Evidence map›Paper›PMID 42156840›Full record

ArticleScientific reports2026

Genetic determinants of drug-induced gingival overgrowth.

Thunchanok Kiattiubolwong, Vorthunju Nakhonsri, Kamornwan Katanyuwong, Thippawan Jaihan, Chamaiporn Klinhom, Chumpol Ngamphiw, Rujipat Wasitthankasem, Mark C Herzberg, Sissades Tongsima, Piranit Nik Kantaputra

Abstract read
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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3 · Its place in the literature

Who cites it

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No citing paper in PubMed yet.

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

10 authors.

Thunchanok Kiattiubolwong *Center of Excellence in Medical Genetics Research, Faculty of Dentistry, Chiang Mai University, Chiang Mai, Thailand.
Vorthunju Nakhonsri *National Center for Genetic Engineering and Biotechnology (BIOTEC), Thailand Science Park, Pathum Thani, 12120, Thailand.
Kamornwan KatanyuwongDivision of Neurology, Department of Pediatrics, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.
Thippawan JaihanDivision of Neurology, Department of Pediatrics, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.
Chamaiporn KlinhomHang Dong Hospital, Hang Dong, Chiang Mai, 50230, Thailand.
Chumpol NgamphiwNational Center for Genetic Engineering and Biotechnology (BIOTEC), Thailand Science Park, Pathum Thani, 12120, Thailand.
Rujipat WasitthankasemNational Center for Genetic Engineering and Biotechnology (BIOTEC), Thailand Science Park, Pathum Thani, 12120, Thailand.
Mark C HerzbergDepartment of Diagnostic and Biological Sciences, School of Dentistry, University of Minnesota, Minneapolis, MN, 55455, USA.
Sissades TongsimaNational Center for Genetic Engineering and Biotechnology (BIOTEC), Thailand Science Park, Pathum Thani, 12120, Thailand. sissades.ton@biotec.or.th.
Piranit Nik KantaputraCenter of Excellence in Medical Genetics Research, Faculty of Dentistry, Chiang Mai University, Chiang Mai, Thailand. dentaland17@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Drug-induced gingival overgrowth (DIGO) is a multifactorial adverse effect associated with calcium channel blockers and antiepileptic drugs, yet genetic susceptibility-particularly in Asian populations-remains poorly defined. We performed whole-genome sequencing in 74 Thai individuals, including 36 DIGO cases and 38 drug-exposed nonresponder controls. A genome-wide association study was conducted with adjustment for amlodipine exposure, which showed a significant association with DIGO. Complementary analyses included gene-based testing using Multi-marker Analysis of GenoMic Annotation, fine-mapping with Sum of Single Effects, haplotype analysis, and receiver operating characteristic-based risk modeling. Although no single nucleotide polymorphisms (SNPs) reached genome-wide significance, we identified 350 lead SNPs across 34 genes showing strong associations with DIGO (p < 0.001). After multiple-testing correction, six genes/SNPs remained statistically significant (p < 0.05), representing the most robust findings. Haplotype analysis implicated TTC7B, RWDD1, TOM1L1, C1QL2, and BBS1 as DIGO risk genes. These genes, not previously linked to DIGO, are involved in cellular trafficking, phosphoinositide signaling, ciliary function, and protein regulation. Our findings indicate that DIGO susceptibility is driven by genetically determined cellular response pathways in the presence of amlodipine rather than by pharmacokinetic mechanisms. The absence of associations with CYP2C9 and HLA variants previously reported in other populations highlights the importance of ethnically diverse pharmacogenomic studies.

Indexed as

Calcium Channel BlockersGenetic Predisposition to DiseaseGingival OvergrowthAmlodipineAnticonvulsantsFemaleGenome-Wide Association StudyHaplotypesHumansPolymorphism, Single NucleotideWhole Genome SequencingAmlodipineAnticonvulsantsCalcium Channel BlockersCalcium channel blockerGenetic susceptibilityGingival hyperplasiaGingival hypertrophyGingival overgrowthRisk factors for gingival enlargement

Identifiers

PMID42156840
PMCPMC13388721

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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.