Evidence map›Paper›PMID 31723047›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Genomic sites hypersensitive to ultraviolet radiation.

Sanjay Premi, Lynn Han, Sameet Mehta, James Knight, Dejian Zhao, Meg A Palmatier, Karl Kornacker, Douglas E Brash

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.9field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

55 citing papers in PubMed, 94 citations in OpenAlex.

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  10. IncRNA-ZFAS1, an Emerging Gate-Keeper in DNA Damage-Dependent Transcriptional Regulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Sanjay PremiDepartment of Therapeutic Radiology, Yale School of Medicine, New Haven, CT 06520-8040.
Lynn HanDepartment of Therapeutic Radiology, Yale School of Medicine, New Haven, CT 06520-8040.
Sameet MehtaDepartment of Genetics, Yale Center for Genome Analysis, Yale School of Medicine, New Haven, CT 06520-8005.ORCID 0000-0002-3029-3217
James KnightDepartment of Genetics, Yale Center for Genome Analysis, Yale School of Medicine, New Haven, CT 06520-8005.
Dejian ZhaoDepartment of Genetics, Yale Center for Genome Analysis, Yale School of Medicine, New Haven, CT 06520-8005.
Meg A PalmatierDepartment of Therapeutic Radiology, Yale School of Medicine, New Haven, CT 06520-8040.
Karl KornackerKarl Kornacker & Associates, LLC, Worthington, OH 43085; karl.kornacker@gmail.com douglas.brash@yale.edu.
Douglas E BrashDepartment of Therapeutic Radiology, Yale School of Medicine, New Haven, CT 06520-8040; karl.kornacker@gmail.com douglas.brash@yale.edu.
Yale University · USYale Cancer Center · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Yale Pathology Tissue Services Shared ResourceP30CA016359 · NCI · YALE UNIVERSITY · PI Eric P. Winer · 1985 to 2026
$85.0M
Yale SPORE in Skin CancerP50CA121974 · NCI · YALE UNIVERSITY · PI MARCUS W BOSENBERG, Harriet M. Kluger · 2006 to 2026
$43.9M
Applying Genomic Dosimeters of UV Damage to Predicting Skin Cancer RiskR01ES030562 · NIEHS · YALE UNIVERSITY · PI BRASH, DOUGLAS E · 2019 to 2024
$2.6M
High Performance Computing Instrumentation for the Yale Center for Genome AnalysiS10OD018521 · OD · YALE UNIVERSITY · PI MANE, SHRIKANT M · 2015 to 2015
$890k
NCATS NIH HHS UL1 TR001863NCI NIH HHS P30 CA016359NCI NIH HHS P50 CA121974NIEHS NIH HHS R01 ES030562NIH HHS S10 OD018521
6 · The paper itself

Abstract

If the genome contains outlier sequences extraordinarily sensitive to environmental agents, these would be sentinels for monitoring personal carcinogen exposure and might drive direct changes in cell physiology rather than acting through rare mutations. New methods, adductSeq and freqSeq, provided statistical resolution to quantify rare lesions at single-base resolution across the genome. Primary human melanocytes, but not fibroblasts, carried spontaneous apurinic sites and TG sequence lesions more frequent than ultraviolet (UV)-induced cyclobutane pyrimidine dimers (CPDs). UV exposure revealed hyperhotspots acquiring CPDs up to 170-fold more frequently than the genomic average; these sites were more prevalent in melanocytes. Hyperhotspots were disproportionately located near genes, particularly for RNA-binding proteins, with the most-recurrent hyperhotspots at a fixed position within 2 motifs. One motif occurs at ETS family transcription factor binding sites, known to be UV targets and now shown to be among the most sensitive in the genome, and at sites of mTOR/5' terminal oligopyrimidine-tract translation regulation. The second occurs at A

Indexed as

5' Untranslated RegionsCells, CulturedDNA DamageFibroblastsGene Expression RegulationGenome, HumanHigh-Throughput Nucleotide SequencingHumansMelanocytesMelanomaMutationPromoter Regions, GeneticProtein BiosynthesisPyrimidine DimersPyrimidine NucleotidesSkin Neoplasms5' Untranslated RegionsMTOR protein, humanPyrimidine DimersPyrimidine NucleotidesTOR Serine-Threonine Kinasescyclobutane pyrimidine dimerETSmelanomaTOP tractUV

Identifiers

PMID31723047
PMCPMC6883822
OpenAlexW2983095819

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.