Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification

By M. Gorre, M. Mohammed, K. Ellwood, N. Hsu, R. Paquette, P. Rao, C. Sawyers. Science, 2001

3,268 citations recorded by the source corpus.

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

View Paper: https://www.semanticscholar.org/paper/968dd259bae7033c3e96c46e5ab0e385266d0b0f

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. Y. Luqmani
2. W. Kaelin
3. William C. Hahn
4. C. Ashby
5. Andreas Hochhaus
6. S. Morrison
7. C. Sawyers
8. Zhesheng Chen

In Hematology

1. E. Scholar
2. A. Arora
3. Y. Luqmani
4. William Pao
5. Andrew K. Joe
6. P. Jänne
7. W. Kaelin
8. I. Weinstein

In Public Health, Environmental and Occupational Health

1. Y. Luqmani
2. K. Strebhardt
3. S. Morrison

Citations in the corpus

• The discovery of receptor tyrosine kinases: targets for cancer therapy (2004, background): “Important questions — such as the definition of the optimal dose and schedule of drug administration and the issue of drug resistance that has been seen in imatinib-treated CM”
• The structure of Dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants. (2006, background): “ABL dependent and BCR-ABL independent, such as overexpression of other tyrosine kinases, may also occur (9, 10).”
• ERBB receptors and cancer: the complexity of targeted inhibitors (2005, background): “However, imatinib-resistance can arise and has been associated with acquired mutations in the BCR–ABL kinase domai”
• Systems biology approaches for advancing the discovery of effective drug combinations (2015, background): “In cancer, drug resistance can occur through mutation of the drug target [11], amplification of an alternate pathway [12], or intrinsic resistance of a subset of the cancer cells [13].”
• Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy. (2007, neutral): “Median age, y (range) 59 (24-79) 59 (24-79) 59 (24-79)”
• The Concept of Synthetic Lethality in the Context of Anticancer Therapy (2005, background): “Decades of clinical experience, including recent examples of imatinib mesylate resistanc”
• Targeting the cancer kinome through polypharmacology (2010, positive): “The strongest evidence in favour of this hypothesis is the discovery of resistance mutations after kinase inhibitor treatment in CML, GIST, lung cancer and a myeloproliferative disorder known as hyper-eosinophilic syndrome 22–26 .”