ArticleCell cycle (Georgetown, Tex.)2008
Transforming human blood stem and progenitor cells: a new way forward in leukemia modeling.
Article in Cell cycle (Georgetown, Tex.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- PTP4A2 promotes leukemogenesis through inhibiting the p53 tumor suppressor signaling pathway in leukemia-initiating cells.Blood advances · 2026Article
- Characterizing the impact of MLL fusion variants and fusion partners on leukemia plasticity using a human CRISPR-engineered MLL-rearranged leukemia model.Neoplasia (New York, N.Y.) · 2026Article
- ALKBH1 Drives Tumorigenesis and Drug Resistance via tRNA-decoding Reprogramming and Codon-biased Translation.Cancer discovery · 2025Article
- Distinct phases of cellular signaling revealed by time-resolved protein synthesis.Nature chemical biology · 2024Article
- Advances in molecular characterization of pediatric acute megakaryoblastic leukemia not associated with Down syndrome; impact on therapy development.Frontiers in cell and developmental biology · 2023Review
- MLL::AF9 degradation induces rapid changes in transcriptional elongation and subsequent loss of an active chromatin landscape.Molecular cell · 2022Article
- SLC5A3-Dependent Myo-inositol Auxotrophy in Acute Myeloid Leukemia.Cancer discovery · 2022Article
- SCP4-STK35/PDIK1L complex is a dual phospho-catalytic signaling dependency in acute myeloid leukemia.Cell reports · 2022Article
- ZNF521 Enhances MLL-AF9-Dependent Hematopoietic Stem Cell Transformation in Acute Myeloid Leukemias by Altering the Gene Expression Landscape.International journal of molecular sciences · 2021Article
- Development and characterization of a DNA aptamer for MLL-AF9 expressing acute myeloid leukemia cells using whole cell-SELEX.Scientific reports · 2021Article
- Targeting CD33 in Chemoresistant AML Patient-Derived Xenografts by CAR-CIK Cells Modified with an Improved SB Transposon System.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- Zoledronic acid inhibits the growth of leukemic MLL-AF9 transformed hematopoietic cells.Heliyon · 2020Article
- Article
- Pharmacological Rac1 inhibitors with selective apoptotic activity in human acute leukemic cell lines.Oncotarget · 2017Article
- Protease-activated receptor-1 inhibits proliferation but enhances leukemia stem cell activity in acute myeloid leukemia.Oncogene · 2017Article
- UBASH3B/Sts-1-CBL axis regulates myeloid proliferation in human preleukemia induced by AML1-ETO.Leukemia · 2016Article
- Therapeutic antagonists of microRNAs deplete leukemia-initiating cell activity.The Journal of clinical investigation · 2014Article
- The rate of spontaneous mutations in human myeloid cells.Mutation research · 2013Article
- Transcription factor RUNX1 promotes survival of acute myeloid leukemia cells.The Journal of clinical investigation · 2013Article
- AML cells are differentially sensitive to chemotherapy treatment in a human xenograft model.Blood · 2013Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
MLL-AF9 (MA9) is a leukemia fusion gene formed upon translocation of the AF9 gene on chromosome 9 and the MLL gene on chromosome 11. MA9 is commonly found in acute myeloid leukemia (AML) and occasionally in acute lymphoid leukemia and is associated with intermediate to poor outcome. The specific signaling pathways downstream of MA9 are still poorly understood. We have recently described a model system whereby we expressed the MA9 fusion gene in human CD34(+) Umbilical Cord Blood (UCB) cells and showed that these cells transformed to acute myeloid or lymphoid leukemia when injected into immunodeficient mice. The Mixed Lineage Leukemia (MLL) oncogenes are unique in this model system in that they promote full transformation of primary human blood cells, while all other leukemia-associated oncogenes tested thus far have induced only partial phenotypes. Here we provide an update on the use of this system for modeling human leukemia and its potential application for therapeutic testing of novel compounds to treat the disease. We focus specifically on the Rho family of small guanosine triphosphatases (GTPases) as potential therapeutic targets, which we have implicated in the pathogenesis of AML associated with MA9 expression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.