Abstract
For acute myeloid leukemia (AML), identification of activating mutations in the FMS-like tyrosine kinase-3 (FLT3) has led to the development of several FLT3-inhibitors. Here we present clinical and next generation sequencing data at the time of progression of a patient on a novel FLT3-inhibitor clinical trial (ASP2215) to show that employing therapeutic interventions with these novel targeted therapies can lead to consequences secondary to selective pressure and clonal evolution of cancer. We describe novel findings alongside data on treatment directed towards actionable aberrations acquired during the process. (Clinical Trial: NCT02014558; registered at: 〈. https://clinicaltrials.gov/ct2/show/NCT02014558〉).
| Original language | English (US) |
|---|---|
| Pages (from-to) | 7-10 |
| Number of pages | 4 |
| Journal | Leukemia Research Reports |
| Volume | 5 |
| DOIs | |
| State | Published - 2016 |
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Keywords
- Acute Leukemia
- ASP2215
- Clonal evolution
- FMS-like tyrosine kinase-3 (FLT3) inhibitors
- Philadelphia chromosome (BCR-ABL)
- Ponatinib
ASJC Scopus subject areas
- Hematology
- Oncology
Cite this
Clonal evolution of AML on novel FMS-like tyrosine kinase-3 (FLT3) inhibitor therapy with evolving actionable targets. / Kasi, Pashtoon M.; Litzow, Mark R; Patnaik, Mrinal M; Hashmi, Shahrukh K.; Gangat, Naseema.
In: Leukemia Research Reports, Vol. 5, 2016, p. 7-10.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Clonal evolution of AML on novel FMS-like tyrosine kinase-3 (FLT3) inhibitor therapy with evolving actionable targets
AU - Kasi, Pashtoon M.
AU - Litzow, Mark R
AU - Patnaik, Mrinal M
AU - Hashmi, Shahrukh K.
AU - Gangat, Naseema
PY - 2016
Y1 - 2016
N2 - For acute myeloid leukemia (AML), identification of activating mutations in the FMS-like tyrosine kinase-3 (FLT3) has led to the development of several FLT3-inhibitors. Here we present clinical and next generation sequencing data at the time of progression of a patient on a novel FLT3-inhibitor clinical trial (ASP2215) to show that employing therapeutic interventions with these novel targeted therapies can lead to consequences secondary to selective pressure and clonal evolution of cancer. We describe novel findings alongside data on treatment directed towards actionable aberrations acquired during the process. (Clinical Trial: NCT02014558; registered at: 〈. https://clinicaltrials.gov/ct2/show/NCT02014558〉).
AB - For acute myeloid leukemia (AML), identification of activating mutations in the FMS-like tyrosine kinase-3 (FLT3) has led to the development of several FLT3-inhibitors. Here we present clinical and next generation sequencing data at the time of progression of a patient on a novel FLT3-inhibitor clinical trial (ASP2215) to show that employing therapeutic interventions with these novel targeted therapies can lead to consequences secondary to selective pressure and clonal evolution of cancer. We describe novel findings alongside data on treatment directed towards actionable aberrations acquired during the process. (Clinical Trial: NCT02014558; registered at: 〈. https://clinicaltrials.gov/ct2/show/NCT02014558〉).
KW - Acute Leukemia
KW - ASP2215
KW - Clonal evolution
KW - FMS-like tyrosine kinase-3 (FLT3) inhibitors
KW - Philadelphia chromosome (BCR-ABL)
KW - Ponatinib
UR - http://www.scopus.com/inward/record.url?scp=84954149212&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84954149212&partnerID=8YFLogxK
U2 - 10.1016/j.lrr.2016.01.002
DO - 10.1016/j.lrr.2016.01.002
M3 - Article
AN - SCOPUS:84954149212
VL - 5
SP - 7
EP - 10
JO - Leukemia Research Reports
JF - Leukemia Research Reports
SN - 2213-0489
ER -