We are analyzing https://link.springer.com/article/10.1007/s12185-010-0706-6.

Title:
Expanded distribution of the T315I mutation among hematopoietic stem cells and progenitors in a chronic myeloid leukemia patient during imatinib treatment | International Journal of Hematology
Description:
T315I mutation of the ABL-kinase domain in chronic myeloid leukemia (CML) confers resistance to imatinib (IM) as well as second-generation tyrosine kinase inhibitors (TKIs). We report a chronic-phase CML patient undergoing IM treatment, who showed the overt existence of the T315I mutation after 15 months. We retrospectively analyzed the distribution of the T315I mutation using the invader assay and direct DNA sequencing among FACSAria-sorted populations from bone marrow cells: total mononuclear cells (TMC), hematopoietic stem cells (HSC)/Thy-1+, HSC/Thy-1−, common myeloid progenitors (CMP), granulocyte macrophage progenitors (GMP), and megakaryocyte erythroid progenitors (MEP), at 0, 3, 6, 9, and 12 months after IM treatment. T315I was barely detectable by 12 months in TMC, but detectable in 19.2% of HSC/Thy-1− and 46.4% of MEP at diagnosis, and finally expanded into all populations. These results suggest that the monitoring of gene mutations in HSC and progenitors at diagnosis might be helpful for the early detection of TKI-resistant CML patients and facilitate appropriate therapeutic decision.
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Keywords {🔍}

article, leukemia, chronic, myeloid, imatinib, pubmed, google, scholar, mutation, cells, cas, stem, progenitors, minami, bcrabl, privacy, cookies, content, journal, cml, access, nagoya, information, publish, research, search, hematology, hematopoietic, treatment, kajiguchi, abe, resistance, kinase, patients, therapy, data, log, expanded, distribution, patient, october, yosuke, tyrosine, months, hscthy, diagnosis, gene, mutations, discover, leukaemia,

Topics {✒️}

bcr-abl-kinase domain occur month download article/chapter bcr-abl mutation status bcr-abl t315i mutation bcr-abl gene bcr-abl kinase mutations tki-resistant cml patients chronic myeloid leukemia article international journal abl-kinase domain bcr-abl transcript chronic myelogenous leukemia privacy choices/manage cookies full article pdf related subjects common myeloid progenitors mutation conferring resistance hematopoietic stem cells cancer stem cells progression-inhibitory effect bone marrow cells total mononuclear cells gene mutations blast-crisis cml direct dna sequencing natl cancer inst tosei general hospital kajiguchi contributed equally nagoya university school conditions privacy policy european economic area journal finder publish granulocyte macrophage progenitors megakaryocyte erythroid progenitors granulocyte-macrophage progenitors accepting optional cookies toshihito ohno facsaria-sorted populations author information authors t315i mutation check access instant access article minami article log im treatment tomohiro kajiguchi akihiro abe scientific research imatinib treatment article cite

Questions {❓}

BCR-ABL kinase mutations in chronic myeloid leukemia: not quite enough to cause resistance to imatinib therapy?
Selecting optimal second-line tyrosine kinase inhibitor therapy for chronic myeloid leukemia patients after imatinib failure: does the BCR-ABL mutation status really matter?

Schema {🗺️}

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         headline:Expanded distribution of the T315I mutation among hematopoietic stem cells and progenitors in a chronic myeloid leukemia patient during imatinib treatment
         description:T315I mutation of the ABL-kinase domain in chronic myeloid leukemia (CML) confers resistance to imatinib (IM) as well as second-generation tyrosine kinase inhibitors (TKIs). We report a chronic-phase CML patient undergoing IM treatment, who showed the overt existence of the T315I mutation after 15 months. We retrospectively analyzed the distribution of the T315I mutation using the invader assay and direct DNA sequencing among FACSAria-sorted populations from bone marrow cells: total mononuclear cells (TMC), hematopoietic stem cells (HSC)/Thy-1+, HSC/Thy-1−, common myeloid progenitors (CMP), granulocyte macrophage progenitors (GMP), and megakaryocyte erythroid progenitors (MEP), at 0, 3, 6, 9, and 12 months after IM treatment. T315I was barely detectable by 12 months in TMC, but detectable in 19.2% of HSC/Thy-1− and 46.4% of MEP at diagnosis, and finally expanded into all populations. These results suggest that the monitoring of gene mutations in HSC and progenitors at diagnosis might be helpful for the early detection of TKI-resistant CML patients and facilitate appropriate therapeutic decision.
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