NAR Cancer 2025 impact factor rises to 4.6; other metrics at journal home page. Appreciate our authors, reviewers, editors. Encourage submissions at intersection of cancer and nucleic acids fields–full info and details of forthcoming "Seeds of Cancer" collection at academic.oup.com/narcancer/pa...

Call for Papers

NAR Cancer is a peer-edited, not-for-profit, Open Access journal published by Oxford University Press. In seven years, it has established a reputation for high-

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PARP inhibitors work in BRCA-mutant cancers, but resistance is common. Buckley-Benbow et al. show loss of CHTF18-RFC2/5 sensitizes cells via replicative gaps (not recombination defects), and isn’t rescued by 53BP1 loss—highlighting new therapeutic targets. academic.oup.com/narcancer/ar...

Loss of CHTF18–RFC2/5 leads to replicative gaps and sensitivity to PARP inhibitors

Abstract. The use of PARP inhibitors (PARPi) has profoundly changed the treatment of BRCA1/BRCA2-mutated cancers. Despite this, acquired resistance to PARP

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Can SMC5/6 status help guide precision cancer therapy? A new NAR Cancer study links deleterious SMC5/6 variants to tumor mutational burden and immunotherapy responses, driven via POLE dysfunction and mismatch repair deficiency.https://academic.oup.com/narcancer/article/8/2/zcag012/8688771

Disruption of the structural maintenance of chromosomes 5/6 complex enables tumor mutagenesis

Abstract. The structural maintenance of chromosomes (SMC) 5/6 complex is conserved and essential for mammalian development. SMC5/6 germline variants in cel

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Few cancer driver mutations have been identified in promoters, maybe for technical reasons. New assay targets >3,000 promoters — hits in CDK4, SMAD3, and GATA3 in breast cancer provide promising leads for functional follow-up. academic.oup.com/narcancer/ar... #CancerGenomics #NonCoding #Promoters

Sensitive detection of somatic mutations in GC-rich cancer gene promoters

Abstract. Somatic mutations in protein-coding genes and noncoding regulatory regions are the major drivers of cancer. Only a relatively small number of som

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Testicular germ cell cancer risk is rising, with disproportionate impact on Hispanic men. New NAR Cancer study of Mexican patients found 7 genes and 3 new genetic variants linked to risk. Inclusive research promotes fair, effective precision medicine. #HealthEquity academic.oup.com/narcancer/ar...

Uncovering novel germline variants associated with testicular germ cell tumors by exome sequencing

Abstract. Testicular germ cell tumors (TGCT) are highly heritable malignancies that display increasing incidence worldwide, with rising mortality rates par

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How does c-MYC overexpression drive transcriptional rewiring in cancer? Sundaram et al report a plausible mechanism involving co-option of TRE/AP1 sites, mainly at enhancers, rising with MYC levels and linked to repression. academic.oup.com/narcancer/ar...

MYC and AP-1 oncogenes cooperatively bind enhancers to rewire transcription

Abstract. The transcription factor c-MYC (MYC) is deregulated in ~70% of human cancers. Through de novo motif discovery analysis on published MYC ChIP-seq

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HSF1 drives cancer stress resilience but is hard to target—clever screen identifies spliceosome helicase DHX8 as a druggable regulator of HSF1 splicing→HSF1 program gone, cancer loses stress defenses. Editor's Choice in NAR Cancer. #PrecisionOncology #Spliceosome academic.oup.com/narcancer/ar...

Human DEAH-box helicase 8 regulates HSF1-mediated stress response and cancer-associated pre-mRNA splicing in tumour cells

Abstract. Transcription factor heat shock factor 1 (HSF1) orchestrates the cellular stress response, promoting malignant transformation, unchecked prolifer

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Introducing IGIS, a versatile, scalable platorm to investigate synthetic lethal relationships between cancer therapeutic targets. Haracska et al. describe the platform and validate it by investigation of BRCA1–RAD18 interplay. New in NAR Cancer. academic.oup.com/narcancer/ar...

Advancing inducible gene-inactivation systems to explore synthetic lethality

Abstract. Synthetic lethality offers opportunities to identify therapeutic targets for cancer research, facilitating the development of targeted tumour the

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Kavalipati, Aponte, et al. reveal actionable ways to overcome CDK4/6 resistance in HR+ breast cancer — a step toward smarter combination therapies and better patient outcomes. New in NAR Cancer: academic.oup.com/narcancer/ar...

NAR Cancer presents a curated collection of 17 articles on how advances in understanding the DNA damage response are reshaping cancer therapy. Explore the collection and read the editorial from guest editors Li Lan and Elise Fouquerel. New targets and new tools. academic.oup.com/narcancer/pa...

5th Anniversary Thematic Collection: Manipulating DNA Repair and the DNA Damage Response to Improve Cancer Therapy

This collection is coordinated with the journal’s virtual 5th Anniversary Symposium and is focused on exploitation of the DNA damage response for

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Terrific on-line seminar - Feb 19 noon EST. Kyungjae Myung, Recent NAR Cancer author, now Director of IBS Center at Ulsan National institute, Korea. "Investigation of genomic integrity & translation for potential clinical applications." Columbia Social DNAing: columbiacuimc.zoom.us/webinar/regi...

Welcome! You are invited to join a webinar: Social DNAing Webinar. After registering, you will receive a confirmation email about joining the webinar.

Welcome! You are invited to join a webinar: Social DNAing Webinar. After registering, you will receive a confirmation email about joining the webinar.

columbiacuimc.zoom.us

New in NAR Cancer: PARP14 binds ssDNA via RRM domains and engages MRE11 at reversed forks, causing stress-induced DSBs—clarifying PARP14’s role in promoting chemosensitivity in BRCA-deficient cells. academic.oup.com/narcancer/ar...

The RRM domains of PARP14 mediate replication fork degradation in BRCA2-deficient cells

Abstract. Degradation of reversed replication forks by nucleases has emerged as a major mechanism of chemosensitivity in BRCA-deficient cells. We previousl

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Early oncogenic perturbations persist for decades, while overt tumorigenesis is constrained. How? CALL FOR PAPERS. NAR Cancer thematic collection. Gabriella Ficz (Queen Mary University London) and Yvonne Fondufe-Mittendorf (Van Andel Institute), eds. For details: academic.oup.com/narcancer/pa...

Seeds of Cancer, Decades of Silence: Ageing and Environmental Control of Tumour Latency

Editors: Gabriella Ficz, PhD Barts Cancer Institute (CRUK), Queen Mary University, London, UK g.ficz@qmul.ac.uk Yvonne Fondufe-Mittendorf, PhD Van Andel Inst

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Insights into how Rad 18 shapes oral cancer genomes by promoting error-free lesion bypass during DNA replication. Read more about how gene-environment interactions determine cancer risk in an NAR Cancer Article from Anand, Williams, Vaziri, and UNC coworkers. academic.oup.com/narcancer/ar...

Differential roles of Rad18 in repressing carcinogen- and oncogene-driven mutagenesis in vivo

Abstract. The DNA repair protein RAD18 activates “Y-family” trans-lesion synthesis (TLS) DNA polymerases that are DNA damage-tolerant and potentially error

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New in NAR Cancer: Colón-Rios, Glazer, and coworkers model PARPi resistance in the IDH1-mutant setting and offer a strategy to overcome resistance by treating with the receptor tyrosine kinase inhibitor, cediranib - mechanism involves suppression of re-activated HDR factors. doi.org/10.1093/narc...

PARP inhibitor resistance in IDH1-mutant cancers due to loss of end protection factors, 53BP1 and REV7

Abstract. Acquired resistance presents a major challenge for targeted therapies, with initially responsive tumors eventually reverting underlying vulnerabi

doi.org

Fantastic speaker lineup, co-organized by NAR Cancer Editorial Board member John Tainer. One of a select few conferences that NAR Journals will extend sponsorship to this year.

Fusion Conferences@fusionconf.bsky.social · 9mo ago

⏰ Only 1 week left! Registration for #DRRSC26 closes soon - don’t miss out on being part of this exciting conference. 📅 Deadline: 25 November 2025 Click here to Register: bit.ly/49oHUCi #FusionStructuralMolBio #FusionDNA

James Watson, Co-Discoverer of the Structure of DNA, Is Dead at 97 www.nytimes.com/2025/11/07/s...

James Watson, Co-Discoverer of the Structure of DNA, Is Dead at 97

nytimes.com

Excited to share: NAR Cancer Editor's Choice review article from Kyungjae Myung and colleagues provides a snapshot of the blossoming field of DNA damage response- and repair-targeted therapeutics. Focus is on small molecules currently in clnical trials. academic.oup.com/narcancer/ar...

Congratulations to Forment, O’Connor and coworkers on an Editors' Choice study in NAR Cancer, unraveling the mechanism by which addition of PARP inhibitors to AR pathway inhibitor therapy improves prostate cancer survival, even in the absence of HRR defects. academic.oup.com/narcancer/ar...

Androgen receptor inhibition extends PARP inhibitor activity in prostate cancer models beyond BRCA mutations and defects in homologous recombination repair

Abstract. Clinical trials show benefit of the combination of poly(ADP-ribose) polymerase inhibitors (PARPi) with androgen receptor (AR) pathway inhibitors

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New in NAR Cancer: Loss of uL14 downregulates antigen processing and presentation components in melanoma cell lines - alters peptide pool available for presentation to create an escape mechanism from immune surveillance. From Anna Dopler and coworkers.

Liam Faller@liamfaller.bsky.social · 11mo ago

Here's the latest from the lab! In it we dive into the role of ribosomal proteins in antigen processing and presentation! academic.oup.com/narcancer/ar...

Evaluation of 49 mRNA modification regulators across subtypes in human breast cancer reveals potential biomarkers and therapeutic targets. New in NAR Cancer, from Carlos Paula, Erik Dassi, Francesca Aguilo and coworkers at University of Trento and Umeå University. academic.oup.com/narcancer/ar...

Analysis of the mRNA modification machinery alterations in breast cancer through the SCAN-B cohort

Abstract. Epitranscriptomic modifications regulate gene expression and have been implicated in cancer, including breast cancer. Using the SCAN-B cohort, we

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We described Ku-RNA binding in 1998, but had to wait 27 years for Zha and coworkers to discover the significance. A lesson in patience. 2/2 pubs.acs.org/doi/10.1021/...

Characterization of the RNA Binding Properties of Ku Protein†

Ku protein, a heterodimer of 70 and 83 kDa polypeptides, is the regulatory component of the DNA-dependent protein kinase (DNA-PK). Ku protein binds to DNA ends and is essential for DNA double-strand b...

pubs.acs.org

Congrats to our Editorial Board member Shan Zha for amazing study attributing essentiality of Ku protein in primates to modulation of RNA-driven innate immunity. 1/2 www.nature.com/articles/s41...

Ku limits RNA-induced innate immunity to allow Alu expansion in primates - Nature

Studies on the essentiality of Ku in human cells reveal that Ku interacts with diverse double-stranded RNA molecules, including antisense Alu, and enables tolerance of Alu sequence expansion in p...

nature.com

N6-methyladenosine in R-loop homeostasis. Short review in NAR Cancer from Chun-Long Chen and coworkers. Effects on transcription, repair, centromere and telomere stability, and R-loop dynamics. Targeting as a cancer therapeutic strategy. academic.oup.com/narcancer/ar...

m6A modification in R-loop homeostasis: a potential target for cancer therapeutics

Abstract. R-loops or DNA–RNA hybrids are prominent nucleic acid structures that commonly arise during transcription. These structures play important biolog

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Beyond BRCA status: machine-learning assisted multichannel imaging platform for cell-by-cell analysis of HR competency, enabling patient stratification. “Editor’s Choice” in NAR Cancer. academic.oup.com/narcancer/ar...

Automated machine learning profiling with MAP-HR for quantifying homologous recombination foci in patient samples

Abstract. Accurate visualization and quantification of homologous recombination (HR)-associated foci in readily available patient samples are critical for

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New insights into gene regulation in melanoma, the deadliest skin cancer: SETD6-catalyzed methylation of BRD4 and chromatin-localized interaction with MITF. From Tzofit Elbaz Biton, Dan Levy, and coworkers, published in NAR Cancer. academic.oup.com/narcancer/ar...

SETD6 mediates selective interaction and genomic occupancy of BRD4 and MITF in melanoma cells

Abstract. Aberrant transcriptional programs mediate malignant transformation of melanoma, the most aggressive form of skin cancer. The lysine methyltransfe

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Our sister journal, Nucleic Acids Research, has opened a search for an Executive Editor. Great opportunity for mid-career or senior investigator looking to be part of a great team, handle 100-150 papers per year, and attend the annual EE meeting. Details at: academic.oup.com/nar/pages/ex...

NAR seeks a new Executive Editor

Overview of the Journal Nucleic Acids Research (NAR) is a leading open access molecular biology journal published by Oxford University Press. It provides rapid

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Are key cancer driver mutations amenable to editing by endogenous ADAR enzymes? The scope of correctable mutations is charted for the first time in an Editor's Choice paper, newly published in NAR Cancer. From Rona Merdler-Rabinowicz and colleagues. academic.oup.com/narcancer/ar...

A systematic evaluation of the therapeutic potential of endogenous-ADAR editors in cancer prevention and treatment

Abstract. Adenosine deaminases acting on RNA (ADAR) enzymes constitute a natural cellular mechanism that induces A-to-I(G) editing, introducing genetic cha

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New in NAR Cancer. A critical examination of mutations in conserved m6A motifs: low recurrence and maybe not a primary mechanism for altering gene function. From Luis A. Diaz and coworkers, @mskcancercenter.bsky.social academic.oup.com/narcancer/ar...

Watch the replay of Elise Fouquerel and Rob Sobol's talks at today's NAR Cancer 5th anniversary symposium (offered in collaboration with Social DNAing). Special thanks to guest host Li Lan. Link to video at the Social DNAing website: www.cancer.columbia.edu/research/pro...