ReviewNature genetics1998
Translocations, cancer and the puzzle of specificity.
Review in Nature genetics, 1998. 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
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
26 citing papers in PubMed, 103 citations in OpenAlex.
- Fusion genes in cancers: Biogenesis, functions, and therapeutic implications.Genes & diseases · 2025Review
- "Putting the cart before the horse": an update on promiscuous gene fusions in soft tissue tumors.Virchows Archiv : an international journal of pathology · 2025Review
- Hematopoietic and Chronic Myeloid Leukemia Stem Cells: Multi-Stability versus Lineage Restriction.International journal of molecular sciences · 2022Review
- Article
- Computational Detection of Known Pathogenic Gene Fusions in a Normal Tissue Database and Implications for Genetic Disease Research.Frontiers in genetics · 2020Article
- GEFT aberrant expression in soft tissue sarcomas.Translational cancer research · 2019Article
- Article
- Advances in sarcoma genomics and new therapeutic targets.Nature reviews. Cancer · 2011Review
- The myxoid/round cell liposarcoma fusion oncogene FUS-DDIT3 and the normal DDIT3 induce a liposarcoma phenotype in transfected human fibrosarcoma cells.The American journal of pathology · 2006Article
- Non-reciprocal chromosomal bridge-induced translocation (BIT) by targeted DNA integration in yeast.Chromosoma · 2005Article
- Directing oncogenic fusion genes into stem cells via an SCL enhancer.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Modeling first-hit functions of the t(12;21) TEL-AML1 translocation in mice.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Role of the TEL-AML1 fusion gene in the molecular pathogenesis of childhood acute lymphoblastic leukaemia.Oncogene · 2004Review
- Reciprocal translocations in Saccharomyces cerevisiae formed by nonhomologous end joining.Genetics · 2004Article
- Molecular genetics of pediatric soft tissue tumors: clinical application.The Journal of molecular diagnostics : JMD · 2003Review
- The pathogenetic role of oncogenes deregulated by chromosomal translocation in B-cell malignancies.International journal of hematology · 2003Review
- Fusions of the SYT and SSX genes in synovial sarcoma.Oncogene · 2001Review
- Loss of drug-stimulated topoisomerase II DNA breaks in living cells is different at two unrelated loci.Nucleic acids research · 2000Article
- Aberrant ALK tyrosine kinase signaling. Different cellular lineages, common oncogenic mechanisms.The American journal of pathology · 2000Article
- Association of EWS-FLI1 type 1 fusion with lower proliferative rate in Ewing's sarcoma.The American journal of pathology · 2000Article
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
The finding of acquired chromosomal translocations that are consistently associated with specific tumour types supports the premise of lineage-specific mechanisms of tumorigenesis. We review the evidence indicating that the specificity of these translocations and the corresponding gene fusions is related to biological constraints at the level of recombination, expression, and protein function. A dynamic relationship between the gene fusion and the cellular environment is proposed in which the environment influences the selection of oncogenic fusions and the oncogenic fusion in turn influences the cellular environment.
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.