Yazar "Haznedaroglu, Ibrahim C." seçeneğine göre listele
Listeleniyor 1 - 9 / 9
Sayfa Başına Sonuç
Sıralama seçenekleri
Öğe The Clinical Impact of Low Doses of Dasatinib in Patients with Chronic Myeloid Leukemia(Akad Doktorlar Yayinevi, 2012) Aksu, Salih; Sahin, Fahri; Uz, Burak; Yavuz, Selim A.; Atay, Hilmi; Kelkitli, Engin; Turgut, Mehmet; Pehlivan, Mustafa; Akay, Meltem O.; Guray, Emel; Demir, Muzaffer; Kahraman, Selda; Demirkan, Fatih; Paydas, Semra; Saydam, Güray; Haznedaroglu, Ibrahim C.We report our experience in 41 patients with chronic phase (CF)-chronic myeloid leukemia (CML) who had discontinued imatinib switched to dasatinib, retrospectively. The CF-CML patients received dasatinib at starting dose of 100 once daily. Dose adjustment were observed in 11 patients, respectively. In case of other circumstances, treatment has been continued with a lower dose if needed. The median dose of dasatinib was 100 mg daily (range: 50 to 140 mg). We conclude that even low-dose dasatinib therapy is an effective and safe in second line treatment of CML patients patients.Öğe Efficacy and safety of ruxolitinib in patients with myelofibrosis: a retrospective and multicenter experience in Turkey(Tubitak Scientific & Technical Research Council Turkey, 2021) Soyer, Nur; Ali, Ridvan; Turgut, Mehmet; Haznedaroglu, Ibrahim C.; Yilmaz, Fergun; Aydogdu, Ismet; Pir, AliBackground/aim: The aim of this study is to assess the efficacy and safety of ruxolitinib in patients with myelofibrosis. Materials and methods: From 15 centers, 176 patients (53.4% male, 46.6% female) were retrospectively evaluated. Results: The median age at ruxolitinib initiation was 62 (28-87) and 100 (56.8%) of all were diagnosed as PMF. Constitutional symptoms were observed in 84.7%. The median initiation dose of ruxolitinib was 30 mg (10-40). Dose change was made in 69 (39.2%) patients. Forty seven (35.6%) and 20 (15.2%) of 132 patients had hematological and nonhematological adverse events, respectively. The mean spleen sizes before and after ruxolitinib treatment were 219.67 +/- 46.79 mm versus 199.49 +/- 40.95 mm, respectively (p < 0.001). There was no correlation between baseline features and subsequent spleen response. Overall survival at 1-year was 89.5% and the median follow up was 10 (1-55) months. We could not show any relationship between survival and reduction in spleen size (p = 0.73). Conclusion: We found ruxolitinib to be safe, well tolerated, and effective in real-life clinical practice in Turkey. Ruxolitinib dose titration can provide better responses in terms of not only clinical benefit but also for long term of ruxolitinib treatment.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, FilizBruton'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.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, AliPhosphatidylinositol 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.Öğe Leukemic stem cells shall be searched in the bone marrow before "tyrosine kinase inhibitor-discontinuation" in chronic myeloid leukemia(Wiley, 2021) Ilhan, Osman; Narli Ozdemir, Zehra; Dalva, Klara; Arslan, Aysenur; Okay Ozgeyik, Mufide; Ipek, Senay; Haznedaroglu, Ibrahim C.Background Leukemic stem cells (LSCs) of chronic myeloid leukemia (CML), persisting in the bone marrow (BM) niche, could be responsible for the relapses within the patients of whom the treatment-free remission (TFR) had been attempted. We assessed the presence of the CML LSCs in the peripheral blood (PB) and concurrently in the BM in the patients with chronic-phase CML (CP CML). Patients and Methods Thirty-eight patients with CP CML were included into the study. CD45(+)/CD34(+)/CD38(-) cells with positive CD26 expression were considered as CML LSCs (CD26(+) LSC) by using multiparameter flow cytometry (FCM). Results Mean BCR-ABL, PB LSC, and BM LSC were 58.528 IS (37.405-83.414 IS), 237.5 LSC/mu L (16-737.5 LSC/mu L), and 805 LSC/10(6) WBCs (134.6-2470 LSC/10(6) WBCs), respectively, in newly diagnosed CML patients. in the patients with BCR-ABL positive hematopoiesis, mean BCR-ABL, PB LSCs, and BM LSCs were 30.09 IS (0.024-147.690 IS), 13.5 LSC/mu L (0-248.7 LSC/mu L) and 143.5 LSC/10(6) WBCs (9-455.2 LSC/10(6) WBCs), respectively. No CML LSCs were detected in PB of patients who achieved deep molecular response (DMR). BM LSCs of the patients who were in DMR were 281.1 LSC/10(6) WBCs (3.1-613.7 LSC/10(6) WBCs). The amount of PB LSCs was highest in patients with newly diagnosed CML (P < .001). Conclusion LSCs persisted in the BM of the patients with DMR, whereas there was no LSCs in the peripheral blood. The investigation of the CML LSCs in bone marrow before deciding TKI discontinuation could be justified to achieve and maintain stable TFR.Öğe Multicenter Retrospective Analysis of Turkish Patients with Chronic Myeloproliferative Neoplasms(Galenos Yayincilik, 2017) Soyer, Nur; Haznedaroglu, Ibrahim C.; Comert, Melda; Cekdemir, Demet; Yilmaz, Mehmet; Unal, Ali; Cagliyan, Gulsum; Bilgir, Oktay; Ilhan, Osman; Ozdemirkiran, Fusun; Kaya, Emin; Sahin, Fahri; Vural, Filiz; Saydam, GürayObjective: Chronic myeloproliferative neoplasms (CMPNs) that include polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF) are Philadelphia-negative malignancies characterized by a clonal proliferation of one or several lineages. The aim of this report was to determine the demographic features, disease characteristics, treatment strategies, and survival rates of patients with CMPNs in Turkey. Materials and Methods: Across all of Turkey, 9 centers were enrolled in the study. We retrospectively evaluated 708 CMPN patients' results including 390 with ET, 213 with PV, and 105 with PMF. Results: The JAK2V617F mutation was found positive in 86% of patients with PV, in 51.5% of patients with ET, and in 50.4% of patients with PMF. Thrombosis and bleeding at diagnosis occurred in 20.6% and 7.5% of PV patients, 15.1% and 9% of ET patients, and 9.5% and 10.4% of PMF patients, respectively. Six hundred and eight patients (85.9%) received cytoreductive therapy. The most commonly used drug was hydroxyurea (89.6%). Leukemic and fibrotic transformations occurred at rates of 0.6% and 13.2%. The estimated overall survival in PV, ET, and PMF patients was 89.7%, 85%, and 82.5% at 10 years, respectively. There were no significant differences between survival in ET, PV, and PMF patients at 10 years. Conclusion: Our patients' results are generally compatible with the literature findings, except for the relatively high survival rate in PMF patients. Hydroxyurea was the most commonly used cytoreductive therapy. Our study reflects the demographic features, patient characteristics, treatments, and survival rates of Turkish CMPN patients.Öğe Retrospective Evaluation of Patients Treated with Dasatinib for Philadelphia Positive Leukemias: Turkish Experience of 16 Months(Akad Doktorlar Yayinevi, 2009) Saydam, Güray; Haznedaroglu, Ibrahim C.; Temiz, Yesim; Soysal, Teoman; Sucak, Gulsan; Tombuloglu, Murat; Ozdogu, Hakan; Yavuz, Selim; Altintas, Abdullah; Ozet, Gulsum; Gulbas, Zafer; Ferhanoglu, Burhan; Ilhan, OsmanThis retrospective study was conducted on 114 CML patients with a mean treatment duration of 7.94 +/- 4.53 months. Disease status distribution among patients was 78.1% in chronic, 7.9% in accelerated, 14% in blastic phases. The last imatinib doses in chronic, accelerated and blastic phases were 609.72 +/- 171.29, 714.29 +/- 106.90, and 569.23 +/- 160.13, respectively. Complete hematologic response was 66.3% and 44.4% in chronic and accelerated phases, respectively. Molecular response was evaluated by bcr/abl transcript levels in RT-PCR. Complete molecular response was 27.0% in chronic, 11.1% in accelerated and 18.8% in blastic phases. Of 99 patients 77 (77.8%) were alive. 16th month-OS for 99 patients was 78% in Kaplan-Meier survival analysis. No adverse event was reported in 69.2% of patients, whereas disease progression and grade 1-2 myelosupression were the most frequently reported events. Most patients had complete hematological response. Dasatinib treatment was well-tolerated and resulted in favorable outcomes with mostly mild side effects.Öğe Retrospective Evaluation of Patients Treated with Dasatinib for Philadelphia Positive Leukemias: Turkish Experience of 16 Months(Akad Doktorlar Yayinevi, 2009) Saydam, Güray; Haznedaroglu, Ibrahim C.; Temiz, Yesim; Soysal, Teoman; Sucak, Gulsan; Tombuloglu, Murat; Ozdogu, Hakan; Yavuz, Selim; Altintas, Abdullah; Ozet, Gulsum; Gulbas, Zafer; Ferhanoglu, Burhan; Ilhan, OsmanThis retrospective study was conducted on 114 CML patients with a mean treatment duration of 7.94 +/- 4.53 months. Disease status distribution among patients was 78.1% in chronic, 7.9% in accelerated, 14% in blastic phases. The last imatinib doses in chronic, accelerated and blastic phases were 609.72 +/- 171.29, 714.29 +/- 106.90, and 569.23 +/- 160.13, respectively. Complete hematologic response was 66.3% and 44.4% in chronic and accelerated phases, respectively. Molecular response was evaluated by bcr/abl transcript levels in RT-PCR. Complete molecular response was 27.0% in chronic, 11.1% in accelerated and 18.8% in blastic phases. Of 99 patients 77 (77.8%) were alive. 16th month-OS for 99 patients was 78% in Kaplan-Meier survival analysis. No adverse event was reported in 69.2% of patients, whereas disease progression and grade 1-2 myelosupression were the most frequently reported events. Most patients had complete hematological response. Dasatinib treatment was well-tolerated and resulted in favorable outcomes with mostly mild side effects.Öğe Turkish Chronic Myeloid Leukemia Study: Retrospective Sectional Analysis of CML Patients(Galenos Yayincilik, 2013) Sahin, Fahri; Saydam, Güray; Comert, Melda; Uz, Burak; Yavuz, Akif Selim; Turan, Esra; Yonal, Ipek; Atay, Hilmi; Keltikli, Engin; Turgut, Mehmet; Pehlivan, Mustafa; Akay, Meltem Olga; Gurkan, Emel; Paydas, Semra; Kahraman, Selda; Demirkan, Fatih; Kirkizlar, Onur; Akpinar, Seval; Pamuk, Gulsum Emel; Demir, Muzaffer; Ozbas, Hasan Mucahit; Sonmez, Mehmet; Gulturk, Mine; Salihoglu, Ayse; Eskazan, Ahmet Emre; Ar, Cem; Sahin, Handan Haydaroglu; Ongoren, Seniz; Baslar, Zafer; Aydin, Yildiz; Yenere, Mustafa Nuri; Tuzuner, Nukhet; Ferhanoglu, Burhan; Haznedaroglu, Ibrahim C.; Ilhan, Osman; Soysal, TeomanObjective: here have been tremendous changes in treatment and follow-up of patients with chronic myeloid leukemia (CML) in the last decade. Especially, regular publication and updating of NCCN and ELN guidelines have provided enermous rationale and base for close monitorization of patients with CML. But, it is stil needed to have registry results retrospectively to evaluate daily CML practices. Materials and Methods: In this article, we have evaluated 1133 patients' results with CML in terms of demographical features, disease status, response, resistance and use of second-generation TKIs. Results: The response rate has been found relatively high in comparison with previously published articles, and we detected that there was a lack of appropriate and adequate molecular response assessment. Conclusion: We concluded that we need to improve registry systems and increase the availability of molecular response assessment to provide high-quality patient care.
