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. Horita M, Andreu EJ, Benito A, Arbona C, Sanz C, Benet I, et al. Blockade of the Bcr-Abl kinase activity induces apoptosis of chronic myelogenous leukemia cells by suppressing signal transducer and activator of transcription 5-dependent expression of Bcl-xL. J Exp Med. 2000; 191:977-84. 24. Dresemann G. Imatinib and hydroxyurea in pretreated progressive glioblastoma multiforme: a patient series. Ann Oncol. 2005; 16:1702-8. 10.1093/annonc/mdi317 25. Reardon DA, Egorin MJ, Quinn JA, Rich JN, Gururangan S, Vredenburgh JJ, et al. Phase II study of imatinib mesylate plus

of equilibrium and periodic solutions of a delay equation modeling leukemia, Works of the Middle Volga Mathematical Society, 11(2009); arXiv:1001.5354. [5] A. V. Ion, R.M. Georgescu, Bautin bifurcation in a delay differential equation modeling leukemia, Nonlinear Analysis, 82(2013), 142-157. [6] Y. A. Kuznetsov, Elements of applied bifurcation theory, Applied Mathematical Sciences, 112, Springer, New York, 1998. [7] L. Pujo-Menjouet, M. C. Mackey, Contribution to the study of periodic chronic myelogenous leukemia, C. R. Biologies, 327(2004), 235-244. [8] L. Pujo


Myeloproliferative neoplasms (MPN) are haematological diseases, characterized by clonal hematopoiesis. Hemostasis abnormalities are among the most critical and frequent complications, affecting the quality of life and a possible reason for death. Thrombotic complications are common and multifactorial. Our aim was to study some genetic thrombophilia factors – Factor V Leiden (FVL), G20210A mutation in prothrombin gene (PR G20210A) and PLA2 allele polymorphism of glycoprotein IIIa gene (GPIIIa gene), and their frequency and association with thrombotic risk in both Philadelphia-positive and Philadelphia-negative MPN – chronic myelogenous leukemia (CML), polycythemia vera (PV), essential thrombocythemia (ET), and primary and secondary myelofibrosis (MF). In our patient population, PLA2 allele polymorphism of GPIIIa gene proved to be the most common and significantly associated with thrombotic complications – 26.85% of our patients were carriers, and 24.14% of them reported thrombotic complications.


Background: Myeloid sarcoma (MS) is a solid malignant tumour associated with infiltration of immature myeloid precursor cells in an extramedullary site. The term MS has replaced the term granulocytic sarcoma and chloroma, which were used in the past. MS in the oral cavity is very uncommon, with less of 40 cases reported until recently. Case Report: We report the first case, the features, and the diagnostic sequence, of intraoral MS with bilateral palatal involvement, which presented as an initial manifestation, and preceded the appearance of acute myeloid leukaemia (AML). Diagnostic confirmation of such oral mucosal lesions usually requires biopsy, histopathological examination with additional immunohistochemical investigation. MS can occur during the course of acute or chronic myelogenous leukaemia, and myelodysplastic syndromes. In the vast majority of the reported cases, only one site was involved with a single intraoral MS lesion, and the cases predominantly associated with AML. Conclusion: The majority of intraoral MS occurs in patients with known AML, but in some of them, presented as an initial manifestation, and preceded the appearance of the disease. Therefore, clinicians should carefully evaluate all unusual oral lesions of unknown origin.

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References 1. Demetri GD, von Mehren M, Blanke CD, Van den Abbeele AD, Eisenberg B, Roberts PJ, et al. Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors. N Engl J Med. 2002; 347:472-80. 2. Schwetz BA. New Treatment for Chronic Myelogenous Leukemia. JAMA. 2001; 286:35. 3. Cohen MH, Williams G, Johnson JR, Duan J, Gobburu J, Rahman A, et al. Approval summary for imatinib mesylate capsules in the treatment of chronic myelogenous leukemia. Clin Cancer Res. 2002; 8: 935-42. 4. Ayoub WS, Geller SA, Tran T, Martin P, Vierling JM

References 1. Copland M. Chronic myelogenous leukemia stem cells: What's new? Curr Hematol Malig Rep. 2009;4(2):66-73. 2. Deininger M, Goldman J, Melo J. The molecular biology of chronic myeloid leukemia. Blood. 2000;96:3343-3356. 3. Serpa M, Sanabani SS, Dorliac-Llacer PE, Conchon M. Molecular measurement of BCR-ABL transcript variations in chronic myeloid leukemia patients in cytogenetic remission. BMC Blood Disorders. 2010;10:7. 4. Pavlu J, Richard MSz, Goldman JM, Apperley JF. Three decades of transplantation for chronic myeloid leukemia: what have we learned

other chronic myelogenous leukemia cells. Science. 1984; 225: 72-74. 5. Druker BJ, Tamura S, Buchdunger E, et al. Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells. Nat Med. 1996; 2: 561-566. 6. Goldman JM, Melo JV. Chronic Myeloid leukemia - advances in biology and new approaches to treatment. N Engl J Med. 2003; 349(15): 1451-64. 7. Hughes TP, Kaeda J, Branford S, Rudzi Z, Hochhaus A, Hensly ML, et al. Frequency of major molecular response to imatinib or intereferon alfa plus cytarabine in newly diagnosed chronic

References Mitelman F. ISCN 1995: an international system for human cytogenetic nomenclature (1995): recommendations of the International Standing Committee of Human Cytogenetic Nomeclature, Memphis, TN, October 1994. Basel: Karger. 1995; 1-4. Rowley JD. A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining. Nature 1973; 243(5405): 290-293. Becher R, Korn WM, Prescher G. Use of fluorescence in situ hybridization and comparative genomic hybridization in the cytogenetic analysis of

PW, et al . Quantitative measure of c-abl and p15 methylation in chronic myelogenous leukemia: biological implications. Blood 2000;95:2990–2. Nguyen TT Mohrbacher AF Tsai YC Groffen J Heisterkamp N Nichols PW et al Quantitative measure of c-abl and p15 methylation in chronic myelogenous leukemia: biological implications Blood 2000 95 2990 2 7 Issa Jp, kantarjian HP. Introduction emerging role of epigenetic therapy: Focus on Decitabine. Semin Hematol 2005;42(3 Suppl 2):S1-2. Issa Jp KantarJian HP. Introduction emerging role of epigenetic therapy: Focus on