ArticleGenes & cancer2010
Duplication of Subcytoband 11E2 of Chromosome 11 Is Regularly Associated with Accelerated Tumor Development in v-abl/myc-Induced Mouse Plasmacytomas.
Article in Genes & cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Copy number gains of chromosome 17 identified by dual in situ hybridization in non-small cell lung cancer tissue correlate with overexpression of c-Myc.Translational cancer research · 2022Article
- Assessment of the clinical relevance of 17q25.3 copy number and three-dimensional telomere organization in non-small lung cancer patients.Journal of cancer research and clinical oncology · 2016Article
- Changes in Nuclear Orientation Patterns of Chromosome 11 during Mouse Plasmacytoma Development.Translational oncology · 2015Article
- Distinct nuclear orientation patterns for mouse chromosome 11 in normal B lymphocytes.BMC cell biology · 2014Article
- Selected telomere length changes and aberrant three-dimensional nuclear telomere organization during fast-onset mouse plasmacytomas.Neoplasia (New York, N.Y.) · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromosome 11 aberrations constitute the second most frequent chromosomal aberration in mouse plasmacytomas (PCTs) in which both the myc and abl oncogenes are constitutively expressed. In these tumors, previous G-banding studies had revealed numerical aberrations including duplication of the entire chromosome 11 or segments of telomeric bands D and E. The trisomy of chromosome 11 was always associated with accelerated pristane + v-abl/myc-induced PCT development. In the present study, PCT development was studied in a unique BALB/c congenic mouse strain, (T38HxBALB/c) F1, carrying a reciprocal translocation between chromosomes X and 11. After v-abl/myc induction, PCTs in this strain had acquired a nonrandom duplication of subcytoband 11E2. This duplication was always associated with accelerated PCT development. Corresponding synteny regions in the human and rat are changed in many tumors and involved in duplication, amplification, or translocation events. Thus, together with these synteny data, our findings strongly suggest a causal involvement of 11E2 in the acceleration of v-abl/myc-induced PCTs.
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