ArticleThe oncologist2011
FLT3 inhibition as therapy in acute myeloid leukemia: a record of trials and tribulations.
Article in The oncologist, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 45 citations in OpenAlex.
- Exosomal biomarkers in leukemia: translational potential and regulatory challenges for precision medicine applications.Frontiers in immunology · 2025Review
- FLT3L-dependent dendritic cells control tumor immunity by modulating Treg and NK cell homeostasis.Cell reports. Medicine · 2023Article
- Role of Biomarkers in FLT3 AML.Cancers · 2022Review
- CD52 is a novel target for the treatment of FLT3-ITD-mutated myeloid leukemia.Cell death discovery · 2021Article
- Article
- Design of FLT3 Inhibitor - Gold Nanoparticle Conjugates as Potential Therapeutic Agents for the Treatment of Acute Myeloid Leukemia.Nanoscale research letters · 2015Article
- Preclinical antitumor activity of ST7612AA1: a new oral thiol-based histone deacetylase (HDAC) inhibitor.Oncotarget · 2015Article
- The antitumor compound triazoloacridinone C-1305 inhibits FLT3 kinase activity and potentiates apoptosis in mutant FLT3-ITD leukemia cells.Acta pharmacologica Sinica · 2015Article
- Synergistic cytotoxicity of sorafenib with busulfan and nucleoside analogs in human FMS-like tyrosine kinase 3 internal tandem duplications-positive acute myeloid leukemia cells.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2014Article
- Preclinical antitumor activity of SST0116CL1: a novel heat shock protein 90 inhibitor.International journal of oncology · 2014Article
- FLT3 kinase inhibitor TTT-3002 overcomes both activating and drug resistance mutations in FLT3 in acute myeloid leukemia.Cancer research · 2014Article
- Drug repurposing screen identifies lestaurtinib amplifies the ability of the poly (ADP-ribose) polymerase 1 inhibitor AG14361 to kill breast cancer associated gene-1 mutant and wild type breast cancer cells.Breast cancer research : BCR · 2014Article
- Novel therapeutics in acute myeloid leukemia.Current hematologic malignancy reports · 2014Review
- Treatment of relapse of acute myeloid leukemia after allogeneic hematopoietic stem cell transplantation.Current hematologic malignancy reports · 2014Review
- Reversal of acquired drug resistance in FLT3-mutated acute myeloid leukemia cells via distinct drug combination strategies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Article
- Emergence of polyclonal FLT3 tyrosine kinase domain mutations during sequential therapy with sorafenib and sunitinib in FLT3-ITD-positive acute myeloid leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Article
- Using functional genomics to overcome therapeutic resistance in hematological malignancies.Immunologic research · 2013Review
- Article
- Gene mutations and molecularly targeted therapies in acute myeloid leukemia.American journal of blood research · 2013Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is a hematologic malignancy with a poor prognosis. Approximately one quarter of the patients with AML also carry an internal tandem duplication (ITD) mutation in the gene encoding FMS-like tyrosine kinase 3 (FLT3), which has a significantly deleterious impact on prognosis. The ITD mutation renders FLT3 constitutively active and leads to uncontrolled proliferation of the leukemic blast. Over the course of the last decade, a variety of compounds have been developed in preclinical and clinical studies as potent inhibitors of FLT3. Many of the earlier agents under investigation, such as lestaurtinib, midostaurin, and sunitinib, were initially developed as inhibitors of other tyrosine kinases and as targeted therapies in a variety of malignancies. These compounds have been demonstrated to have some efficacy in clinical trials of AML, mainly manifesting as transient decreases in circulating blasts correlating with effective in vivo suppression of the FLT3 target. Nevertheless, the cumbersome pharmacokinetics of some compounds and the suboptimal specificity and potency of others have limited their therapeutic efficacy. In the last few years, newer, more potent and specific agents have been under investigation, with the leading example being AC220. This agent has shown significant promise in early phases of clinical investigation, and is currently in more advanced clinical trials. Hope remains that FLT3 inhibition will be become an effective therapeutic adjunct to our current treatment approach to AML.
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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.