WOS

Permanent URI for this collectionhttps://hdl.handle.net/11443/932

Browse

Subject: search.filters.subject.Acute leukemia

Search Results

Now showing 1 - 2 of 2
  • No Thumbnail Available
    Item
    Different Kinetics and Risk Factors for Isolated Extramedullary Relapse after Allogeneic Hematopoietic Stem Cell Transplantation in Children with Acute Leukemia
    (ELSEVIER SCIENCE INC, 2021-01-01) Hazar, Volkan; Ozturk, Gulyuz; Yalcin, Koray; Uygun, Vedat; Aksoylar, Serap; Kupesiz, A.; Bozkaya, Ikbal Ok; Karagun, Barbaros Sahin; Bozkurt, Ceyhun; Ileri, Talia; Atay, Didem; Kocak, Ulker; Karasu, Gulsun Tezcan; Yesilipek, Akif; Gokce, Muge; Kansoy, Savas; Kintrup, Gulen Tuysuz; Karakukcu, Musa; Okur, Fatma Visal; Ertem, Mehmet; Kaya, Zuhre; Gursel, Orhan; Yaman, Yontem; Ozbek, Namik; Antmen, Bulent; Tufekci, Ozlem; Albayrak, Canan; Aksoy, Basak Adakli; Sezgin, Gulay; Albayrak, Davut; Evim, Melike Sezgin; Zengin, Emine; Pekpak, Esra; Transpl, Turkish Pediat Bone Marrow
    Relapse after allogeneic hematopoietic stem cell transplantation (allo-HSCT) remains the most frequent cause of post-transplantation mortality. Isolated extramedullary (EM) relapse (iEMR) after HSCT is relatively rare and not well characterized, particularly in pediatric patients. We retrospectively analyzed 1527 consecutive pediatric patients with acute leukemia after allo-HSCT to study the incidence, risk factors, and outcome of iEMR compared with systemic relapse. The 5 -year cumulative incidence of systemic relapse (either bone marrow {[}BM] only or BM combined with EMR) was 24.8\%, and that of iEMR was 5.5\%. The onset of relapse after allo-HSCT was significantly longer in EM sites than in BM sites (7.19 and 5.58 months, respectively
  • No Thumbnail Available
    Item
    Aberrant Hypermethylation of APC Tumor Supressor Gene in Acute Leukemia Patients
    (AKAD DOKTORLAR YAYINEVI, 2017-01-01) Hatirnaz, Ozden N. G.; Firtina, Sinem; Erbilgin, Yucel; Ozbek, Ugur; Sayitoglu, Muge
    Wingless Type (WNT) signaling pathway is an evolutionarily conserved pathway that is crucial for the cell fate determination, survival and expansion of lymphocyte progenitors. It has been demonstrated that deregulated WNT signaling is one of the participating mechanism underlying lymphoid leukemogenesis. Inactivating mutations and methylation in Adenomatous Polyposis Coli (APC) gene, a negative regulator of WNT pathway, can cause ligand independent WNT pathway simulation. In this study, promoter methylation and expression of the APC gene is evaluated in childhood lymphoid and myeloid acute leukemia patients (n=118) and representative cell lines by using methylation specific PCR (MS-PCR) and real time quantitative PCR (QRT-PCR). APC gene promoter found hypermethylated in the 56\% of childhood acute leukemia patients {[}49.2\% of B-cell acute lymphoblastic leukemia (B-ALL), 62.5\% of T-cell acute lymphoblastic leukemia (T-ALL) and 64.1\% of Acute myeloid leukemia (AML)]. To evaluate the reflection of promoter methylation, APC mRNA levels were examined and found that all acute lymphoblastic leukemia subgroups have statistically lower APC expression levels compared to controls. Although there was no association with clinical parameters, promoter hypermethylation of APC gene seems to be a common epigenetic event in acute leukemia and leading to differential expression levels among different acute leukemia phenotypes.