Selection and characterization of BCR-ABL positive cell lines with differential sensitivity to the tyrosine kinase inhibitor STI571: diverse mechanisms of resistance.

By F. Mahon, M. Deininger, B. Schultheis, J. Chabrol, J. Reiffers, J. Goldman, J. Melo. Blood, 2000

839 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Public Health, Environmental and Occupational Health

View Paper: https://www.semanticscholar.org/paper/275aceccf5e9824e2fd89e439510f35fb34df57c

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. Dan Pinkel
2. Donna Albertson
3. Terence P. Speed
4. C. Sawyers
5. Y. Luqmani

In Hematology

1. Adi F. Gazdar
2. E. Scholar
3. A. Arora
4. Y. Luqmani

In Public Health, Environmental and Occupational Health

1. Y. Luqmani

Citations in the corpus

• Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. (2005, background): “Relapse is often associated with point mutations in Bcr-Abl that reduce the binding affinity of imatinib, or occasionally with amplification of the BCR-ABL gene (Gorre et al., 2001; Cowan-Jacob et al., 2004; le Coutre et al., 2000; Weisberg and Griffin, 2000; Mahon et al., 2000; Campbell et al., 200”
• Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia. (2002, background): “Samples from 32 CML patients who relapsed after a hematoefflux by multidrug resistance pumps (Mahon et al., 2000).”
• Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer. (2007, neutral): “Bcr-Abl fusion protein (Druker et al., 2001; Mahon et al., 2000).”
• Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukemia in myeloid blast crisis: results of a phase II study. (2002, neutral): “Median age, y (range) 56 (19-81) 57 (19-81) 52 (20-73) 56 (19-81)”
• A collection of breast cancer cell lines for the study of functionally distinct cancer subtypes. (2006, background): “Specifically, we found that increases in the levels of p27 (CDKN1B) protein and translocation of p27 to the nucleus were associated with cell cycle arrest as measured by inhibition of BrdUrd incorporation—probably due to inhibition of the formation of CCNE1-CDK2 complexes (Lane et al., 2000; Nahta e”