ArticleMolecular and cellular biology1994
Chromosome breakage at a major fragile site associated with P-glycoprotein gene amplification in multidrug-resistant CHO cells.
Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 71 citations in OpenAlex.
- Novel role for non-homologous end joining in the formation of double minutes in methotrexate-resistant colon cancer cells.Journal of medical genetics · 2015Article
- How a replication origin and matrix attachment region accelerate gene amplification under replication stress in mammalian cells.PloS one · 2014Article
- Characterization at nucleotide resolution of the homogeneously staining region sites of insertion in two cancer cell lines.Nucleic acids research · 2013Article
- The role of fragile sites in sporadic papillary thyroid carcinoma.Journal of thyroid research · 2012Article
- ATR preferentially interacts with common fragile site FRA3B and the binding requires its kinase activity in response to aphidicolin treatment.Mutation research · 2010Article
- Evidence for a novel mechanism for gene amplification in multiple myeloma: 1q12 pericentromeric heterochromatin mediates breakage-fusion-bridge cycles of a 1q12 approximately 23 amplicon.British journal of haematology · 2009Article
- Mechanisms of change in gene copy number.Nature reviews. Genetics · 2009Review
- Plasmodium falciparum pfmdr1 amplification, mefloquine resistance, and parasite fitness.Antimicrobial agents and chemotherapy · 2009Article
- Redox regulation of multidrug resistance in cancer chemotherapy: molecular mechanisms and therapeutic opportunities.Antioxidants & redox signaling · 2009Review
- Genome position and gene amplification.Genome biology · 2007Article
- Identification of transgene integration loci of different highly expressing recombinant CHO cell lines by FISH.Cytotechnology · 2006Article
- Chromosomal instability at common fragile sites in Seckel syndrome.American journal of human genetics · 2004Article
- Article
- Genomic instability driven by the human T-cell leukemia virus type I (HTLV-I) oncoprotein, Tax.Oncogene · 2002Article
- High-resolution mapping of the 11q13 amplicon and identification of a gene, TAOS1, that is amplified and overexpressed in oral cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Enhanced flexibility and aphidicolin-induced DNA breaks near mammalian replication origins: implications for replicon mapping and chromosome fragility.Nucleic acids research · 2000Article
- Gene amplification in a p53-deficient cell line requires cell cycle progression under conditions that generate DNA breakage.Molecular and cellular biology · 1998Article
- Selective entrapment of extrachromosomally amplified DNA by nuclear budding and micronucleation during S phase.The Journal of cell biology · 1998Article
- Intrachromosomal telomere-like DNA sequences in Chinese hamster.Mammalian genome : official journal of the International Mammalian Genome Society · 1996Article
- Colour thresholding in video imaging.Journal of anatomy · 1995Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Recent studies of several drug-resistant Chinese hamster cell lines suggested that a breakage-fusion-bridge mechanism is frequently involved in the amplification of drug resistance genes. These observations underscore the importance of chromosome breakage in the initiation of DNA amplification in mammalian cells. However, the mechanism of this breakage is unknown. Here, we propose that the site of chromosome breakage consistent with the initial event of P-glycoprotein (P-gp) gene amplification via the breakage-fusion-bridge cycle in three independently established multidrug-resistant CHO cells was located at 1q31. This site is a major chromosome fragile site that can be induced by methotrexate and aphidicolin treatments. Pretreatments of CHO cells with methotrexate or aphidicolin enhanced the frequencies of resistance to vinca alkaloid and amplification of the P-gp gene. These observations suggest that chromosome fragile sites play a pivotal role in DNA amplification in mammalian cells. Our data are also consistent with the hypothesis that gene amplification can be initiated by stress-induced chromosome breakage that is independent of modes of action of cytotoxic agents. Drug-resistant variants may arise by their growth advantage due to overproduction of cellular target molecules via gene amplification.
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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.