Identification of AML1-ETO modulators by chemical genomics
Somatic rearrangements of transcription factors are common abnormalities in the acute leukemias. With rare exception, however, the resultant protein products have remained largely intractable as pharmacologic targets. One example is AML1-ETO, the most common translocation reported in acute myeloid l...
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Published in | Blood Vol. 113; no. 24; pp. 6193 - 6205 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Washington, DC
Elsevier Inc
11.06.2009
Americain Society of Hematology American Society of Hematology |
Series | Myeloid Neoplasia |
Subjects | |
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Abstract | Somatic rearrangements of transcription factors are common abnormalities in the acute leukemias. With rare exception, however, the resultant protein products have remained largely intractable as pharmacologic targets. One example is AML1-ETO, the most common translocation reported in acute myeloid leukemia (AML). To identify AML1-ETO modulators, we screened a small molecule library using a chemical genomic approach. Gene expression signatures were used as surrogates for the expression versus loss of the translocation in AML1-ETO–expressing cells. The top classes of compounds that scored in this screen were corticosteroids and dihydrofolate reductase (DHFR) inhibitors. In addition to modulating the AML1-ETO signature, both classes induced evidence of differentiation, dramatically inhibited cell viability, and ultimately induced apoptosis via on-target activity. Furthermore, AML1-ETO–expressing cell lines were exquisitely sensitive to the effects of corticosteroids on cellular viability compared with nonexpressers. The corticosteroids diminished AML1-ETO protein in AML cells in a proteasome- and glucocorticoid receptor–dependent manner. Moreover, these molecule classes demonstrated synergy in combination with standard AML chemotherapy agents and activity in an orthotopic model of AML1-ETO–positive AML. This work suggests a role for DHFR inhibitors and corticosteroids in treating patients with AML1-ETO–positive disease. |
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AbstractList | Abstract
Somatic rearrangements of transcription factors are common abnormalities in the acute leukemias. With rare exception, however, the resultant protein products have remained largely intractable as pharmacologic targets. One example is AML1-ETO, the most common translocation reported in acute myeloid leukemia (AML). To identify AML1-ETO modulators, we screened a small molecule library using a chemical genomic approach. Gene expression signatures were used as surrogates for the expression versus loss of the translocation in AML1-ETO–expressing cells. The top classes of compounds that scored in this screen were corticosteroids and dihydrofolate reductase (DHFR) inhibitors. In addition to modulating the AML1-ETO signature, both classes induced evidence of differentiation, dramatically inhibited cell viability, and ultimately induced apoptosis via on-target activity. Furthermore, AML1-ETO–expressing cell lines were exquisitely sensitive to the effects of corticosteroids on cellular viability compared with nonexpressers. The corticosteroids diminished AML1-ETO protein in AML cells in a proteasome- and glucocorticoid receptor–dependent manner. Moreover, these molecule classes demonstrated synergy in combination with standard AML chemotherapy agents and activity in an orthotopic model of AML1-ETO–positive AML. This work suggests a role for DHFR inhibitors and corticosteroids in treating patients with AML1-ETO–positive disease. Somatic rearrangements of transcription factors are common abnormalities in the acute leukemias. With rare exception, however, the resultant protein products have remained largely intractable as pharmacologic targets. One example is AML1-ETO, the most common translocation reported in acute myeloid leukemia (AML). To identify AML1-ETO modulators, we screened a small molecule library using a chemical genomic approach. Gene expression signatures were used as surrogates for the expression versus loss of the translocation in AML1-ETO–expressing cells. The top classes of compounds that scored in this screen were corticosteroids and dihydrofolate reductase (DHFR) inhibitors. In addition to modulating the AML1-ETO signature, both classes induced evidence of differentiation, dramatically inhibited cell viability, and ultimately induced apoptosis via on-target activity. Furthermore, AML1-ETO–expressing cell lines were exquisitely sensitive to the effects of corticosteroids on cellular viability compared with nonexpressers. The corticosteroids diminished AML1-ETO protein in AML cells in a proteasome- and glucocorticoid receptor–dependent manner. Moreover, these molecule classes demonstrated synergy in combination with standard AML chemotherapy agents and activity in an orthotopic model of AML1-ETO–positive AML. This work suggests a role for DHFR inhibitors and corticosteroids in treating patients with AML1-ETO–positive disease. |
Author | Corsello, Steven M. Ross, Kenneth N. Stegmaier, Kimberly Golub, Todd R. Chow, Kwan T. Stone, Richard M. Kung, Andrew L. Roti, Giovanni Galinsky, Ilene DeAngelo, Daniel J. |
Author_xml | – sequence: 1 givenname: Steven M. surname: Corsello fullname: Corsello, Steven M. organization: Department of Pediatric Oncology, Dana-Farber Cancer Institute and Children's Hospital Boston, Harvard Medical School, MA – sequence: 2 givenname: Giovanni surname: Roti fullname: Roti, Giovanni organization: Department of Pediatric Oncology, Dana-Farber Cancer Institute and Children's Hospital Boston, Harvard Medical School, MA – sequence: 3 givenname: Kenneth N. surname: Ross fullname: Ross, Kenneth N. organization: The Broad Institute of Harvard University and Massachusetts Institute of Technology, Cambridge – sequence: 4 givenname: Kwan T. surname: Chow fullname: Chow, Kwan T. organization: Department of Pediatric Oncology, Dana-Farber Cancer Institute and Children's Hospital Boston, Harvard Medical School, MA – sequence: 5 givenname: Ilene surname: Galinsky fullname: Galinsky, Ilene organization: Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA – sequence: 6 givenname: Daniel J. surname: DeAngelo fullname: DeAngelo, Daniel J. organization: Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA – sequence: 7 givenname: Richard M. surname: Stone fullname: Stone, Richard M. organization: Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA – sequence: 8 givenname: Andrew L. surname: Kung fullname: Kung, Andrew L. organization: Department of Pediatric Oncology, Dana-Farber Cancer Institute and Children's Hospital Boston, Harvard Medical School, MA – sequence: 9 givenname: Todd R. surname: Golub fullname: Golub, Todd R. organization: Department of Pediatric Oncology, Dana-Farber Cancer Institute and Children's Hospital Boston, Harvard Medical School, MA – sequence: 10 givenname: Kimberly surname: Stegmaier fullname: Stegmaier, Kimberly email: kimberly_stegmaier@dfci.harvard.edu organization: Department of Pediatric Oncology, Dana-Farber Cancer Institute and Children's Hospital Boston, Harvard Medical School, MA |
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Keywords | Chromosomal aberration Abnormal chromosome C8 Modulator Hematology Abnormal chromosome Abnormal chromosome G21 Genome Hybrid gene Chromosome translocation |
Language | English |
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Notes | S.M.C. and G.R. contributed equally to this work. |
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Snippet | Somatic rearrangements of transcription factors are common abnormalities in the acute leukemias. With rare exception, however, the resultant protein products... Abstract Somatic rearrangements of transcription factors are common abnormalities in the acute leukemias. With rare exception, however, the resultant protein... |
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SubjectTerms | Acetylation Animals Antineoplastic Agents - pharmacology Apoptosis - drug effects Biological and medical sciences Cell Differentiation Cell Proliferation - drug effects Chromosome aberrations Combinatorial Chemistry Techniques Core Binding Factor Alpha 2 Subunit - antagonists & inhibitors Core Binding Factor Alpha 2 Subunit - genetics Core Binding Factor Alpha 2 Subunit - metabolism Flow Cytometry Gene Expression Profiling Genomics Hematologic and hematopoietic diseases Histone Deacetylase Inhibitors Histone Deacetylases - metabolism Histones - metabolism Humans Immunoblotting Male Medical genetics Medical sciences Mice Mice, Inbred NOD Myeloid Cells - drug effects Myeloid Cells - metabolism Myeloid Neoplasia Neoplasms - drug therapy Neoplasms - genetics Neoplasms - metabolism Oligonucleotide Array Sequence Analysis Oncogene Proteins, Fusion - antagonists & inhibitors Oncogene Proteins, Fusion - genetics Oncogene Proteins, Fusion - metabolism Pharmaceutical Preparations - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics RNA, Messenger - metabolism RNA, Small Interfering - pharmacology RUNX1 Translocation Partner 1 Protein Translocation, Genetic |
Title | Identification of AML1-ETO modulators by chemical genomics |
URI | https://dx.doi.org/10.1182/blood-2008-07-166090 https://www.ncbi.nlm.nih.gov/pubmed/19377049 https://pubmed.ncbi.nlm.nih.gov/PMC2699238 |
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