BCR-ABL1 kinase domain mutations may persist at very low levels for many years and lead to subsequent TKI resistance

Author:

Parker W T,Yeoman A L,Jamison B A,Yeung D T,Scott H S,Hughes T P,Branford S

Publisher

Springer Science and Business Media LLC

Subject

Cancer Research,Oncology

Reference16 articles.

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2. Branford S, Hughes T (2006a) Detection of BCR-ABL mutations and resistance to imatinib mesylate. In Myeloid Leukemia: Methods and Protocols, Methods in Molecular Medicine, Illand H, Hertzgerg M, Marlton P (eds) Vol. 125, pp 93–106. Totawa, Humana Press: New Jersey.

3. Branford S, Hughes T (2006b) Diagnosis and monitoring of chronic myeloid leukemia by qualitative and quantitative RT-PCR. In Myeloid Leukemia: Methods and Protocols, Methods in Molecular Medicine, Illand H, Hertzgerg M, Marlton P (eds) Vol. 125, pp 69–92. Humana Press: Totawa, New Jersey.

4. Branford S, Melo JV, Hughes TP (2009) Selecting optimal second-line tyrosine kinase inhibitor therapy for chronic myeloid leukemia patients after imatinib failure: does the BCR-ABL mutation status really matter? Blood 114: 5426–5435.

5. Ding L, Ley TJ, Larson DE, Miller CA, Koboldt DC, Welch JS, Ritchey JK, Young MA, Lamprecht T, McLellan MD, McMichael JF, Wallis JW, Lu C, Shen D, Harris CC, Dooling DJ, Fulton RS, Fulton LL, Chen K, Schmidt H, Kalicki-Veizer J, Magrini VJ, Cook L, McGrath SD, Vickery TL, Wendl MC, Heath S, Watson MA, Link DC, Tomasson MH, Shannon WD, Payton JE, Kulkarni S, Westervelt P, Walter MJ, Graubert TA, Mardis ER, Wilson RK, DiPersio JF (2012) Clonal evolution in relapsed acute myeloid leukaemia revealed by whole-genome sequencing. Nature 481: 506–510.

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