Topics and Trends in Most Cited DNA Repair Mechanisms Papers

Ranked by citations 18 months after publication

Class of 2026 (Papers Published in 2024)

What topics and trends defined most-cited DNA Repair Mechanisms research in the Class of 2026?

The Class of 2026 is defined by a shift towards targeted interventions and high-resolution methodologies. Surges in synthetic lethality and replication stress research underscore a focus on exploiting DNA repair vulnerabilities, while advanced structural techniques are reshaping our understanding of complex repair machinery.

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Updated July 19, 2026

At a glance

Field
DNA Repair Mechanisms
Cohort label
Class of 2026 (2024 publications)
Papers analyzed
3401
Papers ranked
20
Top topics in ranked papers
Homologous recombination, DNA double-strand breaks, PARP inhibitor
Publication window
Jan 1, 2024 – Dec 31, 2024
Eligibility
Research articles; reviews excluded
Citation window
18 months post-publication
18m citation range
37–343
Data source
OpenAlex · Retrieved July 2026
License
CC BY 4.0

Rankings

20 papers ranked by 18-month citation count

#1 of 3,401
34318m citations

NBS1 lactylation is required for efficient DNA repair and chemotherapy resistance

Hengxing Chen, Yun Li, Huafu Li et al.Nature202410.1038/s41586-024-07620-9

Yulong He, Axel Behrens, Dong Yin, Changhua ZhangSun Yat-sen University, China

NBS1 lactylationlysine 388 (K388)Warburg effectlactate accumulationHomologous recombinationDNA double-strand breaksMRN complexTIP60lysine lactyltransferaseHDAC3de-lactylaselactate dehydrogenase A (LDHA)stiripentolChemoresistanceneoadjuvant chemotherapyGenome integrityanaerobic glycolysisDNA repair efficacy
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#2 of 3,401
11218m citations

Transcription–replication conflicts underlie sensitivity to PARP inhibitors

Angeliki Karamichali, Giacomo G Rossetti et al.Nature202410.1038/s41586-024-07217-2

Thanos D. HalazonetisUniversity of Geneva, Switzerland

PARP inhibitorPARP1Homologous recombination deficiencyTranscription-replication conflictsTIMELESSTIPINReplication fork protectionearly S phasesynthetic lethalityDNA double-strand breakstrapped PARPstranscription elongation inhibitionPARP1 enzymatic activityHR-deficient cancersreplisome progression
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#3 of 3,401
7618m citations

PARP1-DNA co-condensation drives DNA repair site assembly to prevent disjunction of broken DNA ends

Nagaraja Chappidi et al.Cell202410.1016/j.cell.2024.01.015

Simon AlbertiTechnische Universität Dresden, Germany

DNA double-strand breaksDSB sitesPARP1PARylationPARP1-DNA co-condensationDNA end synapsisbottom-up biochemistry reconstitutionPARP1 multimersBiomolecular condensatesFUSDNA end tetheringmechanical forces on DNAeffector protein recruitmenthierarchical DSB condensate assemblyDNA repairbroken DNA end stabilizationPARP1 release from DNA
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#4 of 3,401
7618m citations

Cell-type-specific CAG repeat expansions and toxicity of mutant Huntingtin in human striatum and cerebellum

Kert Mätlik et al.Nature Genetics202410.1038/s41588-024-01653-6

Nathaniel HeintzThe Rockefeller University, United States

CAG repeat expansionsmutant Huntingtinstriatumcerebellummedium spiny neuronscholinergic interneuronsPurkinje neuronsfluorescence-activated nuclear sortingMSH2MSH3MutSβFAN1mutant ATXN3SCA3somatic instabilitycell-type-specific degenerationnucleolytic excisionCAG slip-outsstriatal toxicity
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#5 of 3,401
7318m citations

Structure and repair of replication-coupled DNA breaks

Raphael Pavani, Veenu Tripathi et al.Science202410.1126/science.ado3867

Raphael Pavani, Veenu Tripathi, André NussenzweigNational Cancer Institute, United States

CRISPR-Cas9 nicking enzymesreplication fork collapseDNA nicksleading-strand nickslagging-strand nicksSingle-ended double-strand breaksDouble-ended double-strand breaksHomologous recombinationDNA end resectionBRCA153BP1RAD51 filament formationReplication fork protectionHR-deficient cancersgenomic scarringreplication-coupled DNA breaks
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#6 of 3,401
6918m citations

The ribotoxic stress response drives UV-mediated cell death

Niladri K Sinha et al.Cell202410.1016/j.cell.2024.05.018

Alban Ordureau, Sergi Regot, Rachel GreenJohns Hopkins University School of Medicine, United States

ultraviolet radiationribotoxic stress responseDNA damage responseribosomal collisionsZAK kinaseUV-induced apoptosistime-resolved phosphoproteomicsGCN2negative-feedback modulesphosphodegron autophosphorylationZAK degradationChemogenetic approachsingle-cell imagingRNA damagecell fate determinationhomeostasis-tolerance-death regimesnucleic acid damage sentinel
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#7 of 3,401
6918m citations

Discovery of WRN inhibitor HRO761 with synthetic lethality in MSI cancers

Stephane Ferretti, Jacques Hamon, Ruben de Kanter, Clemens Scheufler et al.Nature202410.1038/s41586-024-07350-y

Henrik Möbitz, Marta Cortés-CrosNovartis BioMedical Research, Switzerland

WRN inhibitorHRO761synthetic lethalityMicrosatellite instabilityWRN helicaseallosteric inhibitionD1 helicase domainD2 helicase domainDNA damage inductionp53-independent mechanismWRN degradationmicrosatellite-stable cellsPatient-derived xenograft modelsimmune checkpoint inhibitorsgenetic screenspharmacological validationoral treatmenttumor growth inhibition
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#9 of 3,401
4818m citations

The PARP1 selective inhibitor saruparib (AZD5305) elicits potent and durable antitumor activity in patient-derived BRCA1/2-associated cancer models

Andrea Herencia-Ropero et al.Genome Medicine202410.1186/s13073-024-01370-z

Alba Llop‐Guevara, Judith Balmaña, Violeta SerraVall d'Hebron Institute of Oncology (VHIO), Spain

saruparib (AZD5305)PARP inhibitorolaparibBRCA1/BRCA2 pathogenic alterationsPALB2Homologous recombination deficiencyPatient-derived xenograft modelsreversion mutationshypomorphic BRCA1RAD51 foci formationReplication stressGenomic instabilityceralasertibATR inhibitorcarboplatin combinationPARP inhibitor resistancepreclinical complete response ratesynthetic lethality
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#11 of 3,401
4618m citations

Targeting ATR in patients with cancer

Natalie Y L Ngoi et al.Nature Reviews Clinical Oncology202410.1038/s41571-024-00863-5

Katharina SchlacherThe University of Texas MD Anderson Cancer Center, United States

ATRATR inhibitorcancer therapyDNA damage responseReplication stresssynthetic lethalityATM deficiencycheckpoint inhibitionmonotherapyCombination therapyclinical trialspatient stratificationbiomarkersResistance mechanisms
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#12 of 3,401
4518m citations

Early oxidative stress and DNA damage in Aβ-burdened hippocampal neurons in an Alzheimer’s-like transgenic rat model

Morgan K Foret et al.Communications Biology202410.1038/s42003-024-06552-4

A. Claudio Cuello, Sonia Do CarmoMcGill University, Canada

intraneuronal amyloid betaMcGill-R-Thy1-APP transgenic ratlaser microdissectionhippocampal neuronspre-plaque oxidative stressDNA double stranded breaksγH2AX fociErcc2FanccSod2GsrIdh1XPDErcc6RAD51Fen1Sirt6Grin2bTOP2βmaladaptive synaptic plasticity
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#13 of 3,401
4318m citations

Mechanism of BRCA1–BARD1 function in DNA end resection and DNA protection

Ilaria Ceppi, Maria Rosaria Dello Stritto et al.Nature202410.1038/s41586-024-07909-9

Petr ĆejkaUniversità della Svizzera italiana, Switzerland

BRCA1–BARD1DNA end resectionHomologous recombinationdouble-strand break repairEXO1 nucleaseDNA2 nucleaseWRN helicaseBloom helicaseMRN complexphosphorylated CtIPBRCA1–C complexBRCT repeatsCtIP S327A mutation53BP1RAD51Replication fork protectionNon-homologous end joiningReplication stress
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#14 of 3,401
4118m citations

Endogenous aldehyde-induced DNA–protein crosslinks are resolved by transcription-coupled repair

Yasuyoshi Oka et al.Nature Cell Biology202410.1038/s41556-024-01401-2

Tomoo OgiNagoya University, Japan

DNA-protein crosslinks (DPCs)DPCsaldehyde-induced DNA damageTranscription-coupled repairTCRRuijs-Aalfs syndromeAMeD syndromeDPC sequencingformaldehyde-induced DPCsp97/VCPproteasomeTFIISRNAPII transcript cleavageTranscription-coupled DPC repairaldehyde clearanceCockayne syndromemetabolic genotoxin
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#15 of 3,401
4118m citations

DNA mismatch and damage patterns revealed by single-molecule sequencing

Mei Hong Liu, Benjamin M Costa et al.Nature202410.1038/s41586-024-07532-8

Gilad D. EvronyNew York University Grossman School of Medicine, United States

DNA mismatchDNA damage patternssingle-molecule sequencingmismatch detectionsequencing error profilingbase modificationssequencing accuracyerror signaturesDNA damagelong-read sequencingnucleotide misincorporationdamage-induced mutationssingle-molecule resolutionsequencing artifacts
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#16 of 3,401
3918m citations

YBX1 promotes homologous recombination and resistance to platinum-induced stress in ovarian cancer by recognizing m5C modification

Huangyang Meng et al.Cancer Letters202410.1016/j.canlet.2024.217064

Lin Zhang, Wenjun ChengThe First Affiliated Hospital of Nanjing Medical University, China

YBX1m5C modificationHomologous recombinationplatinum resistanceovarian cancerPatient-derived organoidsCHD3 mRNAPABPC1mRNA stabilitychromatin accessibilityapoptotic stressSU056YBX1 inhibitororthotopic xenograft modelsplatinum-based chemotherapyDNA damage response
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#17 of 3,401
3918m citations

Structural basis for RNA polymerase II ubiquitylation and inactivation in transcription-coupled repair

Goran Kokic et al.Nature Structural & Molecular Biology202410.1038/s41594-023-01207-0

Patrick Cramer, Martijn S. LuijsterburgMax Planck Institute for Multidisciplinary Sciences, Germany

Transcription-coupled repairTCRRNA polymerase IIPol II ubiquitylationCRL4CSAELOF1UVSSACryo-electron microscopyligase neddylationTFIISPol II porePol II inactivationRNA polymerase II pausingDNA lesion removalTFIIS-like elementsite-specific ubiquitylation
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#18 of 3,401
3818m citations

A p62-dependent rheostat dictates micronuclei catastrophe and chromosome rearrangements

Sara Martin et al.Science202410.1126/science.adj7446

Stefano SantaguidaEuropean Institute of Oncology IRCCS, Italy

p62/SQSTM1micronucleichromosomal instabilityChromosomal rearrangementschromothripsisMicronucleus ruptureESCRT-dependent repairautophagic degradationmitochondrial proximityoxidation-driven homo-oligomerizationmicronuclear envelope repairAutophagy receptorendosomal sorting complex required for transportColorectal cancerprognostic marker
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#19 of 3,401
3718m citations

Transcription-coupled repair of DNA–protein cross-links depends on CSA and CSB

Christopher J Carnie, Aleida C Acampora et al.Nature Cell Biology202410.1038/s41556-024-01391-1

Christopher J. Carnie, Stephen P. Jackson, Julian StingeleCancer Research UK Cambridge Institute, United Kingdom

DNA-protein crosslinks (DPCs)DPCsTranscription-coupled repairCSACSBCockayne syndromeRNA polymerase IIubiquitylationDPC sequencinggenome-wide mapping of DNA-protein adductstranscription blockageTranscription restartNucleotide excision repairDPC-inducing agentsActively transcribed genesneurological features
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#20 of 3,401
3718m citations

Transcription-coupled DNA–protein crosslink repair by CSB and CRL4CSA-mediated degradation

Qing Yu, Melanie van der Woude et al.Nature Cell Biology202410.1038/s41556-024-01394-y

Jurgen A. MarteijnErasmus University Medical Center, Netherlands

DNA-protein crosslinks (DPCs)DPCsTranscription-coupled DPC repairCSBCSACRL4CSARNA polymerase IITranscription-coupled repairTC-NERSPRTNproteasome-mediated degradationUVSSAXPAE3 ubiquitin ligaseDPC-stalled RNA polymerase IIproteolysis-mediated DPC removaltranscription-blocking DPCsactive gene repair
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Dominant research themes and year-over-year shifts in DNA Repair Mechanisms

What Topics Define the Class of 2026?

The Class of 2026 highlights a significant focus on targeted therapies and complex DNA damage repair systems. Homologous recombination and DNA double-strand breaks remain prominent topics, reflecting ongoing efforts to map out intricate repair pathways and their implications for genomic stability. Additionally, the presence of PARP inhibitors indicates a continuing translational interest in exploiting repair deficiencies for cancer treatment, highlighting the bench-to-bedside evolution of DNA repair research.

Leading research themes
Leading research themes

How Did Topics Shift from the Class of 2025 to the Class of 2026?

A notable shift towards advanced therapeutic strategies and specialized cellular models is evident in the transition to the Class of 2026. Topics such as replication stress and synthetic lethality experienced substantial growth, underscoring a pivot towards exploiting vulnerabilities in cancer cell replication. The rise in patient-derived xenograft models and cryo-electron microscopy signifies a methodological leap toward personalized medicine and high-resolution structural analysis. Conversely, broad topics like general DNA damage response saw a relative decline, suggesting a maturation of the field toward more specific, actionable targets.

How topics shifted year over year
How topics shifted year over year
Methodology

PRI identifies high-impact research using a transparent, topic-agnostic framework applied consistently across scientific domains. Bibliographic records are drawn from OpenAlex, including publication dates, citation relationships, and document types.

This ranking covers the Class of 2026 cohort: journal articles published in 2024. Reviews and other non-article document types are excluded to ensure comparability.

Research impact is quantified with an 18-month post-publication citation window—the number of citing works published within 18 months of each paper's publication date. This metric captures early impact while controlling for publication age.

An LLM-based relevance classifier then reviews each candidate's title and abstract to confirm substantive alignment with the target domain. Only papers classified as relevant appear in the final ranking.

Zheng Su, Tinsley Li, Thematic Shifts in Early-High-Impact Cancer Genomics and Diagnostics Research: A Bibliometric and Semantic Analysis. bioRxiv 2026.07.04.736459; doi: https://doi.org/10.64898/2026.07.04.736459

Full methodologyGitHubbioRxiv preprint

Cite this ranking

Pepkio Research Index (PRI). Topics and Trends in Most Cited DNA Repair Mechanisms Papers, Class of 2026. https://pri.pepkio.com/top-papers/dna-repair-mechanisms/2026. Accessed 2026-07-19.

Zheng Su, Tinsley Li, Thematic Shifts in Early-High-Impact Cancer Genomics and Diagnostics Research: A Bibliometric and Semantic Analysis. bioRxiv 2026.07.04.736459; doi: https://doi.org/10.64898/2026.07.04.736459