ArticleOncotarget2017
The implication of FLT3 amplification for FLT targeted therapeutics in solid tumors.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
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- Acute myeloid leukemia: from NGS, through scRNA-seq, to CAR-T. dissect cancer heterogeneity and tailor the treatment.Journal of experimental & clinical cancer research : CR · 2023Review
- A Multicenter, Open-Label, Phase I/II Study of FN-1501 in Patients with Advanced Solid Tumors.Cancers · 2023Article
- Recent Advances in the Development of Anti-FLT3 CAR T-Cell Therapies for Treatment of AML.Biomedicines · 2022Review
- Head to head evaluation of second generation ALK inhibitors brigatinib and alectinib as first-line treatment for ALK+ NSCLC using anOncotarget · 2021Article
- TM4SF4 and LRRK2 Are Potential Therapeutic Targets in Lung and Breast Cancers through Outlier Analysis.Cancer research and treatment · 2021Article
- FMS-like tyrosine kinase 3 (FLT3) amplification in patients with metastatic colorectal cancer.Cancer science · 2021Observational
- Article
- Sunitinib in Patients with Metastatic Colorectal Cancer (mCRC) with FLT-3 Amplification: Results from the Targeted Agent and Profiling Utilization Registry (TAPUR) Study.Targeted oncology · 2020Article
- Increased Risk of Acute Myelogenous Leukemia After Early Onset but Not Late-Onset Colorectal Cancer.American journal of clinical oncology · 2020Article
- Cell-free DNA analysis reveals POLR1D-mediated resistance to bevacizumab in colorectal cancer.Genome medicine · 2020Article
- Treatment of Acute Myeloid Leukemia in the Era of Genomics-Achievements and Persisting Challenges.Frontiers in genetics · 2020Review
- Targeting Receptor Kinases in Colorectal Cancer.Cancers · 2019Review
- Pharmacogenomic landscape of patient-derived tumor cells informs precision oncology therapy.Nature genetics · 2018Article
Corrections and comments
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Authors and funding
18 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the patients with solid cancers harboring Fms-like tyrosine kinase 3 (FLT3) amplification using targeted sequencing of tumor tissue specimen and FISH assay. Simultaneously, FLT3-amplified patient-derived cells (PDCs) were generated to evaluate the sensitivity to FLT3 inhibition. A patient with metastatic colon cancer who was previously treated with more than 3rd line cytotoxic chemotherapy was found to have FLT3 amplification and then received regorafenib showing partial response. In two PDC cell lines with FLT3 amplification, FLT3 mRNA expression was increased, however, the growth of tumor cells was not significantly inhibited by either regorafenib or sorafenib which is known to block the activity FLT3. Additional drug combinations with mTOR inhibitor did not affect the cell proliferation of PDC. FLT3 amplification in solid cancers is infrequently observed using targeted genomic profile, as yet, FLT3 amplification does not seem to be an actionable target or a proper biomarker for FLT3 inhibitor sensitivity.
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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.