Cited by 143Chronic Myeloid Leukemia TreatmentsProtein Tyrosine PhosphatasesAcute Myeloid Leukemia Research

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Expression of Interferon Consensus Sequence Binding Protein (ICSBP) Is Downregulated in Bcr-Abl-Induced Murine Chronic Myelogenous Leukemia-Like Disease, and Forced Coexpression of ICSBP Inhibits Bcr-Abl-Induced Myeloproliferative Disorder

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Hao, Sheryl X., Ren, Ruibao·2000·Molecular and Cellular Biology

DOI 10.1128/mcb.20.4.1149-1161.2000PMC PMC85233

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Abstract

Chronic myelogenous leukemia (CML) is a clonal myeloproliferative disorder resulting from the neoplastic transformation of a hematopoietic stem cell. The majority of cases of CML are associated with the (9;22) chromosome translocation that generates the bcr-abl chimeric gene. Alpha interferon (IFN-alpha) treatment induces hematological remission and prolongs life in 75% of CML patients in the chronic phase. It has been shown that mice deficient in interferon consensus sequence binding protein (ICSBP), a member of the interferon regulatory factor family, manifest a CML-like syndrome. We have shown that expression of Bcr-Abl in bone marrow (BM) cells from 5-fluorouracil (5-FU)-treated mice by retroviral transduction efficiently induces a myeloproliferative disease in mice resembling human CML. To directly test whether icsbp can function as a tumor suppressor gene, we examined the effect of ICSBP on Bcr-Abl-induced CML-like disease using this murine model for CML. We found that expression of the ICSBP protein was significantly decreased in Bcr-Abl-induced CML-like disease. Forced coexpression of ICSBP inhibited the Bcr-Abl-induced colony formation of BM cells from 5-FU-treated mice in vitro and Bcr-Abl-induced CML-like disease in vivo. Interestingly, coexpression of ICSBP and Bcr-Abl induced a transient B-lymphoproliferative disorder in the murine model of Bcr-Abl-induced CML-like disease. Overexpression of ICSBP consistently promotes rather than inhibits Bcr-Abl-induced B lymphoproliferation in a murine model where BM cells from non-5-FU-treated donors were used, indicating that ICSBP has a specific antitumor activity toward myeloid neoplasms. We also found that overexpression of ICSBP negatively regulated normal hematopoiesis. These data provide direct evidence that ICSBP can act as a tumor suppressor that regulates normal and neoplastic proliferation of hematopoietic cells.

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Authors: Hao, S. X., & Ren, R.
Affiliations: Brandeis University (US)
ORCID: Ren, Ruibao
Venue: Molecular and Cellular Biology
Publisher: Informa UK Limited
Published: 2000-02-01
Volume: 20
Issue: 4
Pages: 1149-1161
ISSN: 0270-7306 (ISSN-L)
1098-5549
DOI: 10.1128/mcb.20.4.1149-1161.2000
PMC: PMC85233
OpenAlex: W2096038076
Cited by: 143
References: 48
Citations by year: 2026: 1 · 2023: 1 · 2021: 5 · 2020: 2 · 2019: 1 · 2018: 2 · 2017: 3 · 2016: 10 · 2015: 6 · 2014: 4 · 2013: 5 · 2012: 6
FWCI: 7.42
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: journals.asm.org/non-commercial-tdm-license (tdm)
Locations: Molecular and Cellular Biology (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Cancer Institute (CA68008, R01CA068008)
Topics: Health Sciences › Medicine › Hematology › Chronic Myeloid Leukemia Treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
Keywords: IRF8, BCR-ABL, chronic myeloid leukemia, myeloproliferative neoplasms, tumor suppressor, interferon regulatory factors, B-cell lymphoproliferative disorders, hematopoietic regulation, bone marrow cells, retroviral transduction, colony formation
MeSH terms: Interferon Regulatory Factor-8, Animals, Antimetabolites, Antineoplastic, B-Lymphocytes, Base Sequence, Colony-Forming Units Assay, Disease Models, Animal, Fluorouracil, Hematopoiesis, Humans, Interferons, Lymphoproliferative Disorders, Male, Mice, Inbred BALB C, Myeloproliferative Disorders, Repressor Proteins, Translocation, Genetic, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Down-Regulation, Bone Marrow Transplantation, Genes, abl, Consensus Sequence, DNA Primers, Interferon Regulatory Factors, Mice

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Expression of Interferon Consensus Sequence Binding Protein (ICSBP) Is Downregulated in Bcr-Abl-Induced Murine Chronic Myelogenous Leukemia-Like Disease, and Forced Coexpression of ICSBP Inhibits Bcr-Abl-Induced Myeloproliferative Disorder

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