ArticleScientific reports2016
Using genome-wide CRISPR library screening with library resistant DCK to find new sources of Ara-C drug resistance in AML.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 74 citations in OpenAlex.
- Nucleotide Metabolism in Health and Disease.MedComm · 2026Review
- Enhancing the Nucleoside Analog Response with Translational Therapeutic Approaches to Overcome Resistance.Cells · 2026Review
- Recent advances in drug delivery and treatment strategies for acute myeloid leukemia.International journal of pharmaceutics · 2025Review
- Identification of Target Genes Using Innovative Screening Systems.Pathology international · 2025Review
- Modified screening of MYC promotor region elements using the CRISPR library in ovarian cancer.Journal of ovarian research · 2025Article
- The E3 ubiquitin ligase Herc1 modulates the response to nucleoside analogs in acute myeloid leukemia.Blood advances · 2024Article
- Application of single cell sequencing technology in ovarian cancer research (review).Functional & integrative genomics · 2024Review
- Genome-wide CRISPR screening identifies critical role of phosphatase and tensin homologous (Journal of Zhejiang University. Science. B · 2024Article
- Upregulation of HOXA3 by isoform-specific Wilms tumour 1 drives chemotherapy resistance in acute myeloid leukaemia.British journal of haematology · 2024Article
- Use of CRISPR-based screens to identify mechanisms of chemotherapy resistance.Cancer gene therapy · 2023Review
- Article
- Dexamethasone enhances venetoclax-induced apoptosis in acute myeloid leukemia cells.Medical oncology (Northwood, London, England) · 2023Article
- Indirect CRISPR screening with photoconversion revealed key factors of drug resistance with cell-cell interactions.Communications biology · 2023Article
- A review on CRISPR/Cas: a versatile tool for cancer screening, diagnosis, and clinic treatment.Functional & integrative genomics · 2023Review
- The genomic landscape of sensitivity to arsenic trioxide uncovered by genome-wide CRISPR-Cas9 screening.Frontiers in oncology · 2023Article
- Article
- Proliferation and Self-Renewal Are Differentially Sensitive to NRASG12V Oncogene Levels in an Acute Myeloid Leukemia Cell Line.Molecular cancer research : MCR · 2022Article
- Cellular Target Deconvolution of Small Molecules Using a Selection-Based Genetic Screening Platform.ACS central science · 2022Article
- Identification of the Factor That Leads Human Mesenchymal Stem Cell Lines into Decellularized Bone.Bioengineering (Basel, Switzerland) · 2022Article
- Review
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) can display de novo or acquired resistance to cytosine arabinoside (Ara-C), a primary component of induction chemotherapy. To identify genes capable of independently imposing Ara-C resistance, we applied a genome-wide CRISPR library to human U937 cells and exposed to them to Ara-C. Interestingly, all drug resistant clones contained guide RNAs for DCK. To avoid DCK gene modification, gRNA resistant DCK cDNA was created by the introduction of silent mutations. The CRISPR screening was repeated using the gRNA resistant DCK, and loss of SLC29A was identified as also being capable of conveying Ara-C drug resistance. To determine if loss of Dck results in increased sensitivity to other drugs, we conducted a screen of 446 FDA approved drugs using two Dck-defective BXH-2 derived murine AML cell lines and their Ara-C sensitive parental lines. Both cell lines showed an increase in sensitivity to prednisolone. Guide RNA resistant cDNA rescue was a legitimate strategy and multiple DCK or SLC29A deficient human cell clones were established with one clone becoming prednisolone sensitive. Dck-defective leukemic cells may become prednisolone sensitive indicating prednisolone may be an effective adjuvant therapy in some cases of DCK-negative AML.
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