Gene expression changes associated with progression and response in chronic myeloid leukemia.

By J. Radich, Hongyue Dai, M. Mao, V. Oehler, Janell M. Schelter, Brian J. Druker, C. Sawyers, N. Shah, W. Stock, C. Willman and 2 more. Proceedings of the National Academy of Sciences of the United States of America, 2006

609 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/bd57d699ab46c15f590666cf538c660fe29a4b47

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. D. J. Barnes
2. J. Melo
3. Brian J. Druker

In Hematology

1. J. Melo
2. Brian J. Druker

Citations in the corpus

• Chronic myeloid leukaemia as a model of disease evolution in human cancer (2007, background): “This has been likened to being unable to predict where on the 'clock' of disease progression an individual lies at the time of diagnosi”
• The biology of CML blast crisis. (2004, background): “For example, SOCS2, thought to normally play a part in negative regulation of proliferation, has been found to up-regulated in advanced phases of CML.(30,46) Elastase (ELA2) and BMI2 have been found in microarray studies to be implicated in progression, and these may be associated with disease respo”
• Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia. (2007, background): “Surprisingly, even in the molecular age, a complete blood count and the old-fashioned Sokal risk score based on simple clinical data remain the mainstay of prognostication, although microarray data are maturing.(56) For now however, the best option is to use benchmarks of response to identify failur”