A
Attila Kiss
Researcher at University of Debrecen
Publications - 103
Citations - 994
Attila Kiss is an academic researcher from University of Debrecen. The author has contributed to research in topics: Transplantation & Bone marrow. The author has an hindex of 17, co-authored 97 publications receiving 895 citations.
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Calcein assay for multidrug resistance reliably predicts therapy response and survival rate in acute myeloid leukaemia.
Éva Karászi,Katalin Jakab,László Homolya,Gergely Szakács,Zsolt Holló,Béla Telek,Attila Kiss,L. Rejto,Sarolta Nahajevszky,Balázs Sarkadi,János Kappelmayer +10 more
TL;DR: The calcein assay can be used as a quantitative, standardized, inexpensive screening test in a routine clinical laboratory setting, and identifies AML patients with unfavourable therapy responses.
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Factor XIII: a marker of mono- and megakaryocytopoiesis.
TL;DR: FXIII subunit α could be considered as a common marker of megakaryo‐ and monocytopoiesis and its immunomorphological detection might provide a useful diagostic tool for identifying normal and perhaps also malignant differentiation forms of these cell lines.
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Abnormalities of chromosome 1 in relation to human malignant diseases
TL;DR: The frequency, types, and time of the occurrence of chromosome 1 aberrations and their relation to the stage of the disease were studied in 317 patients with various malignant diseases.
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Alterations of P53 and RB genes and the evolution of the accelerated phase of chronic myeloid leukemia.
Zoltan Beck,Attila Kiss,Ferenc D. Tóth,Judit Szabó,Attila Bacsi,Erzsébet Balogh,Ágnes Borbély,Béla Telek,Eszter Kovács,Éva Oláh,Kálmán Rák +10 more
TL;DR: Using the single-strand conformation polymorphism and heteroduplex analyses, the P53 and RB genes were analyzed in cell samples from patients with chronic myeloid leukemia both at diagnosis and at the onset of accelerated phase of the disease.
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Frequent methylation of p16INK4A and p14ARF genes implicated in the evolution of chronic myeloid leukaemia from its chronic to accelerated phase.
Etelka Nagy,Zoltan Beck,Attila Kiss,Eszter Csoma,Béla Telek,József Kónya,Éva Oláh,Kálmán Rák,Ferenc D. Tóth +8 more
TL;DR: The data indicate that p16(INK4A) and p14(ARF) are primary targets for inactivation by promoter methylation in the acceleration of CML.