ArticleNeoplasia (New York, N.Y.)
c-Myc-induced extrachromosomal elements carry active chromatin.
Article in Neoplasia (New York, N.Y.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- Review
- Leveraging extrachromosomal DNA to fine-tune trials of targeted therapy for glioblastoma: opportunities and challenges.Nature reviews. Clinical oncology · 2022Review
- Guilt by association: EcDNA as a mobile transactivator in cancer.Trends in cancer · 2022Review
- Extrachromosomal DNA in Cancer.Annual review of genomics and human genetics · 2022Review
- Extrachromosomal DNA: An Emerging Hallmark in Human Cancer.Annual review of pathology · 2022Review
- CircleBase: an integrated resource and analysis platform for human eccDNAs.Nucleic acids research · 2022Article
- Pioneering insights of extrachromosomal DNA (ecDNA) generation, action and its implications for cancer therapy.International journal of biological sciences · 2022Review
- Small ring has big potential: insights into extrachromosomal DNA in cancer.Cancer cell international · 2021Review
- Histone Lysine Methylation Dynamics ControlCancer discovery · 2020Article
- The biogenesis and roles of extrachromosomal oncogene involved in carcinogenesis and evolution.American journal of cancer research · 2020Review
- Small Circular DNAs in Human Pathology.The Malaysian journal of medical sciences : MJMS · 2014Article
- c-MYC-induced genomic instability.Cold Spring Harbor perspectives in medicine · 2014Review
- A review of the past, present, and future directions of neoplasia.Neoplasia (New York, N.Y.) · 2005Review
- c-Myc induces chromosomal rearrangements through telomere and chromosome remodeling in the interphase nucleus.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Murine Pre-B lymphocytes with experimentally activated MycER show both chromosomal and extrachromosomal gene amplification. In this report, we have elucidated the size, structure, and functional components of c-Myc-induced extrachromosomal elements (EEs). Scanning electron microscopy revealed that EEs isolated from MycER-activated Pre-B+ cells are an average of 10 times larger than EEs isolated from non-MycER-activated control Pre-B- cells. We demonstrate that these large c-Myc-induced EEs are associated with histone proteins, whereas EEs of non-MycER-activated Pre B- cells are not. Immunohistochemistry and Western blot analyses using pan-histone-specific, histone H3 phosphorylation-specific, and histone H4 acetylation-specific antibodies indicate that a significant proportion of EEs analyzed from MycER-activated cells harbors transcriptionally competent and/or active chromatin. Moreover, these large, c-Myc-induced EEs carry genes. Whereas the total genetic make-up of these c-Myc-induced EEs is unknown, we found that 30.2% of them contain the dihydrofolate reductase (DHFR) gene, whereas cyclin C (CCNC) was absent. In addition, 50% of these c-Myc-activated Pre-B+ EEs incorporated bromodeoxyuridine (BrdU), identifying them as genetic structures that self-propagate. In contrast, EEs isolated from non-Myc-activated cells neither carry the DHFR gene nor incorporate BrdU, suggesting that c-Myc deregulation generates a new class of EEs.
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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.