ArticleNeoplasia (New York, N.Y.)2022
Whole-chromosome arm acquired uniparental disomy in cancer development is a consequence of isochromosome formation.
Article in Neoplasia (New York, N.Y.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 10 citations in OpenAlex.
- Genetic modeling of ELP1-associated Sonic hedgehog medulloblastoma identifies MDM2 as a selective therapeutic target.Cancer cell · 2025Article
- SPAG6 Promotes Multiple Myeloma Through Activation of the MAPK/ERK Signaling Pathway.Frontiers in pharmacology · 2025Article
- Insights into the Clinical, Biological and Therapeutic Impact of Copy Number Alteration in Cancer.International journal of molecular sciences · 2024Review
- Gross Chromosomal Rearrangement at Centromeres.Biomolecules · 2023Review
- SETD2 safeguards the genome against isochromosome formation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Fission yeast Srr1 and Skb1 promote isochromosome formation at the centromere.Communications biology · 2023Article
- Prognostic Impact ofCancers · 2022Article
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 2 institutions in 1 country.
Funding
Abstract
Using SNP-based microarray data from The Cancer Genome Atlas (TCGA), we investigated isochromosomes (deletion of one arm and duplication of the other arm) and related acquired uniparental disomy in 12 tumor types. We observed a high frequency of isochromosomes (25.98%) across all type of tumors except thyroid cancers. The highest frequency of isochromosomes was found in lung squamous cell carcinoma (54.18%). Moreover, whole-chromosome arm acquired uniparental disomy (aUPD) was common in the deleted arms of isochromosomes. These data are consistent with whole-chromosome arm aUPD likely being a consequence of isochromosomes formation. Our findings implicated aUPD as occurring through error-prone DNA repair of a deleted arm or segment of a chromosome that leads to homozygosity for existing alterations. Isochromosomes were significantly more frequent in TP53 mutated samples than wild types in 6 types of tumors with loss of TP53 function potentially contributing to development of isochromosomes. Isochromosomes are common alterations in cancer, and losing one arm of a chromosome could result in duplication of the lost arm. Duplication of the remaining arm leads promulgation of the effects on any defects in the remaining allele, due to subsequent homozygosity.
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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.