Fyn is not essential for Bcr-Abl-induced leukemogenesis in mouse bone marrow transplantation models

The Bcr-Abl oncogene causes human Philadelphia chromosome-positive (Ph + ) leukemias, including B-cell acute lymphoblastic leukemia (B-ALL) and chronic myeloid leukemia (CML) with chronic phase (CML-CP) to blast crisis (CML-BC). Previous studies have demonstrated that Src family kinases are required...

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Veröffentlicht in:International journal of hematology 2012-02, Vol.95 (2), p.167-175
Hauptverfasser: Doki, Noriko, Kitaura, Jiro, Uchida, Tomoyuki, Inoue, Daichi, Kagiyama, Yuki, Togami, Katsuhiro, Isobe, Masamichi, Ito, Shinichi, Maehara, Akie, Izawa, Kumi, Kato, Naoko, Oki, Toshihiko, Harada, Yuka, Nakahara, Fumio, Harada, Hironori, Kitamura, Toshio
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container_issue 2
container_start_page 167
container_title International journal of hematology
container_volume 95
creator Doki, Noriko
Kitaura, Jiro
Uchida, Tomoyuki
Inoue, Daichi
Kagiyama, Yuki
Togami, Katsuhiro
Isobe, Masamichi
Ito, Shinichi
Maehara, Akie
Izawa, Kumi
Kato, Naoko
Oki, Toshihiko
Harada, Yuka
Nakahara, Fumio
Harada, Hironori
Kitamura, Toshio
description The Bcr-Abl oncogene causes human Philadelphia chromosome-positive (Ph + ) leukemias, including B-cell acute lymphoblastic leukemia (B-ALL) and chronic myeloid leukemia (CML) with chronic phase (CML-CP) to blast crisis (CML-BC). Previous studies have demonstrated that Src family kinases are required for the induction of B-ALL, but not for CML, which is induced by Bcr-Abl in mice. In contrast, it has been reported that Fyn is up-regulated in human CML-BC compared with CML-CP, implicating Fyn in the blast crisis transition. Here, we aimed to delineate the exact role of Fyn in the induction/progression of Ph + leukemias. We found that Fyn is expressed in mouse hematopoietic cells at varying stages of development, including c-kit + Sca-1 + Lin − cells. Notably, Fyn is highly expressed in some of human lymphomas, but not in human Ph + leukemias including CML-BC. In mouse bone marrow transplantation models, mice transplanted with wild-type or Fyn-deficient bone marrow cells transduced with Bcr-Abl showed no differences in the development of B-ALL or CML-like diseases. Similarly, Fyn deficiency failed to impact the development of myeloid CML-BC induced by Bcr-Abl and Hes1. Elevated expression of Fyn was not found in mouse samples of Bcr-Abl-mediated CML- and CML-BC-like diseases. Thus, Fyn is not required for the pathogenesis of Bcr-Abl-mediated leukemias.
doi_str_mv 10.1007/s12185-011-0994-5
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Previous studies have demonstrated that Src family kinases are required for the induction of B-ALL, but not for CML, which is induced by Bcr-Abl in mice. In contrast, it has been reported that Fyn is up-regulated in human CML-BC compared with CML-CP, implicating Fyn in the blast crisis transition. Here, we aimed to delineate the exact role of Fyn in the induction/progression of Ph + leukemias. We found that Fyn is expressed in mouse hematopoietic cells at varying stages of development, including c-kit + Sca-1 + Lin − cells. Notably, Fyn is highly expressed in some of human lymphomas, but not in human Ph + leukemias including CML-BC. In mouse bone marrow transplantation models, mice transplanted with wild-type or Fyn-deficient bone marrow cells transduced with Bcr-Abl showed no differences in the development of B-ALL or CML-like diseases. Similarly, Fyn deficiency failed to impact the development of myeloid CML-BC induced by Bcr-Abl and Hes1. 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Malignant lymphomas. Malignant reticulosis. 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Previous studies have demonstrated that Src family kinases are required for the induction of B-ALL, but not for CML, which is induced by Bcr-Abl in mice. In contrast, it has been reported that Fyn is up-regulated in human CML-BC compared with CML-CP, implicating Fyn in the blast crisis transition. Here, we aimed to delineate the exact role of Fyn in the induction/progression of Ph + leukemias. We found that Fyn is expressed in mouse hematopoietic cells at varying stages of development, including c-kit + Sca-1 + Lin − cells. Notably, Fyn is highly expressed in some of human lymphomas, but not in human Ph + leukemias including CML-BC. In mouse bone marrow transplantation models, mice transplanted with wild-type or Fyn-deficient bone marrow cells transduced with Bcr-Abl showed no differences in the development of B-ALL or CML-like diseases. Similarly, Fyn deficiency failed to impact the development of myeloid CML-BC induced by Bcr-Abl and Hes1. Elevated expression of Fyn was not found in mouse samples of Bcr-Abl-mediated CML- and CML-BC-like diseases. Thus, Fyn is not required for the pathogenesis of Bcr-Abl-mediated leukemias.</abstract><cop>Japan</cop><pub>Springer Japan</pub><pmid>22189847</pmid><doi>10.1007/s12185-011-0994-5</doi><tpages>9</tpages></addata></record>
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identifier ISSN: 0925-5710
ispartof International journal of hematology, 2012-02, Vol.95 (2), p.167-175
issn 0925-5710
1865-3774
language eng
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source MEDLINE; SpringerNature Journals
subjects Animals
Basic Helix-Loop-Helix Transcription Factors - genetics
Biological and medical sciences
Bone Marrow Transplantation
Chromosome aberrations
Disease Models, Animal
Fusion Proteins, bcr-abl - genetics
Gene Expression Regulation, Leukemic - physiology
Hematologic and hematopoietic diseases
Hematology
Hematopoietic Stem Cells - physiology
Homeodomain Proteins - genetics
Humans
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - physiopathology
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
Lymphoma, B-Cell - genetics
Lymphoma, B-Cell - physiopathology
Lymphoma, T-Cell - genetics
Lymphoma, T-Cell - physiopathology
Medical genetics
Medical sciences
Medicine
Medicine & Public Health
Mice
Mice, Inbred C57BL
Mice, Mutant Strains
Myelodysplastic Syndromes - genetics
Myelodysplastic Syndromes - physiopathology
Oncology
Original Article
Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics
Precursor Cell Lymphoblastic Leukemia-Lymphoma - physiopathology
Proto-Oncogene Proteins c-fyn - genetics
Proto-Oncogene Proteins c-fyn - physiology
Transcription Factor HES-1
title Fyn is not essential for Bcr-Abl-induced leukemogenesis in mouse bone marrow transplantation models
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