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    Central nervous system fungal infections in children with leukemia and undergoing hematopoietic stem cell transplantation: A retrospective multicenter study
    (2022) Karaman, Serap; Kebudi, Rejin; Kızılocak, Hande; Karakaş, Zeynep; Demirağ, Bengü; Evim, Melike Sezgin; Yaralı, Neşe; Kaya, Zühre; Karagün, Barbaros Şahin; Aydoğdu, Selime; Çalışkan, Ümran; Ayhan, Aylin Canbolat; Bahadır, Ayşenur; Çakır, Betül; Güner, Burçak T.; Albayrak, Canan; Karapınar, Deniz Yılmaz; Kazancı, Elif Güner; Ünal, Ekrem; Türkkan, Emine; Akıcı, Ferhan; Bor, Özcan; Vural, Sema; Yılmaz, Şebnem; Apak, Hilmi; Baytan, Birol; Tahta, Neryal Müminoğlu; Güzelküçük, Zeliha; Koçak, Ülker; Antmen, Bülent; Tokgöz, Hüseyin; Fışgın, Tunç; Özdemir, Nihal; Güneş, Adalet Meral; Vergin, Canan; Ünüvar, Ayşegül; Özbek, Namık; Tuğcu, Deniz; Bay, Sema Büyükkapu; Tanyıldız, Hikmet Gülşah; Celkan, Tiraje
    Background: Central nervous system fungal infections (CNSFI) are seen in patients with hematologic malignancies and have high morbidity and mortality. Because of their rarity, there is limited data on CNSFI in children with no established treatment protocols or guidelines. Materials and methods: In this multicenter retrospective study, 51 pediatric patients with leukemia, 6 of whom had undergone bone marrow transplantation, with proven or probable CNSFI were evaluated. Fungal infections were defined as proven or probable based on European Organisation for Research and Treatment of Cancer criteria. Proven CNSFI was diagnosed by appropriate central nervous system (CNS) imaging or tissue sample findings in combination with positive microbiological results of cerebrospinal fluid. A positive culture, microscopic evidence of hyphae, a positive result of the galactomannan assays are defined as positive microbiological evidence. Probable CNSFI was defined as appropriate CNS imaging findings together with proven or probable invasive fungal infections at another focus without CNS when there is no other explanatory condition. Data was collected by using the questionnaire form (Supplemental Digital Content 1, http://links.lww.com/JPHO/A541). Results: Seventeen patients had proven, 34 patients had probable CNSFI. Headaches and seizures were the most common clinical findings. The median time between the onset of fever and diagnosis was 5 days. The most common fungal agent identified was Aspergillus. Sixteen patients received single-agent, 35 received combination antifungal therapy. Surgery was performed in 23 patients. Twenty-two patients (43%) died, 29 of the CNSFI episodes recovered with a 20% neurological sequelae. Conclusion: CNSFIs should be considered in the differential diagnosis in patients with leukemia and refractory/recurrent fever, headache, neurologicalocular symptoms, and a radiologic-serological evaluation should be performed immediately. Early diagnosis and prompt management, both medical and surgical, are essential for improving clinical outcomes.
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    Prognostic evidence of LEF1 isoforms in childhood acute lymphoblastic leukemia
    (Wiley, 2021) Erbilgin, Yücel; Ng, Özden Hatırnaz; Can, İsmail; Fırtına, Sinem; Küçükcankurt, Fulya; Karaman, Serap; Sayıtoğlu, Müge; Gelen, Sema Aylan; Özdemir, Gül Nihal; Yıldırmak, Yıldız; Doğru, Ömer; Tansel, Türkan; Khodzhaev, Khusan; Toluk, Özlem; Özbek, Uğur
    Introduction The lymphoid enhancer factor 1 (LEF1) is a DNA-binding transcription factor that functions in the Wnt signaling pathway. Increased LEF1 activity is associated with progression of several types of cancer including leukemia. Here, we investigated LEF1 isoform expression and genomic variations in acute lymphoblastic leukemia (ALL). Methods LEF1 isoform expression was evaluated by quantitative real-time PCR in 87 newly diagnosed childhood ALL patients and controls. Moreover, Western blot analysis was performed for detection of LEF1 expression and the hotspot region of LEF1 was screened by deep sequencing. Results The LEF1 mRNA expression of B cell ALL patients was higher than the controls (LEF1-total P = .011, LEF1-long P = .026). Moreover, B-ALL samples showing higher total LEF1 expression had significantly shorter relapse-free survival (P = .008) and overall survival (P = .011). Although full-length LEF1 expression was similar to the controls in T-ALL, 50% (n = 15) of the ALL patients had increased full-length LEF1 protein expression. Imbalance between short- and full-length LEF1 isoforms may lead to cell survival in ALL. Beside the LEF1 activation, LEF1 gene variations were rarely observed in our cohort. Conclusion The results indicate that the Wnt pathway may have a pathogenic function in a group of ALL patients and high LEF1-total expression might be a marker for shorter relapse-free survival time in B cell ALL.