ArticleProceedings of the National Academy of Sciences of the United States of America2007
Nonrandom variations in human cancer ESTs indicate that mRNA heterogeneity increases during carcinogenesis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Mistranslation suppresses mistranscription in eukaryotes.Nature communications · 2026Article
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- Phenotypic mutations contribute to protein diversity and shape protein evolution.Protein science : a publication of the Protein Society · 2022Review
- Transcriptional frameshifts contribute to protein allergenicity.The Journal of clinical investigation · 2020Article
- Transcription fidelity and its roles in the cell.Current opinion in microbiology · 2018Review
- A link between transcription fidelity and pausing in vivo.Transcription · 2017Article
- Misincorporation by RNA polymerase is a major source of transcription pausing in vivo.Nucleic acids research · 2017Article
- Systems biology of cancer: entropy, disorder, and selection-driven evolution to independence, invasion and "swarm intelligence".Cancer metastasis reviews · 2013Review
- Heritable change caused by transient transcription errors.PLoS genetics · 2013Article
- Increased frequency of single base substitutions in a population of transcripts expressed in cancer cells.BMC cancer · 2012Article
- Inositol-requiring enzyme 1alpha is a key regulator of angiogenesis and invasion in malignant glioma.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Article
- Potential role of phenotypic mutations in the evolution of protein expression and stability.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
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Authors and funding
17 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Virtually all cancer biological attributes are heterogeneous. Because of this, it is currently difficult to reconcile results of cancer transcriptome and proteome experiments. It is also established that cancer somatic mutations arise at rates higher than suspected, but yet are insufficient to explain all cancer cell heterogeneity. We have analyzed sequence variations of 17 abundantly expressed genes in a large set of human ESTs originating from either normal or cancer samples. We show that cancer ESTs have greater variations than normal ESTs for >70% of the tested genes. These variations cannot be explained by known and putative SNPs. Furthermore, cancer EST variations were not random, but were determined by the composition of the substituted base (b0) as well as that of the bases located upstream (up to b - 4) and downstream (up to b + 3) of the substitution event. The replacement base was also not randomly selected but corresponded in most cases (73%) to a repetition of b - 1 or of b + 1. Base substitutions follow a specific pattern of affected bases: A and T substitutions were preferentially observed in cancer ESTs. In contrast, cancer somatic mutations [Sjoblom T, et al. (2006) Science 314:268-274] and SNPs identified in the genes of the current study occurred preferentially with C and G. On the basis of these observations, we developed a working hypothesis that cancer EST heterogeneity results primarily from increased transcription infidelity.
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