Marked ploidy and BCR-ABL gene amplification in vivo in a patient treated with STI571 [3]

Leukemia

Volumn 15, Issue 11, 2001, Pages 1795-1797

  Sirulink, A ^a   Silver, R T ^b   Najfeld, V ^a  

^a MOUNT SINAI SCHOOL OF MEDICINE   (United States)

^b WEILL CORNELL MEDICAL CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ALPHA INTERFERON; BCR ABL PROTEIN; CYTARABINE; IMATINIB;

ADULT; ANIMAL CELL; BONE MARROW BIOPSY; CASE REPORT; CHROMOSOME DELETION; CHRONIC MYELOID LEUKEMIA; CLINICAL FEATURE; CONTROLLED STUDY; CYTOGENETICS; FEMALE; FLUORESCENCE IN SITU HYBRIDIZATION; GENE AMPLIFICATION; GENE REARRANGEMENT; HUMAN; HUMAN CELL; HUMAN TISSUE; IN VIVO STUDY; LETTER; MOUSE; NONHUMAN; PHILADELPHIA 1 CHROMOSOME; PLOIDY; PRIORITY JOURNAL; TREATMENT OUTCOME;

EID: 0035163226     PISSN: 08876924     EISSN: None     Source Type: Journal    
DOI: 10.1038/sj.leu.2402267     Document Type: Letter

References (6)

1. Induction of chronic myelogenous leukemia in mice by the P210bcr/abl gene of the Philadelphia chromosome
2. Lessons learned from the development of an abl tyrosine kinase inhibitor for chronic myelogenous leukemia
3. Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia
4. Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the Philadelphia chromosome
5. Selection and characterization of BCR-ABL positive cell lines with differential sensitivity to the tyrosine kinase inhibitor ST1571: Diverse mechanism of resistance
6. BCR/ABL gene amplification: A possible mechanism of drug resistance in patients treated with an ABL specific kinase inhibitor