ArticleOncogene2003
Shaping of tumor and drug-resistant genomes by instability and selection.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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Who cites it
29 citing papers in PubMed, 83 citations in OpenAlex.
- Intricate and Cell Type-Specific Populations of Endogenous Circular DNA (eccDNA) inG3 (Bethesda, Md.) · 2017Article
- Fast Bayesian Inference of Copy Number Variants using Hidden Markov Models with Wavelet Compression.PLoS computational biology · 2016Article
- Modulation of breast cancer cell viability by a cannabinoid receptor 2 agonist, JWH-015, is calcium dependent.Breast cancer (Dove Medical Press) · 2016Article
- Genome-wide copy number analysis of cerebrospinal fluid tumor cells and their corresponding archival primary tumors.Genomics data · 2014Article
- Article
- A systems approach defining constraints of the genome architecture on lineage selection and evolvability during somatic cancer evolution.Biology open · 2013Article
- Parsimonious higher-order hidden Markov models for improved array-CGH analysis with applications to Arabidopsis thaliana.PLoS computational biology · 2012Article
- Cooperativity of Rb, Brca1, and p53 in malignant breast cancer evolution.PLoS genetics · 2012Article
- Integration of DNA copy number alterations and transcriptional expression analysis in human gastric cancer.PloS one · 2012Article
- Discovering tumor suppressor genes through genome-wide copy number analysis.Current genomics · 2010Article
- Co-amplified genes at 8p12 and 11q13 in breast tumors cooperate with two major pathways in oncogenesis.Oncogene · 2009Article
- Stromal control of oncogenic traits expressed in response to the overexpression of GLI2, a pleiotropic oncogene.Oncogene · 2009Article
- Adaptive copy number evolution in malaria parasites.PLoS genetics · 2008Article
- Cross-platform array comparative genomic hybridization meta-analysis separates hematopoietic and mesenchymal from epithelial tumors.Oncogene · 2007Article
- Exploiting noise in array CGH data to improve detection of DNA copy number change.Nucleic acids research · 2007Article
- Genome position and gene amplification.Genome biology · 2007Article
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- Article
- Article
- Genetic determinants of methotrexate responsiveness and resistance in colon cancer cells.Oncogene · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Tumors with defects in mismatch repair (MMR) show fewer chromosomal changes by cytogenetic analyses than most solid tumors, suggesting that a greater proportion of the alterations required for malignancy occur in genes with nucleotide sequences susceptible to errors normally corrected by MMR. Here, we used genome-wide microarray comparative genomic hybridization to carry out a higher resolution evaluation of the effect of MMR competence on genomic alterations occurring in 20 cell lines and to determine if characteristic aberrations arise in MMR-proficient and -deficient HCT116 cells undergoing selection for methotrexate resistance. We observed different spectra of aberrations in MMR-proficient compared to -deficient cell lines, as well as among cell lines with different types of MMR-deficiency. We also observed different genetic routes to drug resistance. Resistant MMR-deficient cells most frequently displayed no copy number alterations (16/29 cell pools), whereas all MMR-proficient cells had unique abnormalities involving chromosome 5, including amplicons centered on the target gene, DHFR and/or a neighboring novel locus (7/13 pools). These observations support the concept that tumor genomes are shaped by selection for alterations that promote survival and growth advantage, as well as by the particular dysfunctions in genes responsible for maintenance of genetic integrity.
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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.