MLL rearrangements are induced by low doses of etoposide in human fetal hematopoietic stem cells
During fetal development, the liver serves as the primary hematopoietic organ in which hematopoietic stem cells (HSC) comprise a large proportion of hepatic cell populations. Because HSC are capable of initiating long-term hematopoiesis, injury to these cells during pregnancy may play a role in the...
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Published in | Carcinogenesis (New York) Vol. 27; no. 4; pp. 874 - 881 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Oxford
Oxford University Press
01.04.2006
Oxford Publishing Limited (England) |
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Abstract | During fetal development, the liver serves as the primary hematopoietic organ in which hematopoietic stem cells (HSC) comprise a large proportion of hepatic cell populations. Because HSC are capable of initiating long-term hematopoiesis, injury to these cells during pregnancy may play a role in the development of hematopoietic disorders manifested after birth. Of interest is the role of genetic injury to fetal HSC in the etiology of the infant acute leukemias, which are characterized by chromosomal rearrangements in the 11q23 region involving the mixed lineage leukemia (MLL) gene. These gene fusions also occur in leukemias in adults following chemotherapy with etoposide and other inhibitors of DNA topoisomerase II. We used etoposide as a model compound to determine the sensitivity of human fetal HSC to DNA damage and to determine whether we could induce MLL rearrangements in cultured human fetal HSC. Exposure of HSC to etoposide resulted in a dose-dependent loss of viability, with effects observed at low nanomolar concentrations. DNA strand breaks were observed on exposure to 140 nM etoposide, and higher etoposide concentrations stimulated an increase in early lymphoid populations and elicited G2/M cell cycle arrest. Immunophenotyping of MLL translocations revealed a significant increase in positive flow cytometry events at low etoposide concentrations and were consistent with MLL recombination. MLL translocations were confirmed using fluorescent in situ hybridization. In vitro inhibition of DNA topoisomerase II was observed at ≥25 µM etoposide, but was not evident at lower etoposide concentrations associated with DNA damage. Our data indicate that low acute doses of etoposide can cause DNA strand breaks and chromosomal rearrangements involving MLL in human fetal HSC. Ultimately, such injury may have ramifications with regards to transplacental exposures to environmental chemicals linked to the etiology of infant acute leukemias. |
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AbstractList | During fetal development, the liver serves as the primary hematopoietic organ in which hematopoietic stem cells (HSC) comprise a large proportion of hepatic cell populations. Because HSC are capable of initiating long-term hematopoiesis, injury to these cells during pregnancy may play a role in the development of hematopoietic disorders manifested after birth. Of interest is the role of genetic injury to fetal HSC in the etiology of the infant acute leukemias, which are characterized by chromosomal rearrangements in the 11q23 region involving the mixed lineage leukemia (MLL) gene. These gene fusions also occur in leukemias in adults following chemotherapy with etoposide and other inhibitors of DNA topoisomerase II. We used etoposide as a model compound to determine the sensitivity of human fetal HSC to DNA damage and to determine whether we could induce MLL rearrangements in cultured human fetal HSC. Exposure of HSC to etoposide resulted in a dose-dependent loss of viability, with effects observed at low nanomolar concentrations. DNA strand breaks were observed on exposure to 140 nM etoposide, and higher etoposide concentrations stimulated an increase in early lymphoid populations and elicited G sub(2)/M cell cycle arrest. Immunophenotyping of MLL translocations revealed a significant increase in positive flow cytometry events at low etoposide concentrations and were consistent with MLL recombination. MLL translocations were confirmed using fluorescent in situ hybridization. In vitro inhibition of DNA topoisomerase II was observed at greater than or equal to 25 mu M etoposide, but was not evident at lower etoposide concentrations associated with DNA damage. Our data indicate that low acute doses of etoposide can cause DNA strand breaks and chromosomal rearrangements involving MLL in human fetal HSC. Ultimately, such injury may have ramifications with regards to transplacental exposures to environmental chemicals linked to the etiology of infant acute leukemias. During fetal development, the liver serves as the primary hematopoietic organ in which hematopoietic stem cells (HSC) comprise a large proportion of hepatic cell populations. Because HSC are capable of initiating long-term hematopoiesis, injury to these cells during pregnancy may play a role in the development of hematopoietic disorders manifested after birth. Of interest is the role of genetic injury to fetal HSC in the etiology of the infant acute leukemias, which are characterized by chromosomal rearrangements in the 11q23 region involving the mixed lineage leukemia (MLL) gene. These gene fusions also occur in leukemias in adults following chemotherapy with etoposide and other inhibitors of DNA topoisomerase II. We used etoposide as a model compound to determine the sensitivity of human fetal HSC to DNA damage and to determine whether we could induce MLL rearrangements in cultured human fetal HSC. Exposure of HSC to etoposide resulted in a dose-dependent loss of viability, with effects observed at low nanomolar concentrations. DNA strand breaks were observed on exposure to 140 nM etoposide, and higher etoposide concentrations stimulated an increase in early lymphoid populations and elicited G2/M cell cycle arrest. Immunophenotyping of MLL translocations revealed a significant increase in positive flow cytometry events at low etoposide concentrations and were consistent with MLL recombination. MLL translocations were confirmed using fluorescent in situ hybridization. In vitro inhibition of DNA topoisomerase II was observed at >or=25 microM etoposide, but was not evident at lower etoposide concentrations associated with DNA damage. Our data indicate that low acute doses of etoposide can cause DNA strand breaks and chromosomal rearrangements involving MLL in human fetal HSC. Ultimately, such injury may have ramifications with regards to transplacental exposures to environmental chemicals linked to the etiology of infant acute leukemias. During fetal development, the liver serves as the primary hematopoietic organ in which hematopoietic stem cells (HSC) comprise a large proportion of hepatic cell populations. Because HSC are capable of initiating long-term hematopoiesis, injury to these cells during pregnancy may play a role in the development of hematopoietic disorders manifested after birth. Of interest is the role of genetic injury to fetal HSC in the etiology of the infant acute leukemias, which are characterized by chromosomal rearrangements in the 11q23 region involving the mixed lineage leukemia (MLL) gene. These gene fusions also occur in leukemias in adults following chemotherapy with etoposide and other inhibitors of DNA topoisomerase II. We used etoposide as a model compound to determine the sensitivity of human fetal HSC to DNA damage and to determine whether we could induce MLL rearrangements in cultured human fetal HSC. Exposure of HSC to etoposide resulted in a dose-dependent loss of viability, with effects observed at low nanomolar concentrations. DNA strand breaks were observed on exposure to 140 nM etoposide, and higher etoposide concentrations stimulated an increase in early lymphoid populations and elicited G2/M cell cycle arrest. Immunophenotyping of MLL translocations revealed a significant increase in positive flow cytometry events at low etoposide concentrations and were consistent with MLL recombination. MLL translocations were confirmed using fluorescent in situ hybridization. In vitro inhibition of DNA topoisomerase II was observed at ≥25 µM etoposide, but was not evident at lower etoposide concentrations associated with DNA damage. Our data indicate that low acute doses of etoposide can cause DNA strand breaks and chromosomal rearrangements involving MLL in human fetal HSC. Ultimately, such injury may have ramifications with regards to transplacental exposures to environmental chemicals linked to the etiology of infant acute leukemias. |
Author | Shao, Jing Moneypenny, Craig G. Gallagher, Evan P. Song, Yanyu |
Author_xml | – sequence: 1 givenname: Craig G. surname: Moneypenny fullname: Moneypenny, Craig G. organization: Present address: St. Jude Children's Research Hospital, Division of Molecular Therapeutics Department of Hematology and Oncology, Danny Thomas Research Tower, D5061, 332 North Lauderdale Street, Memphis, TN 38105, USA – sequence: 2 givenname: Jing surname: Shao fullname: Shao, Jing organization: Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA 98105, USA and – sequence: 3 givenname: Yanyu surname: Song fullname: Song, Yanyu organization: Department of Physiological Sciences, University of Florida, Gainesville, FL 32611, USA – sequence: 4 givenname: Evan P. surname: Gallagher fullname: Gallagher, Evan P. organization: Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA 98105, USA and |
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Keywords | Antineoplastic agent Human DNA topoisomerase (ATP-hydrolysing) Enzyme Stem cell Low dose Enzyme inhibitor Hematopoietic cell Etoposide Podophyllotoxine derivatives Isomerases Fetal cell Gene rearrangement Antimitotic |
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SubjectTerms | 4-HNE 4-hydroxynonenal acute lymphoblastic leukemia acute myelogenous leukemia ALL AML Antineoplastic Agents, Phytogenic - pharmacology Biological and medical sciences Carcinogenesis, carcinogens and anticarcinogens Cell Culture Techniques Cell Cycle - drug effects Cell Survival - drug effects DNA Damage DNA topoisomerase II Dose-Response Relationship, Drug Etoposide - pharmacology Female Fetus FISH fluorescence in situ hybridization Gene Rearrangement - drug effects hematopoietic stem cells Hematopoietic Stem Cells - drug effects Histone-Lysine N-Methyltransferase HSC Humans IAL infant acute leukemia kDNA kinetoplast DNA Leukemia - chemically induced Maternal-Fetal Exchange Medical sciences mixed lineage leukemia MLL MoAB monoclonal antibody Myeloid-Lymphoid Leukemia Protein - genetics Phycoerythrin Pregnancy topo II Tumors |
Title | MLL rearrangements are induced by low doses of etoposide in human fetal hematopoietic stem cells |
URI | https://api.istex.fr/ark:/67375/HXZ-M558VGKZ-5/fulltext.pdf https://www.ncbi.nlm.nih.gov/pubmed/16377807 https://www.proquest.com/docview/219393403 https://search.proquest.com/docview/19974618 |
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