ReviewLeukemia2005
Gatekeeper pathways and cellular background in the pathogenesis and therapy of AML.
Review in Leukemia, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 22 citations in OpenAlex.
- Identification of DUSP7 as an RNA Marker for Prognostic Stratification in Acute Myeloid Leukemia: Evidence from Large Population Cohorts.Genetics research · 2023Article
- Dual mTORC2/mTORC1 targeting results in potent suppressive effects on acute myeloid leukemia (AML) progenitors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011Article
- Review
- Peripheral T cell lymphoma: new model + new insight.The Journal of experimental medicine · 2010Article
- Molecular mechanisms underlying deregulation of C/EBPalpha in acute myeloid leukemia.International journal of hematology · 2010Review
- Phosphoinositide 3-kinase/Akt signaling pathway and its therapeutical implications for human acute myeloid leukemia.Leukemia · 2006Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myelogenous leukemia (AML) is characterized by the accumulation of immature cells due to disturbed differentiation and proliferation of the myeloid lineage. Genetic alterations affecting transcription factors and receptor tyrosine kinases have been identified in AML and causally linked to the disease. The goal of this review is to address the role of the different genetic alterations in self-renewal and proliferation and to discuss the cellular background in which these events occur during the pathogenesis of AML. Data from AML samples, clinical studies and mouse models for AML will be used to support the different theories regarding the leukemogenesis of AML. Finally, this review wants to highlight the implication of these findings for the therapy of 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.