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1

Complex translocations with chromosome Philadelphia positive and negative in patients with chronic myelois leukemia [CML]

100%
Stanczak H., Brycz-Witkowska J., Chmarzynska-Mroz E., Malinowska J., Sachs W., Wasiutynski A., Jedrzejczak W. W.
Folia Histochemica et Cytobiologica. Supplement
|
2001
|
tom 39
|
nr 1
2

Monoclonal and bispecific antibodies as novel therapeutics

86%
Booy E. P., Johar D., Maddika S., Pirzada H., Sahib M. M., Gehrke I., Loewen S., Louis S. F., Kadkhoda K., Mowat M., Los M.
Archivum Immunologiae et Therapiae Experimentalis
|
2006
|
tom 54
|
nr 2
3

Cytogenetic studies in chronic myeloid leukemia

86%
Chmarzynska-Mroz E., Brycz-Witkowska J., Stanczak H., Boguradzki A., Wasiutynski A., Jedrzejczak W. W.
Folia Histochemica et Cytobiologica. Supplement
|
2001
|
tom 39
|
nr 1
4

Comparison of two methods used for monitoring low-copy cytomegalovirus infection in a patient with chronic myeloid leukemia after unrelated umbilical cord blood transplantation

86%
Dzieciatkowski T., Przybylski M., Tomaszewska A., Rokicka M., Luczak M.
Archivum Immunologiae et Therapiae Experimentalis
|
2007
|
tom 55
|
nr 3
5

Dasatinib treatment can overcome imatinib and nilotinib resistance in CML patient carrying F3591 mutation of BCR-ABL oncogene

72%
Baranska M., Lewandowski K., Gniot M., Iwola M., Lewandowska M., Komarnicki M.
Journal of Applied Genetics
|
2008
|
tom 49
|
nr 2
201-203
Point mutations of bcr-abl tyrosine kinase are the most frequent causes of imatinib resistance in chronic myeloid leukaemia (CML) patients. In most CML cases with BCR-ABL mutations leading to imatinib resistance the second generation of tyrosine kinase inhibitors (TKI- e.g. nilotinib or dasatinib) may be effective. Here, we report a case of a CML patient who during imatinib treatment did not obtain clinical and cytogenetic response within 12 months of therapy. The sequencing of BCR-ABL kinase domains was performed and revealed the presence of a F359I point mutation (TTC-to-ATC nucleotide change leading to Phe-to-Ile amino acid substitution). After 1 month of nilotinib therapy a rapid progression of clinical symptoms was observed. In the presence of the F359I point mutation only dasatinib treatment overcame imatinib and nilotinib resistance.
6

Influence of BCR-ABL fusion proteins on the course of Ph leukemias

72%
Telegeev G. D., Dubrovska A. N., Dybkov M. V., Maliuta S. S.
Acta Biochimica Polonica
|
2004
|
tom 51
|
nr 3
The hallmark of chronic myeloid leukemia (CML) and a subset of acute lymphoblastic leukemia (ALL) is the presence of the Philadelphia chromosome as a result of the t(9;22) translocation. This gene rearrangement results in the production of a novel oncoprotein, BCR/ABL, a constitutively active tyrosine kinase. There is compelling evidence that the malignant transformation by BCR/ABL is critically de­pendent on its Abl tyrosine kinase activity. Also the bcr part of the hybrid gene takes part in realization of the malignant phenotype. We supposed that additional muta­tions accumulate in this region of the BCR/ABL oncogene during the development of the malignant blast crisis in CML patients. In ALL patients having p210 fusion pro­tein the mutations were supposed to be preexisting. Sequencing of PCR product of the BCR/ABL gene (Dbl, PH region) showed that along with single-nucleotide substitutions other mutations, mostly deletions, had oc­curred. In an ALL patient a deletion of the 5th exon was detected. The size of the de­letions varied from 36 to 220 amino acids. For one case of blast crisis of CML changes in the character of actin organization were observed. Taking into account the functional role of these domains in the cell an etiological role of such mutations on the disease phenotype and leukemia progression is plausible.
7

Interaction of 2-chlorodeoxyadenosine in combination either with interferons or recombinant human tumor necrosis factor alpha on myeloid progenitor cells in vitro

72%
Korycka A., Robak T.
Archivum Immunologiae et Therapiae Experimentalis
|
1996
|
tom 44
|
nr 4
8

Evaluation of monocyte-derived dendritic cells, T regulatory and Th17 cells in chronic myeloid leukemia patients treated with tyrosine kinase inhibitors

58%
Hus I., Tabarkiewicz J., Lewandowska M., Wasiak M., Wdowiak P., Kusz M., Legiec M., Dmoszynska A., Rolinski J.
Folia Histochemica et Cytobiologica
|
2011
|
tom 49
|
nr 1
9
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Molecular follow up of donor lymphocyte infusion in CML children after allogeneic bone marrow transplantation

58%
Ladon D., Pieczonka A., Jolkowska J., Wachowiak J., Witt M.
Journal of Applied Genetics
|
2001
|
tom 42
|
nr 4
10

Liposomal imatinib: an EPR and DSC study

58%
Beni S., Budai M., Noszal B., Grof P.
Cellular and Molecular Biology Letters
|
2005
|
tom 10
|
nr Suppl.
11
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Mechanism, detection and significance of some chromosomal rearrangements in chronic myeloid leukaemia [CML] and acute lymphoblastic leukaemia [ALL]

58%
Ladon D., Witt M.
Journal of Applied Genetics
|
2000
|
tom 41
|
nr 3
12

Plasma membrane phospholipid asymmetry and its maintenance

44%
Roelofsen B., Vermeulen W. P., Op den Kamp J.A.F.
Biophysics of Membrane Transport
|
1994
|
tom 12
|
nr 2
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