The molecular biology of chronic myeloid leukemia.

By M. Deininger, J. Goldman, J. Melo. Blood, 2000

1,713 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/08ec83e002b3345b3b3bffc5ccf1dd4159fe280a

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. Brian J. Druker
2. T. Hunter
3. J. Melo
4. Zhesheng Chen
5. C. Ashby
6. J. Cortes
7. D. J. Barnes
8. K. Borden

In Hematology

1. Brian J. Druker
2. J. Melo
3. T. Hunter
4. M. Greaves
5. Joe Wiemels
6. J. Goldman
7. C. Ashby
8. Zhesheng Chen

In Pathology and Forensic Medicine

1. D. J. Barnes
2. J. Melo

Citations in the corpus

• Mechanisms of BCR–ABL in the pathogenesis of chronic myelogenous leukaemia (2005, neutral): “DH p185 (1-426) p210 (1-902–927) p230 (1–1,176) Y177 Myr GAG BCR F G 1a 1b”
• Chronic myeloid leukemia--advances in biology and new approaches to treatment. (2003, background): “Consistent fusion of ZNF198 to the fibroblast growth factor receptor-1 in the t(8;13) (p11;q12) myeloproliferative syndrome.”
• Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. (2005, background): “The underlying cause of CML is the BCR-ABL oncogene, which results from a reciprocal t(9;22) chromosome translocation in a hematopoietic stem cell (Deininger et al., 2000).”
• MOZ-TIF2, but not BCR-ABL, confers properties of leukemic stem cells to committed murine hematopoietic progenitors. (2004, methodology): “…to the original human tumor, and serial transin this cell compartment in patients with AML, chronic myeloidplantation of the tumor to secondary recipients confirms the leukemia (CML), and ALL (Deininger et al., 2000; Haase et al.,true stem cell nature of these subpopulations of malignant cells.”
• Origins of chromosome translocations in childhood leukaemia (2003, background): “However, progression of CML to an acute phase or blast-cell crisis with differentiation arrest is clearly associated with additional and diverse genetic change”
• Chronic myeloid leukaemia as a model of disease evolution in human cancer (2007, background): “Expression of the NUP98/HOXA9 fusion transcript in the blast crisis of Philadelphia chromosome-positive chronic myelogenous leukaemia with t(7;11)(p15;p15).”
• Oncogenic kinase signalling (2001, background): “The transforming effect of Bcr-Abl is mediated by numerous downstream signalling pathways normally activated by RPTKs, including the Ras-Raf-ERK, JAK-STAT and PI(3)K pathway”
• Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity. (2011, background): “Introduction Chronic myeloid leukemia (CML) originates in a HSC with the reciprocal translocation t(9;22) (1).”
• BCR-ABL tyrosine kinase inhibitors in the treatment of Philadelphia chromosome positive chronic myeloid leukemia: a review. (2010, background): “[8] Deininger MW, Goldman JM, Melo JV.”