ArticleEnvironmental and molecular mutagenesis2017
Variation in organ-specific PIK3CA and KRAS mutant levels in normal human tissues correlates with mutation prevalence in corresponding carcinomas.
Article in Environmental and molecular mutagenesis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 23 citations in OpenAlex.
- Colibactin-associated mutations in the human colon appear to reflect anatomy and early exposure, not oncogenesis.medRxiv : the preprint server for health sciences · 2026Article
- Expansion of preexisting cancer driver mutant clones is induced by the genotoxic carcinogen benzo[b]fluoranthene in MutaMouse lung.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Tissue and Sex-Specific Performance of a Cancer Driver Based Biomarker in rasH2-Tg Mice.Environmental and molecular mutagenesis · 2025Article
- CarcSeq detection of lorcaserin-induced clonal expansion of Pik3ca H1047R mutants in rat mammary tissue.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Alternative polyadenylation is a determinant of oncogenic Ras function.Science advances · 2021Article
- Frequent PIK3CA mutations in eutopic endometrium of patients with ovarian clear cell carcinoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021Article
- Quantification of cancer driver mutations in human breast and lung DNA using targeted, error-corrected CarcSeq.Environmental and molecular mutagenesis · 2020Article
- Extensive rewiring of the EGFR network in colorectal cancer cells expressing transforming levels of KRASNature communications · 2020Article
- Outgrowth of erlotinib-resistant subpopulations recapitulated in patient-derived lung tumor spheroids and organoids.PloS one · 2020Article
- Rationale and Roadmap for Developing Panels of Hotspot Cancer Driver Gene Mutations as Biomarkers of Cancer Risk.Environmental and molecular mutagenesis · 2020Review
- Low-Frequency Mutational Heterogeneity of Invasive Ductal Carcinoma Subtypes: Information to Direct Precision Oncology.International journal of molecular sciences · 2019Article
- Cancer stem cells in progression of colorectal cancer.Oncotarget · 2018Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Large-scale sequencing efforts have described the mutational complexity of individual cancers and identified mutations prevalent in different cancers. As a complementary approach, allele-specific competitive blocker PCR (ACB-PCR) is being used to quantify levels of hotspot cancer driver mutations (CDMs) with high sensitivity, to elucidate the tissue-specific properties of CDMs, their occurrence as tumor cell subpopulations, and their occurrence in normal tissues. Here we report measurements of PIK3CA H1047R mutant fraction (MF) in normal colonic mucosa, normal lung, colonic adenomas, colonic adenocarcinomas, and lung adenocarcinomas. We report PIK3CA E545K MF measurements in those tissues, as well as in normal breast, normal thyroid, mammary ductal carcinomas, and papillary thyroid carcinomas. We report KRAS G12D and G12V MF measurements in normal colon. These MF measurements were integrated with previously published ACB-PCR data on KRAS G12D, KRAS G12V, and PIK3CA H1047R. Analysis of these data revealed a correlation between the degree of interindividual variability in these mutations (as log
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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.