ArticleProceedings of the National Academy of Sciences of the United States of America1984
Aberrant expression of an amplified c-myb oncogene in two cell lines from a colon carcinoma.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1984. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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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
46 citing papers in PubMed, 181 citations in OpenAlex.
- MYB/AKT3 axis is a key driver of ovarian cancer growth, aggressiveness, and chemoresistance.Journal of ovarian research · 2025Article
- Unveiling the mysteries of extrachromosomal circular DNA: from generation to clinical relevance in human cancers and health.Molecular cancer · 2024Review
- Extrachromosomal circular DNA in colorectal cancer: biogenesis, function and potential as therapeutic target.Oncogene · 2023Review
- Review
- Colorectal cancer cell lines show striking diversity of their O-glycome reflecting the cellular differentiation phenotype.Cellular and molecular life sciences : CMLS · 2021Article
- MYB - A regulatory factor in hematopoiesis.Gene · 2018Review
- Reassessing the Potential of Myb-targeted Anti-cancer Therapy.Journal of Cancer · 2018Review
- Adult IDH wild-type lower-grade gliomas should be further stratified.Neuro-oncology · 2017Article
- Genome-wide RNA-Sequencing analysis identifies a distinct fibrosis gene signature in the conjunctiva after glaucoma surgery.Scientific reports · 2017Article
- Article
- Nanocarrier-mediated targeting of tumor and tumor vascular cells improves uptake and penetration of drugs into neuroblastoma.Frontiers in oncology · 2013Article
- Role of c-Myb in the survival of pre B-cell acute lymphoblastic leukemia and leukemogenesis.American journal of hematology · 2012Article
- New tricks from an old oncogene: gene fusion and copy number alterations of MYB in human cancer.Cell cycle (Georgetown, Tex.) · 2010Review
- MYB suppresses differentiation and apoptosis of human breast cancer cells.Breast cancer research : BCR · 2010Article
- Alu elements mediate MYB gene tandem duplication in human T-ALL.The Journal of experimental medicine · 2007Article
- c-Myb is required for progenitor cell homeostasis in colonic crypts.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Review
- HTLV-I Tax transrepresses the human c-Myb promoter independently of its interaction with CBP or p300.Oncogene · 2000Article
- Distinct cellular factors regulate the c-myb promoter through its E2F element.Molecular and cellular biology · 1999Article
- c-Myb is critical for murine colon development.Oncogene · 1999Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Two cell lines (COLO 201 and COLO 205) derived independently from a single adenocarcinoma of the human colon each harbored an approximately 10-fold amplification of the cellular oncogene c-myb and a proportional abundance of the 4-kilobase mRNA derived from c-myb. By contrast, expression of c-myb could not be detected in cells from a variety of other solid tumors, including other colon carcinomas. Analysis of the amplified DNA with restriction endonucleases failed to reveal any topographical abnormalities within c-myb. Neither COLO 201 nor COLO 205 carry the double minute chromosomes and homogeneously staining regions of chromosomes that frequently serve as karyotypic signatures of amplified DNA. Instead, amplified c-myb is carried on what appear to be disomic or trisomic copies of the same anomalous marker chromosome that is characteristic of both COLO 201 and COLO 205. The karyological origin of this abnormal chromosome is not presently apparent. Our findings show c-myb expression by cells outside of the hemopoietic lineage, raise the possibility that amplification and/or ectopic expression of c-myb may have contributed to the genesis of the tumor from which the cells of COLO 201 and COLO 205 arose, and suggest that amplification of cellular oncogenes may be a more common factor in tumorigenesis than might have been suspected from available karyological data.
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