Results 141 to 150 of about 12,771 (176)

Imatinib resistant chronic myelogenous leukemia, BCR-ABL positive by chromosome and FISH analyses but negative by PCR, in a child progressing to acute basophilic leukemia: cytogenetic follow-up

Cancer Genetics and Cytogenetics, 2006
The case of an 11-year-old child with adult-type chronic myeloid leukemia, Philadelphia (BCR-ABL) positive, reverse transcription-polymerase chain reaction negative for the major, minor, and micro breakpoints is presented. In the course of 3 years, the child failed to respond to treatment with hydroxyurea, refused all therapy for 6 months, was ...
Asher M, Moser, Esther, Manor, Ginat, Narkis, Joseph, Kapelushnik   +3 more
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Philadelphia-positive chronic myelogenous leukemia with typical bcr/abl molecular features and atypical, prolonged survival.

Leukemia, 1989
Despite the major breakthrough in the knowledge of the molecular events underlying the t(9;22) translocation, still no consistent data have been found on the evolution of Ph1 positive CML from the chronic to the accelerated or blastic phase of the disease.
Selleri L., Emilia G., Temperani P., Grassilli E., Zucchini P., Tagliafico E., Bonati A., Venezia L., Ferrari S., Torelli U., Torelli G.   +10 more
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Presence or Re-Appearance of BCR-ABL-Positive Cells Years after Allogeneic Bone Marrow Transplantation for Chronic-Phase Chronic Myelogenous Leukemia in Patients in Hematological Remission

Acta Haematologica, 2009
AUogeneic bone marrow transplantation (BMT) is considered to be the only curative therapy for chronic myelogenous leukemia (CML). The cytogenetic marker of CML, the Philadelphia (Ph) chromosome, or the molecular alterations caused by the BCR-ABL gene fusion can be used to monitor the success of treatment.
L, Diekmann, D W, Beelen, K, Quabeck, R, Becher, H, Schulte Holthausen, R, Bützler, U W, Schaefer, B, Opalka   +7 more
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Absence of the hybrid bcr‐abl mRNA in Ph¹‐positive B lymphoblastoid cell lines established from a patient with chronic myelogenous leukemia

International Journal of Cancer, 1987
AbstractThe expression of c‐abl, c‐sis, c‐myc and N‐ras oncogenes was examined in 2 lymphoblastoid cell lines, one with Ph1 (PB‐1049) and the other without Ph1 (LN‐1049), both established from a patient with chronic myelogenous leukemia (CML), and in a Ph1‐positive cell line (PB‐1049‐T) derived from a tumor formed after transplantation of PB‐1049 cells
T, Yamada, T, Oikawa, N, Kuzumaki, N, Takagi, M, Sasaki   +4 more
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Preliminary activity of AMN107, a novel potent oral selective Bcr-Abl tyrosine kinase inhibitor, in newly diagnosed Philadelphia chromosome (Ph)-positive chronic phase chronic myelogenous leukemia (CML-CP)

Journal of Clinical Oncology, 2006
6591 Background: AMN107 is a novel, highly selective oral Bcr-Abl inhibitor which is 20–50-fold more potent than imatinib. High response rates with AMN107 were observed in all CML phases post imatinib failure. Methods: Study Aims: Evaluate the efficacy of AMN107in newly diagnosed Ph-positive CML-CP.
E. Jabbour, F. Giles, J. Cortes, S. O’Brien, F. Ravandi, G. Borthakur, G. Garcia-Manero, L. Letvak, A. Salvado, H. Kantarjian   +9 more
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A Population (Registry) Based Analysis of the Impact of Bcr-Abl Specific Tyrosine Kinase Inhibition on Survival after Diagnosis of Philadelphia Chromosome Positive Chronic Myelogenous Leukemia..

Blood, 2008
Abstract Specific tyrosine kinase inhibition (TKI) of the bcr-abl fusion protein in Philadelphia chromosome positive chronic myelogenous leukemia (CML) was introduced into general use in 2000 after a plenary abstract presentation to ASH in December 1999.
A. Robert Turner, Joanne D Hewitt, Anmmd Kamruzzaman, Loree M. Larratt, Deborah A. Rusnak, Nanette Cox-Kennett, Andrew R. Belch   +6 more
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Patterns of Clonal Evolution in Ph’-Positive Chronic Myelogenous Leukemia (CML) during Chronic Phase: Overall Incidence, Type, Multiplicity, Development Time, Effect on Subsequent Genetic Instability, Sokal Risk, Type of bcr/abl Transcript and Hematological Evolution.

Blood, 2006
Abstract Fifty-two kariotypic abnormalities additional to Philadelphia chromosome (Ph’) were documented at the time of diagnosis or during the course of the disease in 114 CML patients. Five were evaluated only once at the time of diagnosis, while 109 were repeatedly studied overtime during a median period of 138 (1–275)months.
Luzi D, Falchi L, Emili R, Angeletti I, Prontera P, Venti G, Bassetti A, Gubbiotti M, Capparella V, Gentileschi E, Donti E, LIBERATI, Anna Marina   +11 more
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Closely Related BCR/ABL Oncogenes Are Associated with the Distinctive Clinical Biologies of Philadelphia Chromosome Positive Chronic Myelogenous and Acute Lymphocytic Leukemia

1988
The study of oncogene activation in naturally occurring human leukemias provides a useful approach to define the range of growth regulatory mechanisms used by hematopoietic stem cells. Recent analysis of the structural changes created by the Philadelphia chromosome translocation [t(9;22) — (q34;q11)] shows that two alternative regions of the BCR gene ...
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A possible correlation between the type of bcr-abl hybrid messenger RNA and platelet count in Philadelphia-positive chronic myelogenous leukemia.

Blood, 1992
The Philadelphia (Ph1) chromosome, in which the hybrid bcr-abl gene is formed, is thought to be the initial event in chronic myelogenous leukemia (CML). The position of the breakpoint within the breakpoint cluster region (bcr) on Ph1 chromosome and the splicing pattern determine the species of the fused bcr-abl messenger RNA (mRNA).
K, Inokuchi, T, Inoue, A, Tojo, M, Futaki, K, Miyake, T, Yamada, Y, Tanabe, I, Ohki, K, Dan, K, Ozawa   +9 more
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[Regression of the Philadelphia chromosome (bcr/abl)-positive myelo- and megakaryopoiesis after Imatinib (STI571) therapy in chronic myelogenous leukemia (CML)].

Der Pathologe, 2005
In chronic myeloid leukemia following therapy with Imatinib (STI571) hematologic and cytogenetic response is associated with conspicuous changes of bone marrow morphology. However, it is not known to which extent these alterations are accompanied by a loss of the bcr/abl translocation. To study regression of the leukemic cell population we recruited 14
J, Thiele, H M, Kvasnicka, E, Varus, S, Kriener, K, Engels, P, Staib, E S, Ollig, M, Griesshammer, C F, Waller, H, Pfeifer, A, Schmitt-Gräff   +10 more
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