#GenomeInstability
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embo.org
Learn about #cancer signaling, #GenomeInstability and more at the EMBO | FEBS Lecture Course "Cancer research: From fundamental insights to clinical application" in #Spetses, GR, 17–23 August 2026.

Deadline: 1 April

https://meetings.embo.org/event/26-cancerbio
#EMBOCancerResearch #EMBOevents 🧪
January 22, 2026 at 2:15 PM
dimiccolab.bsky.social
Still new on 🦋 but thrilled to share that I will be chairing with @lopeslab.bsky.social the next series of virtual seminars from @genomeiinetwork.bsky.social! Join us for the most exciting, thought-provoking, latest findings in the field! 👇Please repost
#genomeinstability #DDR #Senescence #epigenome
lopeslab.bsky.social Lopes_Lab @lopeslab.bsky.social · Mar 17
Exciting seminar series from Genome integrity italian Network (GiiN), chaired by myself and Raffaella Di Micco! Short talks (2x30’), at convenient time for EU/USA attendees. Big shots and raising stars in an expanding field. See flyers + link to receive email alerts. Please repost to your network!👇
March 18, 2025 at 9:22 AM
yerayhdez.bsky.social
I would like to take this opportunity to use my first "tweet" to say that I am currently seeking a postdoctoral position.

#DDR #PTMs #GenomeInstability
November 16, 2024 at 12:40 PM
alebrambati.bsky.social
Our study highlights RNA as a direct template for DNA repair, revealing RT-DSBR as a previously unrecognized and potentially mutagenic pathway. Huge thanks to the incredible team who made this work possible! (5/5)
🔗 www.nature.com/articles/s41...
#GenomeInstability #DNARepair #RNA #CRISPR #DSB
RNA transcripts serve as a template for double-strand break repair in human cells - Nature Communications
DNA double-stranded breaks threaten genome stability. Here, the authors show that transcript RNA serves as a repair template in human cells and identify Polζ as a key factor in RNA-templated DSB repai...
www.nature.com
May 12, 2025 at 5:49 PM
doksanilab.bsky.social
Thrilled to see our work featured on the cover of Molecular Cell.

The image is an electron micrograph of an i-loop, the DNA structure we propose as a source of eccDNA formation. Almost like catching circular DNA formation in the act.
#eccDNA #CancerResearch #GenomeInstability #DNARepair
May 21, 2026 at 2:46 PM
doksanilab.mastodon.social.ap.brid.gy
Join us at Social DNAing later today to hear more about telomere biology and genome instability : http://cancer.columbia.edu/dna-webinar
#telomere #genomeinstability #cancer @academicchatter
Virtual flyer for a scientific Talk by Dr. Ylli Doksani entitled: Stranger Things at Telomeres Provide Insights into Genome Instability. Part of the DNA dynamics webinar series Social DNAing.
March 12, 2026 at 2:48 PM
genesndiseases.bsky.social
This review highlights the dual nature of R-loops in #GeneRegulation and #GenomeInstability, emphasizing their impact on #DNADamage responses and potential as #therapeutic targets. #medsky

#OpenAccess: www.sciencedirect.com/science/arti...
November 2, 2025 at 12:51 AM
alebrambati.bsky.social
Huge thanks to the incredible team who made this work possible! 🙌

Check out the full preprint here: 🔗 doi.org/10.1101/2025...

#GenomeInstability #DNARepair #RNA #CRISPR #DSB #Genomics

@agnelsfeir.bsky.social @hinashah.bsky.social
doi.org
February 27, 2025 at 3:15 AM
valentinapiano.bsky.social
Happy new year 🎊

For the first time on this platform, I am happy to share the latest collections of papers @biomednews.bsky.social about mitotic cell signalling!

Enjoy reading new cool methods and exciting findings about my favourite phase of the cell cycle!
#mitosis #cellcycle #genomeinstability
January 2, 2025 at 12:17 PM
embo.org
Learn about #cancer signaling, #GenomeInstability and more at the EMBO | FEBS Lecture Course "Cancer research: From fundamental insights to clinical application" in #Spetses, GR, 17–23 August 2026.

Deadline: 1 April

https://meetings.embo.org/event/26-cancerbio
#EMBOCancerResearch #EMBOevents 🧪
March 26, 2026 at 3:25 PM
pombedoc.bsky.social
My former student Josh just had his paper accepted at #Genetics showing that #pombe diploids have intrinsic #genomeinstability . Be identified ploidy-essential genes and a remarkable loss of heterozygosity phenotype that may identify specific fragile sites.

🧬
@genetics-gsa.bsky.social
April 19, 2025 at 3:04 PM
jsantoyo.bsky.social
Roles of chromatin and genome instability in cellular senescence and their relevance to ageing and related diseases. #Chromatin #GenomeInstability #CellularSenescence #Ageing #Genomics #BioSky #SciSky 🧪
www.nature.com/articles/s41...
Roles of chromatin and genome instability in cellular senescence and their relevance to ageing and related diseases - Nature Reviews Molecular Cell Biology
Heterochromatin loss, telomere attrition and DNA damage induce cellular senescence by eliciting genome instability and innate immunity responses, thereby promoting ageing and age-related diseases. Thi...
www.nature.com
November 16, 2024 at 3:10 PM
myesmo.bsky.social
🔍 Before cancer starts, biology leaves clues.
The #ESMO25 session “The hallmarks of pre-cancer” unveils them
📅 17 Oct | 16:00–17:30 | Hall 5.2

🔗 buff.ly/33jC7nK

#GenomeInstability #PhenotypicPlasticity #inflammationa
October 15, 2025 at 8:01 AM
alicefrolov.bsky.social
Copy-Number Signature Architecture of Chromosomal Instability

#CancerGenomics #ChromosomalInstability #CopyNumberSignatures #MutationalSignatures #GenomeInstability #ComputationalOncology #Bioinformatics #DataVisualization
Copy-Number Signature Architecture of Chromosomal Instability I am sharing a visualization summarizing the relative contribution of 11 copy-number (CN) signatures associated with chromosomal instability (CIN) across a pan-cancer cohort. I want to state explicitly at the outset that the underlying data are simulated. The figure is not derived from a specific patient dataset; rather, it is constructed to illustrate a literature-grounded trend consistent with published CIN signature frameworks, and should be interpreted as a conceptual rather than empirical result. The plot adopts a radar bar-style format, with each of the 11 CIN signatures rendered as an angular segment whose radial length encodes its mean relative activity across the simulated cohort. This layout was chosen to emphasize the compositional structure of CIN etiologies within a single sample space, allowing simultaneous inspection of dominant and subdominant signature contributions. Mechanistically, these signatures are intended to reflect distinct genomic scars: impaired homologous recombination and replication stress producing tandem duplications and focal amplifications, defective mitotic segregation and whole-genome doubling generating chromosome-arm and whole-chromosome copy-number changes, and breakage-fusion-bridge cycles yielding characteristic segment-size and copy-number jump distributions. The simulated architecture recapitulates the expected skew, with a small number of signatures accounting for the majority of aggregate activity while lower-frequency signatures capture ecDNA-associated amplification and chromothripsis-like patterns. I offer this figure primarily as a communication and pedagogical aid for discussing how CN feature distributions - segment size, breakpoint count, copy-number state, and change-point magnitude - are decomposed into interpretable components.
August 19, 2026 at 10:52 PM
ezeta.bsky.social
Here you can read the full article:
www.cell.com/molecular-ce...

#MolecularBiology #eccDNA #ecDNA #CancerResearch #GenomeInstability #DNARepair
Damage-induced i-loops generate eccDNA from repetitive elements
Zanella et al. reveal a mechanism of eccDNA formation. Nicks or gaps at repetitive sequences promote i-loop formation that can be excised as eccDNA. Given the abundance of repetitive elements and the ...
www.cell.com
May 21, 2026 at 4:45 PM
alicefrolov.bsky.social
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.
September 6, 2026 at 5:10 PM
zahadyv.bsky.social
4/ Strikingly, T. gondii-induced DNA damage begins just 15 minutes post-infection. This damage, marked by γH2AX foci, predominantly affects cells in the S-phase and is independent of reactive oxygen species (ROS).
#GenomeInstability
December 16, 2024 at 2:02 PM