Mechanisms of disease - The biology of chronic myeloid leukemia

[1] DIFFERENTIAL COMPLEMENTATION OF BCR-ABL POINT MUTANTS WITH C-MYC [J]. SCIENCE, 1994, 264 (5157) : 424 - 426

[2] ALTERATIONS IN THE P53 GENE AND THE CLONAL EVOLUTION OF THE BLAST CRISIS OF CHRONIC MYELOCYTIC-LEUKEMIA [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (17) : 6783 - 6787

[3] Interferon-alpha restores normal beta 1 integrin-mediated inhibition of hematopoietic progenitor proliferation by the marrow microenvironment in chronic myelogenous leukemia [J]. BLOOD, 1996, 87 (09) : 3883 - 3891

[4] BIERNAUX C, 1995, BLOOD, V86, P3118

[5] The presence of typical and atypical BCR-ABL fusion genes in leukocytes of normal individuals: Biologic significance and implications for the assessment of minimal residual disease [J]. BLOOD, 1998, 92 (09) : 3362 - 3367

[6] BROWN RD, 1986, BLOOD, V68, P37

[7] A special fluorescent in situ hybridization technique to study peripheral blood and assess the effectiveness of interferon therapy in chronic myeloid leukemia [J]. BLOOD, 1998, 92 (07) : 2315 - 2321

[8] The ABL genes in normal and abnormal cell development [J]. CRITICAL REVIEWS IN ONCOGENESIS, 1996, 7 (1-2): : 33 - 48

[9] CYTOKINETIC CONSIDERATIONS RELEVANT TO DEVELOPMENT OF A SUCCESSFUL THERAPEUTIC STRATEGY IN CHRONIC MYELOGENOUS LEUKEMIA (CML) [J]. LEUKEMIA & LYMPHOMA, 1993, 11 : 101 - 107

[10] Donor leukocyte infusions in 140 patients with relapsed malignancy after allogeneic bone marrow transplantation [J]. JOURNAL OF CLINICAL ONCOLOGY, 1997, 15 (02) : 433 - 444

[1] DIFFERENTIAL COMPLEMENTATION OF BCR-ABL POINT MUTANTS WITH C-MYC [J]. SCIENCE, 1994, 264 (5157) : 424 - 426

[2] ALTERATIONS IN THE P53 GENE AND THE CLONAL EVOLUTION OF THE BLAST CRISIS OF CHRONIC MYELOCYTIC-LEUKEMIA [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (17) : 6783 - 6787

[3] Interferon-alpha restores normal beta 1 integrin-mediated inhibition of hematopoietic progenitor proliferation by the marrow microenvironment in chronic myelogenous leukemia [J]. BLOOD, 1996, 87 (09) : 3883 - 3891

[4] BIERNAUX C, 1995, BLOOD, V86, P3118

[5] The presence of typical and atypical BCR-ABL fusion genes in leukocytes of normal individuals: Biologic significance and implications for the assessment of minimal residual disease [J]. BLOOD, 1998, 92 (09) : 3362 - 3367

[6] BROWN RD, 1986, BLOOD, V68, P37

[7] A special fluorescent in situ hybridization technique to study peripheral blood and assess the effectiveness of interferon therapy in chronic myeloid leukemia [J]. BLOOD, 1998, 92 (07) : 2315 - 2321

[8] The ABL genes in normal and abnormal cell development [J]. CRITICAL REVIEWS IN ONCOGENESIS, 1996, 7 (1-2): : 33 - 48

[9] CYTOKINETIC CONSIDERATIONS RELEVANT TO DEVELOPMENT OF A SUCCESSFUL THERAPEUTIC STRATEGY IN CHRONIC MYELOGENOUS LEUKEMIA (CML) [J]. LEUKEMIA & LYMPHOMA, 1993, 11 : 101 - 107

[10] Donor leukocyte infusions in 140 patients with relapsed malignancy after allogeneic bone marrow transplantation [J]. JOURNAL OF CLINICAL ONCOLOGY, 1997, 15 (02) : 433 - 444