ReviewOncogene2001
In vivo analysis of the molecular genetics of acute promyelocytic leukemia.
Review in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 59 citations in OpenAlex.
- Choosing the Right Cell Line for Acute Myeloid Leukemia (AML) Research.International journal of molecular sciences · 2023Review
- Genomic Abnormalities as Biomarkers and Therapeutic Targets in Acute Myeloid Leukemia.Cancers · 2021Review
- Efficiency of All-Trans Retinoic Acid on Gastric Cancer: A Narrative Literature Review.International journal of molecular sciences · 2018Review
- Contribution of the C-terminal regions of promyelocytic leukemia protein (PML) isoforms II and V to PML nuclear body formation.The Journal of biological chemistry · 2012Article
- The mechanisms of PML-nuclear body formation.Molecular cell · 2006Article
- Molecular biology in acute leukemia.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2006Review
- Article
- Aberrant promoter methylation of the retinoic acid receptor alpha gene in acute promyelocytic leukemia.Leukemia · 2005Article
- Promyelocytic leukemia protein-induced growth suppression and cell death in liver cancer cells.Cancer gene therapy · 2005Article
- Identification of genes that synergize with Cbfb-MYH11 in the pathogenesis of acute myeloid leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Review
- Growth suppression by acute promyelocytic leukemia-associated protein PLZF is mediated by repression of c-myc expression.Molecular and cellular biology · 2003Article
- Genetic and biological subgroups of low-stage follicular thyroid cancer.The American journal of pathology · 2003Article
- Review
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 promyelocytic leukemia (APL) is a distinct and paradigmatic subtype of myeloid leukemia associated with reciprocal chromosomal translocations always involving the Retinoic Acid Receptor(alpha) (RARalpha) gene on chromosome 17 and variable partner genes (X genes) on different chromosomes. As a consequence of these translocations X-RARalpha and RARalpha-X fusion genes are generated. RARalpha fuses to the PML gene in the vast majority of APL cases, and in a few cases to the PLZF, NPM, NuMA and STAT5b genes respectively. In the last few years, the functions of these aberrant fusion proteins and of the normal gene products involved in these translocations have been extensively characterized in vivo in transgenic and KO animal models. Here we will review the important conclusions, the novel questions and paradoxes that stem from this analysis.
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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.