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@nicolocovelli.bsky.socialOct 9, 2026, 10:01 AM

Whales, on the other hand, have an enhanced capacity to repair DNA lesions before they become permanent mutations in the genome. This is made possible by the overexpression of CIRBP.

👉️ Read more: themolecularcode.substack.com/p/from-whale...
#CancerBiology #MolecularBiology #DNARepair #SciComm

@narjournal.bsky.socialOct 7, 2026, 1:44 AM

14. Targeting DNA repair mechanisms in cancer therapy: the role of #smallmolecule #DNArepair inhibitors - Jeong et al. doi.org/10.1093/narc... “Editor’s Choice” review article detailing the current pipeline of repair inhibitors, synthetic lethality, biomarkers, and their combinations. 15/18

@narjournal.bsky.socialOct 7, 2026, 1:44 AM

⭐ How does the #BRCA network protect genome stability, and how can its vulnerabilities guide #cancertreatment? Explore 17 #NARCancer articles curated for the NAR Journals’ RRS session. #RadiationResearchSocietyMeeting #DNARepair @aibsbiology.bsky.social @nar-cancer-editor.bsky.social 1/18

@sigtrans-sttt.bsky.socialOct 6, 2026, 5:47 AM

Can hyperactive #DNArepair be targeted in #Neuroendocrine #CervicalCarcinoma?

#Multiomics reveals HRR activation and a CAF–IL6–E2F1–BLM axis that limits #PARP inhibitor sensitivity, supporting dual PARP–BLM inhibition.

#STTT #OpenAccess: doi.org/10.1038/s413...

Multi-omics profiling reveals homologous recombination repair hyperactivation as a therapeutic vulnerability in neuroendocrine cervical carcinoma
@nicolocovelli.bsky.socialOct 5, 2026, 10:01 AM

One explanation is that different species have evolved distinct anti-cancer strategies. Bowhead whales evolved a mechanism that allows them to faithfully repair DNA lesions.

👉️ Read more: themolecularcode.substack.com/p/from-whale...

#CancerBiology #MolecularBiology #DNARepair #SciComm

@nicolocovelli.bsky.socialOct 2, 2026, 10:00 AM

How can bowhead whales live for so long with such a low incidence of cancer?
The answer lies in the overexpression of CIRBP that enhances the cell's ability to repair DNA lesions.

👉️ Full story here: themolecularcode.substack.com/p/from-whale...

#CancerBiology #MolecularBiology #DNARepair #SciComm

@genesdev.bsky.socialSep 29, 2026, 3:00 PM

🆕 ADVANCE ONLINE 🆕

RESEARCH PAPER: Human PIF1 clears secondary DNA structures by coupled DNA unwinding and rewinding activities
By Jayachandran et al. and Petr Cejka
➡️ https://ow.ly/IFke50ZRacV

Petr Cejka Institute for Research in Biomedicine Università della Svizzera italiana
#DNA #DNArepair

@cddpress.bsky.socialSep 28, 2026, 11:53 AM

“DDX3X regulates DNA repair pathway choice at double-strand breaks via RNA-DNA hybrid formation”

This work highlights a new mechanism controlling #DNARepair and tumor cell sensitivity to #chemotherapy ⤵️
nature.com/articles/s41...

@mhr-reprodsci.bsky.socialSep 21, 2026, 9:22 AM

Findings:

🔬 Oocytes survived DNA breaks & fertilized.

🔬 Embryos faced DNA damage & developmental delays.

🔬 Offspring showed a spike in de novo (post-zygotic) mutations!

Read it here: academic.oup.com/molehr/advan...
#Genetics #DNARepair #Embryology #ESHRE

@narjournal.bsky.socialSep 16, 2026, 4:43 AM

✨NAR Molecular Medicine✨
⚠️ What happens when #DNArepair can no longer keep up? A study shows that increasing exposure to #NDMA can saturate #MGMT, triggering a burst of #mutations. A striking example of how dose shapes #DNAdamage and #cancerrisk. doi.org/10.1093/narm... @mitpress.bsky.social

@fdadf.bsky.socialSep 14, 2026, 11:39 AM

🚨 Can DNA that does nothing become a cell’s Achilles’ heel?

🧬 Cas9 selectively killed human cells carrying a non-functional target sequence, sparing cells without it.

www.sciencedirect.com/science/arti...

#CRISPR #DNARepair

@sbgrid.bsky.socialSep 10, 2026, 4:05 PM

The not so easy job of protecting our DNA: a publication in @natsmb.nature.com from the lab of Nikola Pavletich at @mskcancercenter.bsky.social in which researchers describe the structure of ATR-ATRIP complex bound to its two activators.
Read more here: buff.ly/S5IWOVw

#SBGrid #DNARepair

@nicolocovelli.bsky.socialSep 10, 2026, 10:00 AM

This reveals how RNA-binding proteins activate DNA-damage sensors, opening precise and reversible strategies to bypass tumor resistance.

📄 Source: www.cell.com/molecular-ce...

#MolecularIntegrity #MolecularBiology #DNARepair #GenomeStability #SciComm

@genesdev.bsky.socialSep 9, 2026, 6:00 PM

RESEARCH PAPER: MRE11 suppresses germline mutagenesis at meiotic double-strand breaks in mice
By Lukaszewicz et al., Scott Keeney, and Maria Jasin
➡️ https://genesdev.cshlp.org/content/40/17-18/1466.full

Memorial Sloan Kettering Cancer Center University of Michigan
#DNArepair #mutagenesis #genome

@alicefrolov.bsky.socialSep 6, 2026, 5:10 PM

Sharing a heatmap from an ongoing methodological exercise: "Age-associated erosion of DNA repair pathway capacity across human tissues"

#DNArepair #DNAdamageResponse #GenomeInstability #BasexcisionRepair #HomologousRecombination #GenomeMaintenance #Mutagenesis

Sharing a heatmap from an ongoing methodological exercise: "Age-associated erosion of DNA repair pathway capacity across human tissues," with the subtitle "Simulated relative repair activity for six core DNA damage response pathways (young vs aged donors)." The visualization arranges six canonical DNA damage response (DDR) pathways along the vertical axis: base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), homologous recombination (HR), non-homologous end joining (NHEJ), and interstrand crosslink repair (the Fanconi anemia pathway). The horizontal axis stratifies representative tissue compartments (hematopoietic, hepatic, dermal, skeletal muscle, cortical neuronal, and intestinal epithelium) in paired young and aged donor columns. Cell values encode relative repair activity normalized within pathway, with the color gradient scaled from low (attenuated capacity) to high (preserved capacity). I want to emphasize that the matrix is simulated. Values were parameterized to reproduce directional trends reported in the literature rather than to represent empirical measurements. The intent is to provide a compact scaffold for discussing pathway and tissue-specific vulnerability, not to assert quantitative effect sizes. The simulated pattern reflects several recurring observations: pronounced decline in double-strand break repair fidelity, particularly HR relative to the more error-prone NHEJ, alongside diminished BER throughput in post-mitotic compartments where oxidative lesion burden accumulates. Neuronal and hematopoietic columns display the steepest attenuation, consistent with reported associations between DDR insufficiency, mutational accumulation, and clonal dynamics. I would welcome critique on the parameterization strategy, particularly the choice to normalize within pathway rather than across tissues, which necessarily obscures absolute cross-pathway baseline differences.