ArticleThe American journal of pathology2003
Amplification and overexpression of the L-MYC proto-oncogene in ovarian carcinomas.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
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Who cites it
24 citing papers in PubMed, 66 citations in OpenAlex.
- Review
- Spatial and temporal intra-tumoral heterogeneity in advanced HGSOC: Implications for surgical and clinical outcomes.Cell reports. Medicine · 2023Article
- Alterations and Co-Occurrence of C-MYC, N-MYC, and L-MYC Expression are Related to Clinical Outcomes in Various Cancers.International journal of stem cells · 2023Article
- c-MYC-Driven Polyamine Metabolism in Ovarian Cancer: From Pathogenesis to Early Detection and Therapy.Cancers · 2023Review
- Incorporation of a histone mutant with H3K56 site substitution perturbs the replication machinery in mouse embryonic stem cells.Journal of molecular cell biology · 2022Article
- Identification of a Vitamin-D Receptor Antagonist, MeTC7, which Inhibits the Growth of Xenograft and Transgenic TumorsJournal of medicinal chemistry · 2022Article
- Article
- Cooperation between ETS transcription factor ETV1 and histone demethylase JMJD1A in colorectal cancer.International journal of oncology · 2020Article
- TheFrontiers in oncology · 2020Article
- Clinical Importance of Myc Family Oncogene Aberrations in Epithelial Ovarian Cancer.JNCI cancer spectrum · 2018Article
- Family matters: How MYC family oncogenes impact small cell lung cancer.Cell cycle (Georgetown, Tex.) · 2017Review
- Evaluation of the use of therapeutic peptides for cancer treatment.Journal of biomedical science · 2017Review
- MYCL is a target of a BET bromodomain inhibitor, JQ1, on growth suppression efficacy in small cell lung cancer cells.Oncotarget · 2016Article
- BPTF is required for c-MYC transcriptional activity and in vivo tumorigenesis.Nature communications · 2016Article
- The lncRNA-MYC regulatory network in cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Review
- MicroRNA related polymorphisms and breast cancer risk.PloS one · 2014Article
- DNA fingerprinting techniques for the analysis of genetic and epigenetic alterations in colorectal cancer.Mutation research · 2010Review
- p27Kip1 mediates addiction of ovarian cancer cells to MYCC (c-MYC) and their dependence on MYC paralogs.The Journal of biological chemistry · 2010Article
- Posttranslational regulation of Myc by promyelocytic leukemia zinc finger protein.International journal of cancer · 2009Article
- Analysis of DNA copy number alterations in ovarian serous tumors identifies new molecular genetic changes in low-grade and high-grade carcinomas.Cancer research · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Gene amplification is an important mechanism of oncogene activation in various human cancers, including ovarian carcinomas (OvCas). We used restriction landmark genomic scanning (RLGS) to detect amplified DNA fragments in the genomes of 47 primary OvCas. Visual analysis of the RLGS gel images revealed several OvCa samples with spots of greater intensity than corresponding spots from normal tissues, indicating possible DNA amplification in specific tumors. Two primary tumors (E1 and S12) shared four high-intensity spots. A recently developed informatics tool termed Virtual Genome Scans was used to compare the RLGS patterns in these tumors with patterns predicted from the human genome sequence. Virtual Genome Scans determined that three of the four fragments localized to chromosome 1p34-35, a region containing the proto-oncogene L-MYC. Sixty-eight primary OvCas, including 40 analyzed by RLGS, were screened by quantitative polymerase chain reaction (PCR) for possible amplification of L-MYC. Ten tumors with increased L-MYC copy number were identified, including tumor E1, which showed an approximately 24-fold increase in copy number compared to normal DNA. Southern analysis of several tumors confirmed the quantitative PCR results. Using sequence tagged site (STS) markers flanking L-MYC, increased DNA copy number in tumor E1 was found to span the region flanking L-MYC between D1S432 and D1S463 ( approximately 3.1 Mb). Other tumors showed amplification only at the L-MYC locus. Using oligonucleotide microarrays, L-MYC was found to be more frequently overexpressed in OvCas than either c-MYC or N-MYC relative to ovarian surface epithelium. Quantitative reverse transcriptase-PCR analysis confirmed elevated L-MYC expression in a substantial fraction of OvCas, including nine of nine tumors with increased L-MYC copy number. The data implicate L-MYC gene amplification and/or overexpression in human OvCa pathogenesis.
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