Prospective analysis of low-level BCR-ABL1 T315I mutation in CD34+ cells of patients with de novo chronic myeloid leukemia
| Authors | |
|---|---|
| Year of publication | 2014 |
| Type | Article in Periodical |
| Magazine / Source | LEUKEMIA & LYMPHOMA |
| MU Faculty or unit | |
| Citation | |
| Doi | http://dx.doi.org/10.3109/10428194.2013.842988 |
| Field | Oncology and hematology |
| Keywords | BCR-ABL1; T315I; CD34+; chronic myeloid leukemia |
| Attached files | |
| Description | Th e detection of BCR – ABL1 kinase domain (KD) mutations is frequently associated with resistance to tyrosine kinase inhibitors (TKIs), which results in an impaired prognosis for patients with chronic myeloid leukemia (CML) [1]. Early detection of these mutations can potentially lead to early therapeutic intervention and optimization of an ongoing treatment strategy. Considering the hematopoiesis hierar- chy, it is expected that BCR – ABL1 mutation clones expand directly from hematopoietic stem cells or early progenitor cells [2]. It has already been reported that BCR – ABL1 KD mutations were detected in these cells before they occurred in bone marrow (BM) or peripheral blood (PB) [3]. Particu- lar focus should be given to the T315I mutation, which is resistant to all approved TKIs (imatinib, nilotinib and dasa- tinib) [4,5], meaning that early detection of this key BCR – ABL1 KD mutation in “ source ” cells could have potential clinical benefits. |