Results 121 to 130 of about 81,803 (228)

Alu and translisin recognition site sequences flanking translocation sites in a novel type of chimeric bcr-abl transcript suggest a possible general mechanism for bcr-abl breakpoints

Haematologica, 2000
BACKGROUND AND OBJECTIVE: We further characterized a novel type of chimeric BCR-ABL mRNA transcript detected in a patient with Philadelphia chromosome positive (Ph+) chronic myeloid leukemia (CML).
G Martinelli, C Terragna, M Amabile, V Montefusco, N Testoni, E Ottaviani, A de Vivo, A Mianulli, G Saglio, S Tura   +9 more
doaj  

Supplementary Fig. S5 from Stromal-mediated protection of tyrosine kinase inhibitor-treated BCR-ABL-expressing leukemia cells

, 2008
Supplementary Fig. S5 from Stromal-mediated protection of tyrosine kinase inhibitor-treated BCR-ABL-expressing leukemia ...
Ilene Galinsky (64265), Arghya Ray (203488), Andrew L. Kung (9710962), Renee D. Wright (15042080), Richard Stone (86371), Ellen Weisberg (203474), Rosemary Barrett (203507), James D. Griffin (203544), Sophia Adamia (203502), Douglas W. McMillin (348456), Constantine Mitsiades (381062)   +10 more
core   +1 more source

Proteosomal degradation of BCR/ABL protein can generate an HLA-A*0301-restricted peptide, but high-avidity T cells recognizing this leukemia-specific antigen were not demonstrated

Haematologica, 2004
BACKGROUND AND OBJECTIVES: Cytotoxic T-lymphocytes (CTL) have been generated in vitro against chronic myeloid leukemia (CML)-associated BCR/ABL-specific peptides.
EF Posthuma, CA van Bergen, MG Kester, RA de Paus, PA van Veelen, AH de Ru, JW Drijfhout, EG Lurvink, R Willemze, JH Falkenburg   +9 more
doaj  

Supplementary Fig. S4 from Stromal-mediated protection of tyrosine kinase inhibitor-treated BCR-ABL-expressing leukemia cells

, 2008
Supplementary Fig. S4 from Stromal-mediated protection of tyrosine kinase inhibitor-treated BCR-ABL-expressing leukemia ...
Ilene Galinsky (64265), Arghya Ray (203488), Andrew L. Kung (9710962), Renee D. Wright (15042080), Richard Stone (86371), Ellen Weisberg (203474), Rosemary Barrett (203507), James D. Griffin (203544), Sophia Adamia (203502), Douglas W. McMillin (348456), Constantine Mitsiades (381062)   +10 more
core   +1 more source

Real-time quantification of different types of bcr-abl transcript in chronic myeloid leukemia

Haematologica, 2001
BACKGROUND AND OBJECTIVES: The most common translocation in chronic myeloid leukemia (CML) t(9;22) (q34;q22) produces the BCR/ABL fusion gene. We set up and evaluated a rapid and reliable real-time reverse-transcription-polymerase chain reaction (RT-PCR)
M Amabile, B Giannini, N Testoni, V Montefusco, G Rosti, C Zardini, C Terragna, S Buonamici, E Ottaviani, S Soverini, M Fiacchini, S Bassi, A de Vivo, E Trabacchi, G Saglio, F Pane, M Baccarani, S Tura, G Martinelli   +18 more
doaj  

Chronic Myeloid Leukemia with Rare e1a3 BCR-ABL Transcript

Pakistan Journal of Medicine and Dentistry
Chronic myelogenous leukemia (CML) results from neoplastic transformation of a hematopoietic stem cell. It is cytogenetically characterized by the presence of Philadelphia chromosome which results from reciprocal translocation t(9;22) that juxtaposes ...
Najia Tabassum, Rubina Ghani, Mohammad Saboor, Moinuddin Moinuddin   +3 more
doaj  

New tyrosine kinase inhibitors in chronic myeloid leukemia

Haematologica, 2005
The deregulated activity of BCR-ABL tyrosine kinase originating from the t(9;22) chromosomal translocation has been shown to be necessary and sufficient for the transformed phenotype of chronic myeloid leukemia (CML) cells. This peculiarity has paved the
G Martinelli, S Soverini, G Rosti, D Cilloni, M Baccarani   +4 more
doaj  

e8a2 BCR–ABL: more frequent than other atypical BCR–ABL variants? [PDF]

Leukemia, 2005
DEMEHRI S, PASCHKA P, SCHULTHEIS B, LANGE T, KOIZUMI T, SUGIMOTO T, BRANFORD S, LIM LC, KEGEL T, MARTINELLI, GIOVANNI, HOCHHAUS A, DRUKER BJ, DEININGER MW   +12 more
openaire   +2 more sources

Role of SOCS proteins in FLT3-ITD and BCR/ABL mediated leukemogenesis [PDF]

, 2010
Acute myeloid/lymphoid leukemia is a fatal hematological malignancy characterized by accumulation of nonfunctional, immature blasts, which interferes with the production of normal blood cells.
Reddy, N. G. Pavan Kumar
core  

BCR/ABL rearrangement and leukemia phenotype [PDF]

Leukemia, 1999
SAGLIO, Giuseppe, PANE F., MARTINELLI G., GUERRASIO, Angelo   +3 more
openaire   +3 more sources