ReviewCancer2011
FLT3 inhibitors in the treatment of acute myeloid leukemia: the start of an era?
Review in Cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 83 citations in OpenAlex.
- A phase I/II study of the Janus kinase (JAK)1 and 2 inhibitor ruxolitinib in patients with relapsed or refractory acute myeloid leukemia.Clinical lymphoma, myeloma & leukemia · 2015Trial
- Predicting Novel Drug Candidates for Pancreatic Neuroendocrine Tumors via Gene Signature Comparison and Connectivity Mapping.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2022Article
- Combined effect of (-)-epigallocatechin-3-gallate and all-trans retinoic acid inBiomedical reports · 2020Article
- Review
- FLT3 inhibitor design using molecular docking based virtual screening for acute myeloid leukemia.Bioinformation · 2019Article
- Insights Into the Pathogenesis of Sweet's Syndrome.Frontiers in immunology · 2019Review
- Management of Adverse Events Associated with Cabozantinib Therapy in Renal Cell Carcinoma.The oncologist · 2018Review
- Aminoisoquinoline benzamides, FLT3 and Src-family kinase inhibitors, potently inhibit proliferation of acute myeloid leukemia cell lines.Future medicinal chemistry · 2017Article
- FLT3 activating mutations display differential sensitivity to multiple tyrosine kinase inhibitors.Oncotarget · 2017Article
- Characteristics of Sweet Syndrome in patients with acute myeloid leukemia.Clinical lymphoma, myeloma & leukemia · 2015Article
- Independent oncogenic and therapeutic significance of phosphatase PRL-3 in FLT3-ITD-negative acute myeloid leukemia.Cancer · 2014Article
- Article
- Investigational FMS-like tyrosine kinase 3 inhibitors in treatment of acute myeloid leukemia.Expert opinion on investigational drugs · 2014Review
- Acute myeloid leukemia in the elderly: do we know who should be treated and how?Leukemia & lymphoma · 2014Review
- Phase I study of quizartinib administered daily to patients with relapsed or refractory acute myeloid leukemia irrespective of FMS-like tyrosine kinase 3-internal tandem duplication status.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2013Article
- Review
- Article
- Extracellular assembly and activation principles of oncogenic class III receptor tyrosine kinases.Nature reviews. Cancer · 2012Review
- Article
- An overview on the role of FLT3-tyrosine kinase receptor in acute myeloid leukemia: biology and treatment.Oncology reviews · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Despite recent modest improvements in the chemotherapy regimens used to treat acute myeloid leukemia (AML), many patients diagnosed with AML ultimately die of the disease. Commonly occurring genetic alterations have been identified that strongly affect the prognosis for patients with AML. These alterations represent possible targets for investigational therapies that could act to specifically halt the aberrant growth of AML cells while limiting damage to normal cells. One such gene is the Fms-like tyrosine kinase 3 (FLT3) gene, which is mutated in approximately 30% of adult patients with AML and has a significant impact on prognosis. In particular, internal tandem duplications in FLT3 confer a poor prognosis to this large subgroup of patients with AML. Agents that target FLT3 are in development for the treatment of patients who have AML and offer a potential paradigm change in the current standard treatment of AML. For this report, the authors reviewed the prognostic significance of genetic alterations observed in AML with a focus on the therapeutic implications of targeting FLT3. The introduction of such agents may be the next major step toward the era of personalized therapy in AML.
Indexed as
Identifiers
What OpenQuestion holds
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.