ReviewInternational journal of hematology2005
Molecular pathogenesis of MLL-associated leukemias.
Review in International journal of hematology, 2005. 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
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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.
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, 49 citations in OpenAlex.
- Article
- Article
- Classifying leukemia types with chromatin conformation data.Genome biology · 2014Article
- Ligand-independent FLT3 activation does not cooperate with MLL-AF4 to immortalize/transform cord blood CD34+ cells.Leukemia · 2014Article
- Cytogenetic as an important tool for diagnosis and prognosis for patients with hypocellular primary myelodysplastic syndrome.BioMed research international · 2014Article
- Genomic characterization of acute leukemias.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2014Review
- Insights into the cellular origin and etiology of the infant pro-B acute lymphoblastic leukemia with MLL-AF4 rearrangement.Leukemia · 2011Review
- t(4;11) leukemias display addiction to MLL-AF4 but not to AF4-MLL.Leukemia research · 2011Article
- Genetic abnormalities and challenges in the treatment of acute myeloid leukemia.Genes & cancer · 2011Article
- E2F-1 directly regulates thrombospondin 1 expression.PloS one · 2010Article
- Challenges and strategies for generating therapeutic patient-specific hemangioblasts and hematopoietic stem cells from human pluripotent stem cells.The International journal of developmental biology · 2010Review
- Elongation factor ELL (Eleven-Nineteen Lysine-rich Leukemia) acts as a transcription factor for direct thrombospondin-1 regulation.The Journal of biological chemistry · 2009Article
- MLL fusions: pathways to leukemia.Cancer biology & therapy · 2009Review
- Article
- Diagnostic microarrays in hematologic oncology: applications of high- and low-density arrays.Molecular diagnosis & therapy · 2009Review
- Aberrant chromatin at genes encoding stem cell regulators in human mixed-lineage leukemia.Genes & development · 2008Article
- A variant-type MLL/SEPT9 fusion transcript in adult de novo acute monocytic leukemia (M5b) with t(11;17)(q23;q25).International journal of hematology · 2008Article
- Article
- HOX proteins and leukemia.International journal of clinical and experimental pathology · 2008Article
- Bimodal degradation of MLL by SCFSkp2 and APCCdc20 assures cell cycle execution: a critical regulatory circuit lost in leukemogenic MLL fusions.Genes & development · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromosome translocations disrupting the MLL gene are associated with various hematologic malignancies but are particularly common in infant and secondary therapy-related acute leukemias. The normal MLL-encoded protein is an essential component of a supercomplex with chromatin-modulating activity conferred by histone acetylase and methyltransferase activities, and the protein plays a key role in the developmental regulation of gene expression, including Hox gene expression. In leukemia, this function is subverted by breakage, recombination, and the formation of chimeric fusion with one of many alternative partners. Such MLL translocations result in the replacement of the C-terminal functional domains of MLL with those of a fusion partner, yielding a newly formed MLL chimeric protein with an altered function that endows hematopoietic progenitors with self-renewing and leukemogenic activity. This potent impact of the MLL chimera can be attributed to one of 2 kinds of activity of the fusion partner: direct transcriptional transactivation or dimerization/oligomerization. Key unresolved issues currently being addressed include the set of target genes for MLL fusions, the stem cell of origin for the leukemias, the role of additional secondary mutations, and the origins or etiology of the MLL gene fusions themselves. Further elaboration of the biology of MLL gene-associated leukemia should lead to novel and specific therapeutic strategies.
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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.