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Miodrag Dragoj, Jasna Bankovic, Ana Podolski-Renic, Sonja Stojkovic Buric, Milica Pesic, Nikola Tanic and Tijana Stankovic
, optimize treatments and enable monitoring disease progression and response to therapy. Molecules that regulate cellular processes essential for maintaining malignant phenotype, such as c-Myc oncogene, stand out as promising candidates to serve as molecular markers. This nuclear phosphoprotein functions as transcriptional regulator of multiple genes and controls cell proliferation, induces apoptosis, and regulates stemness, senescence, metabolism and genome stability ( 4 ). Its expression is deregulated in number of human cancers including breast cancer, Burkitt
burden of schizophrenia in the United States was $156 billion ( 2 ).
Elabela (ELA) is a peptide of 32 amino acids that activates the apelin receptor (APJ) ( 5 , 6 ). It plays a role in various biological events such as self-renewing human embryonic stem cells in embryonic and adult periods, endoderm differentiation, cardiac morphogenesis, bone formation, regulation of blood pressure, water and food intake ( 7 ). ELA appears in many tissues including the APJ such as placenta, heart, kidney, lung, liver, brain, skeletal muscle, gastrointestinal system ( 8 ). Before
Aysun Şentürk Yıkılmaz, Şule Mine Bakanay, Sema Akinci, Murat Alisik, Özcan Erel and İmdat Dilek
is high in ET patients ( 2 , 3 ).
ET is a disease with bone marrow myeloproliferation in which monoclonal proliferation of megakaryocytes is more distinct. Although the pathogenesis of ET is not clearly known, 90% of cases have acquired somatic driver mutations such as JAK2, CALR, and MPL. Hypersensitivity to cytokines such as erythropoietin (EPO), thrombopoietin (TPO), interleukin 3 (IL-3) and stem cell factor (SCF) is known in the etiopathogenesis of ET. Increased free radicals are also known to increase the risk of genetic mutation in neoplastic processes ( 4
Mihaela Cîrstea, Adriana Coliță, Bogdan Ionescu, Alexandra Ghiaur, Didona Vasilescu, Camelia Dobrea, Cerasela Jardan, Mihaela Dragomir, Anca Gheorghe, Zsofia Várady and Anca Roxana Lupu
In the 2016 revision of the World Health Organization classification the term therapy-related myeloid neoplasia (t-MN) defines a subgroup of acute myeloid leukemia (AML) comprising patients who develop myelodysplastic syndrome (MDS-t) or acute myeloid leukemia (AML-t) after treatment with cytotoxic and/or radiation therapy for various malignancies or autoimmune disorders. We report the case of a 36 year old patient with t-MN (t-MDS) after achieving complete remission (CR) of a PML-RARA positive acute promyelocytic leukemia (APL) at 32 months after diagnosis. Initially classified as low risk APL and treated according to the AIDA protocol - induction and 3 consolidation cycles - the patient achieved a complete molecular response in September 2013 and started maintenance therapy. On follow-up PML-RARA transcript remained negative. In January 2016 leukopenia and thrombocytopenia developed and a peripheral blood smear revealed hypogranular and agranular neutrophils. Immunophenotyping in the bone marrow aspirate identified undifferentiated blast cells that did not express cytoplasmic myeloperoxidase. The cytogenetic study showed normal karyotype. The molecular biology tests not identified PMLRARA transcript. A diagnosis of t-MDS (AREB-2 - WHO 2008) was established. Treatment of AML was started with 2 “3+7” regimens and 1 MEC cycle. Two months from diagnosis, while in CR, an allogeneic HSCT from an unrelated HLA compatible donor was performed after myeloablative regimen. An unfavorable clinical evolution was followed by death on day 9 after transplantation. The occurrence of t-MNs during CR of APL represents a particular problem in terms of follow-up and differential diagnosis of relapse and constitutes a dramatic complication for a disease with a favorable prognosis.
This work was supported by the grants PN 41-087 /PN2-099 from the Romanian Ministry of Research and Technology
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