ArticleJCI insight2020
Transcriptomic silencing as a potential mechanism of treatment resistance.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 38 citations in OpenAlex.
- Transcriptomics-based multi-omics approach for optimizing risk stratification in acute myeloid leukemia.Blood science (Baltimore, Md.) · 2026Article
- Deciphering molecular pathways in urological cancers: A gateway to precision therapeutics.Journal of advanced research · 2026Review
- PD-1 transcriptomic landscape across cancers and implications for immune checkpoint blockade outcome.NPJ genomic medicine · 2025Article
- Targeted therapies in biliary tract cancer-when precision becomes imprecise.ESMO gastrointestinal oncology · 2024Review
- Omics-based molecular classifications empowering in precision oncology.Cellular oncology (Dordrecht, Netherlands) · 2024Review
- LAG-3 transcriptomic expression correlates linearly with other checkpoints, but not with clinical outcomes.American journal of cancer research · 2024Article
- Article
- Comprehensive Analysis of Human Epidermal Growth Factor Receptor 2 Through DNA, mRNA, and Protein in Diverse Malignancies.JCO precision oncology · 2023Article
- LAG-3 transcriptomic expression patterns across malignancies: Implications for precision immunotherapeutics.Cancer medicine · 2023Article
- Evolution of the Targeted Therapy Landscape for Cholangiocarcinoma: Is Cholangiocarcinoma the 'NSCLC' of GI Oncology?Cancers · 2023Review
- PD-L1 gene amplification and focality: relationship with protein expression.Journal for immunotherapy of cancer · 2023Article
- Cancer: slaying the nine-headed Hydra.Annals of oncology : official journal of the European Society for Medical Oncology · 2023Review
- High tumor amplification burden is associated withCancer biology & therapy · 2022Article
- Transcriptomics and solid tumors: The next frontier in precision cancer medicine.Seminars in cancer biology · 2022Review
- Tissue-Agnostic Activity of BRAF plus MEK Inhibitor in BRAF V600-Mutant Tumors.Molecular cancer therapeutics · 2022Review
- Individualized Prediction of Drug Response and Rational Combination Therapy in NSCLC Using Artificial Intelligence-Enabled Studies of Acute Phosphoproteomic Changes.Molecular cancer therapeutics · 2022Article
- Genomics and Immunomics in the Treatment of Urothelial Carcinoma.Current oncology (Toronto, Ont.) · 2022Review
- Review
- Use of Circulating Tumour DNA (ctDNA) for Measurement of Therapy Predictive Biomarkers in Patients with Cancer.Journal of personalized medicine · 2022Review
- Therapeutic implications of cancer gene amplifications without mRNA overexpression: silence may not be golden.Journal of hematology & oncology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Next-generation sequencing (NGS) has not revealed all the mechanisms underlying resistance to genomically matched drugs. Here, we performed in 1417 tumors whole-exome tumor (somatic)/normal (germline) NGS and whole-transcriptome sequencing, the latter focusing on a clinically oriented 50-gene panel in order to examine transcriptomic silencing of putative driver alterations. In this large-scale study, approximately 13% of the somatic single nucleotide variants (SNVs) were unexpectedly not expressed as RNA; 23% of patients had ≥1 nonexpressed SNV. SNV-bearing genes consistently transcribed were TP53, PIK3CA, and KRAS; those with lower transcription rates were ALK, CSF1R, ERBB4, FLT3, GNAS, HNF1A, KDR, PDGFRA, RET, and SMO. We also determined the frequency of tumor mutations being germline, rather than somatic, in these and an additional 462 tumors with tumor/normal exomes; 33.8% of germline SNVs within the gene panel were rare (not found after filtering through variant information domains) and at risk of being falsely reported as somatic. Both the frequency of silenced variant transcription and the risk of falsely identifying germline mutations as somatic/tumor related are important phenomena. Therefore, transcriptomics is a critical adjunct to genomics when interrogating patient tumors for actionable alterations, because, without expression of the target aberrations, there will likely be therapeutic resistance.
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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.