sayinalp, Nilgun; Sahin, Fahri; Turgut, Mehmet; Unal, Ali; Vural, Filiz
    Bruton'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-naive 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.
  • Küçük Resim Yok
    Öğe
    Idelalisib at the Crossroads of B-Cell Lymphoproliferative Disorders
    (Akad Doktorlar Yayinevi, 2016) Aksu, Salih; Ayyildiz, Orhan; Etgul, Sezgin; Goker, Hakan; Gunes, Gursel; Haznedaroglu, Ibrahim C.; Ilhan, Osman; Kaynar, Leyla G.; Malkan, Umit Y.; Ozdemir, Evren; Saydam, Güray; Sayinalp, Nilgun; Sahin, Fahri; Turgut, Mehmet; Unal, Ali
    Phosphatidylinositol 3-kinases (PI3Ks) are considered as lipid kinases that are very active in the pathobiology of lymphoproliferative disorders (LPDs). Idelalisib, a selective inhibitor of the delta isoform of PI3K, provides significant clinical efficacy and has an acceptable side-effect profile in the treatment of B-LPDs. The aim of this review is to outline the pharmacobiological basis of idelalisib that is located at the crossroads of B-LPDs. The PI3K signaling pathway with downstream targets including Akt is involved in hematologic malignancies and lymphomas. Idelalisib has been most widely studied in chronic lymphoid leukemia (CLL) and B-lymphoma. The activity of idelalisib in high-risk FL with early relapse following front line immunochemotherapy was recently shown. The unique immunological toxicity pattern of idelalisib was also decribed in this review. Further clinical investigations will help for the better selection of the subsets of the patients with B-LPD that would be best candidates for the clinical utilization of idelalisib. Other indications such as marginal zone lymphoma, mantle cell lymphoma, Waldenstrom's Macroglobulinemia and other B-cell disorders could likely to be expanded. Future clinical and experimental data combined with the next-generation genomics strategies and personalized medicine for the treatment of malignant disorders will enlightened us for better placement of idelalisib in the treatment algorithm of the patients.