ArticleCancer research2013
Kinase pathway dependence in primary human leukemias determined by rapid inhibitor screening.
Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.
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Who cites it
106 citing papers in PubMed, 149 citations in OpenAlex.
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- Lymphoma and Leukemia Cell Vulnerabilities and Resistance Identified by Compound Library Screens.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Single-cell landscape of innate and acquired drug resistance in acute myeloid leukemia.Nature communications · 2024Article
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- Therapeutic biomarkers in acute myeloid leukemia: functional and genomic approaches.Frontiers in oncology · 2024Review
- Clinical forecasting of acute myeloid leukemia using ex vivo drug-sensitivity profiling.Cell reports methods · 2023Article
- Standardized assays to monitor drug sensitivity in hematologic cancers.Cell death discovery · 2023Article
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- Modelling acute myeloid leukemia (AML): What's new? A transition from the classical to the modern.Drug delivery and translational research · 2023Review
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- Treatment for ovarian clear cell carcinoma with combined inhibition of WEE1 and ATR.Journal of ovarian research · 2023Article
- Pharmacological approaches to understanding protein kinase signaling networks.Frontiers in pharmacology · 2023Review
- Ex Vivo Drug Sensitivity Correlates with Clinical Response and Supports Personalized Therapy in Pediatric AML.Cancers · 2022Article
- Therapeutic Targeting of MERTK and BCL-2 in T-Cell and Early T-Precursor Acute Lymphoblastic Leukemia.Cancers · 2022Article
- Comprehensive molecular characterization of a rare case of Philadelphia chromosome-positive acute myeloid leukemia.Cold Spring Harbor molecular case studies · 2022Article
46 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
20 authors at 7 institutions in 3 countries.
Funding
Abstract
Kinases are dysregulated in most cancers, but the frequency of specific kinase mutations is low, indicating a complex etiology in kinase dysregulation. Here, we report a strategy to rapidly identify functionally important kinase targets, irrespective of the etiology of kinase pathway dysregulation, ultimately enabling a correlation of patient genetic profiles to clinically effective kinase inhibitors. Our methodology assessed the sensitivity of primary leukemia patient samples to a panel of 66 small-molecule kinase inhibitors over 3 days. Screening of 151 leukemia patient samples revealed a wide diversity of drug sensitivities, with 70% of the clinical specimens exhibiting hypersensitivity to one or more drugs. From this data set, we developed an algorithm to predict kinase pathway dependence based on analysis of inhibitor sensitivity patterns. Applying this algorithm correctly identified pathway dependence in proof-of-principle specimens with known oncogenes, including a rare FLT3 mutation outside regions covered by standard molecular diagnostic tests. Interrogation of all 151 patient specimens with this algorithm identified a diversity of kinase targets and signaling pathways that could aid prioritization of deep sequencing data sets, permitting a cumulative analysis to understand kinase pathway dependence within leukemia subsets. In a proof-of-principle case, we showed that in vitro drug sensitivity could predict both a clinical response and the development of drug resistance. Taken together, our results suggested that drug target scores derived from a comprehensive kinase inhibitor panel could predict pathway dependence in cancer cells while simultaneously identifying potential therapeutic options.
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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.