Dasatinib treatment can overcome imatinib and nilotinib resistance in CML patient carrying F359I mutation of BCR-ABL oncogene

Barańska, Małgorzata; Lewandowski, Krzysztof; Gniot, Michał; Iwoła, Małgorzata; Lewandowska, Maria; Komarnicki, Mieczysław

doi:10.1007/bf03195613

Cited by 24 publications

(21 citation statements)

References 10 publications

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“…43 Furthermore, rapid progression was observed in a nilotinib-treated patient harboring F359I at commencement of nilotinib. 66 The IC 50 value of this mutation is unknown.…”

mentioning

confidence: 99%

Selecting optimal second-line tyrosine kinase inhibitor therapy for chronic myeloid leukemia patients after imatinib failure: does the BCR-ABL mutation status really matter?

Branford

Melo

Hughes

2009

Blood

170

131

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Preclinical studies of BCR-ABL mutation sensitivity to nilotinib or dasatinib suggested that the majority would be sensitive. Correspondingly, the initial clinical trials demonstrated similar response rates for CML patients after imatinib failure, irrespective of the mutation status. However, on closer examination, clinical evidence now indicates that some mutations are less sensitive to nilotinib (Y253H, E255K/V, and F359V/C) or dasatinib (F317L and V299L). T315I is insensitive to both. Novel mutations (F317I/V/C and T315A) are less sensitive/ insensitive to dasatinib. We refer to these collectively as second-generation inhibitor (SGI) clinically relevant mutations. By in vitro analysis, other mutations confer a degree of insensitivity; however, clinical evidence is currently insufficient to define them as SGI clinically relevant. Here we examine the mutations that are clearly SGI clinically relevant, those with minimal impact on response, and those for which more data are needed. In our series of patients with mutations at imatinib cessation and/or at nilotinib or dasatinib commencement, 43% had SGI clinically relevant mutations, including 14% with T315I. The frequency of SGI clinically relevant mutations was dependent on the disease phase at imatinib failure. The clinical data suggest that a mutation will often be detectable after imatinib failure for which there is compelling clinical evidence that one SGI should be preferred. (Blood. 2009; 114:5426-5435)

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“…43 Furthermore, rapid progression was observed in a nilotinib-treated patient harboring F359I at commencement of nilotinib. 66 The IC 50 value of this mutation is unknown.…”

mentioning

confidence: 99%

Selecting optimal second-line tyrosine kinase inhibitor therapy for chronic myeloid leukemia patients after imatinib failure: does the BCR-ABL mutation status really matter?

Branford

Melo

Hughes

2009

Blood

170

131

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“…Currently, there are more than 100 mutations associated with imatinib resistance, and the majority of them affect the P-loop (amino acids 248–255), T315, M351, and F359V [11,12]. F359I in the catalytic domain is an uncommon point mutation and has been associated with moderate imatinib resistance in vitro [13] and with imatinib and/or nilotinib resistance in two cases, one of which was overcome with dasatinib [14,15]. Currently, there is no in vitro data to support the sensitivity of F359I to dasatinib [16]; instead, the clinical data demonstrated the efficacy of dasatinib against BCR-ABL that presents with the F359V mutation [17].…”

Section: Discussionmentioning

confidence: 99%

Dasatinib Overrides Imatinib Resistance Mediated by the F359I Residue Mutation in Two Patients with Chronic Myeloid Leukemia

Serpa¹,

Sanabani²,

Dorlhíac-Llacer³

et al. 2011

Acta Haematol

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Despite the beneficial effects of imatinib mesylate, some patients may either not respond or respond suboptimally. Here, we report two chronic myelogenous leukemia patients; one had a suboptimal response according to European LeukemiaNet criteria (a major molecular response was not achieved after 18 months of standard-dose imatinib therapy) and the other had failure with a standard dose of imatinib. At the time of the suboptimal response in patient 1 and the failure in patient 2, we were able to detect the F359I mutation in the BCR-ABL tyrosine kinase domain using DNA sequencing in both patients. Therefore, it was decided to change the therapeutic regimen to dasatinib at a dose of 100 mg once daily in both patients. This change resulted in the achievement of complete cytogenetic remission in patient 1 after 4 months and a major molecular response within 2 and 3 months in both patients. Detection of the F359I mutation in our two cases likely explains the suboptimal response to imatinib in case 1 and the failure in case 2. This implies that in such cases dasatinib should be considered to effectively suppress the mutated clones.

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“…69,84 A patient who developed a F359I mutation on imatinib that was unresponsive to nilotinib eventually responded to dasatinib treatment. 85 A patient who acquired T315A on dasatinib, in addition to two mutations on imatinib (triple compound mutation) responded to combination treatment with imatinib and dasatinib. 69 However, it should be noted that a proportion of patients develop resistance to dasatinib or nilotinib in the absence of any BCR-ABL mutation, indicating that alternative mechanisms of resistance exist.…”

confidence: 99%

Impact ofBCR-ABLmutations on patients with chronic myeloid leukemia

Hochhaus¹,

Rosée²,

Müller³

et al. 2011

Cell Cycle

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Dasatinib treatment can overcome imatinib and nilotinib resistance in CML patient carrying F359I mutation of BCR-ABL oncogene

Cited by 24 publications

References 10 publications

Selecting optimal second-line tyrosine kinase inhibitor therapy for chronic myeloid leukemia patients after imatinib failure: does the BCR-ABL mutation status really matter?

Selecting optimal second-line tyrosine kinase inhibitor therapy for chronic myeloid leukemia patients after imatinib failure: does the BCR-ABL mutation status really matter?

Dasatinib Overrides Imatinib Resistance Mediated by the F359I Residue Mutation in Two Patients with Chronic Myeloid Leukemia

Impact ofBCR-ABLmutations on patients with chronic myeloid leukemia

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