Andrew Blackford
@andrewblackford.bsky.social
Associate professor and CRUK Senior Fellow, University of Copenhagen and University of Oxford. My lab researches how DNA repair defects and loss of genome stability cause disease, including cancer.
https://icmm.ku.dk/english/research-groups/blackford-group
https://icmm.ku.dk/english/research-groups/blackford-group
Congratulations, looks like a great resource!
November 13, 2025 at 1:54 PM
Congratulations, looks like a great resource!
Very nice work, congratulations Arnab & team!
November 3, 2025 at 10:06 AM
Very nice work, congratulations Arnab & team!
See also the elegant and complementary study from the @durocher1.bsky.social lab, also out on bioRxiv: www.biorxiv.org/content/10.1...
Mitotic single-stranded DNA suppression by DDIAS
Incomplete DNA replication and chromosome breakage during mitosis pose major threats to chromosome segregation. The CIP2A-TOPBP1 complex acts to mitigate this peril, but its exact role is not yet unde...
www.biorxiv.org
September 10, 2025 at 3:26 PM
See also the elegant and complementary study from the @durocher1.bsky.social lab, also out on bioRxiv: www.biorxiv.org/content/10.1...
Finally, we are particularly grateful to the patients and their families for their participation in this study.
September 10, 2025 at 3:23 PM
Finally, we are particularly grateful to the patients and their families for their participation in this study.
The work was led by our star postdoc Kaima Tsukada & is the result of a great collaboration with labs of @fenaochs.bsky.social, @profstewartlab.bsky.social, @tcr-miller.bsky.social, @antonywoliver.bsky.social, Zafar Iqbal & others not on Bluesky.
September 10, 2025 at 3:22 PM
The work was led by our star postdoc Kaima Tsukada & is the result of a great collaboration with labs of @fenaochs.bsky.social, @profstewartlab.bsky.social, @tcr-miller.bsky.social, @antonywoliver.bsky.social, Zafar Iqbal & others not on Bluesky.
We have also identified patients with bi-allelic mutations in DDIAS and CIP2A, who present with severe neurological phenotypes, revealing the pathological consequences of the failure to resolve DNA lesions during mitosis.
September 10, 2025 at 3:21 PM
We have also identified patients with bi-allelic mutations in DDIAS and CIP2A, who present with severe neurological phenotypes, revealing the pathological consequences of the failure to resolve DNA lesions during mitosis.
In brief: DDIAS is a mitosis-specific TOPBP1-binding protein that acts downstream of TOPBP1-CIP2A. DDIAS also has a ssDNA-binding domain, & mutation of this domain or loss of TOPBP1 binding leads to chromosomal breaks & micronuclei, as well as synthetic lethality in cells deficient in BRCA1 or BRCA2
September 10, 2025 at 3:20 PM
In brief: DDIAS is a mitosis-specific TOPBP1-binding protein that acts downstream of TOPBP1-CIP2A. DDIAS also has a ssDNA-binding domain, & mutation of this domain or loss of TOPBP1 binding leads to chromosomal breaks & micronuclei, as well as synthetic lethality in cells deficient in BRCA1 or BRCA2
Congrats Beth, fantastic work!
August 15, 2025 at 7:16 AM
Congrats Beth, fantastic work!
Congratulations!
August 1, 2025 at 8:33 AM
Congratulations!
Congratulations Ernst, great to see your work in print. Predictomes is a fantastic resource for the field!
February 26, 2025 at 6:40 PM
Congratulations Ernst, great to see your work in print. Predictomes is a fantastic resource for the field!