Kops Lab

@kopslab.bsky.social

Interested in all things chromosome segregation and aneuploidy | Director & PI at Hubrecht Institute

As a cell biology lab, we acknowledge the decades-long impressive efforts to uncover evolutionary relationships using advanced phylogenomics methods. These approaches undergo continuous improvements that lead to adjustments of data interpretation, as is the case in every scientific field. (1/3)

Bungo Akiyoshi@bungoakiyoshi.bsky.social · 6mo ago

BTW when I talked to a cell biologist this week and explained that bacterial-origin proteins were used to determine the root of the eukaryotic tree of life, the person was surprised by that approach. So it's not just me who has issues with this approach.

Our story on the kinetochore composition of the ciliate Tetrahymena thermophila is out now on bioRxiv! We find surprisingly many orthologs of conventional kinetochore components, but also components that have very different evolutionary origins. A 🧵 (1/11) Check it out here: tinyurl.com/4ectm9x4

tinyurl.com

Ever wondered how chromosomal instability (CIN) influences tumorigenesis? And how does it contribute to shaping the tumor microenvironment? In our latest preprint, we used the CiMKi model to induce and monitor skin tumors across five levels of CIN tinyurl.com/52tuk88z Here's what we find (1/5):

Non-cell-autonomous mechanisms of tumor initiation and relapse by chromosomal instability

Chromosomal instability (CIN) is a hallmark of cancer, and a primary cause of genetic heterogeneity in tumors. Depending on the degree of CIN and the affected tissue, CIN can promote or suppress tumor...

tinyurl.com

Our new preprint is out! We revisit the associations between p53 status and cancer aneuploidy using TCGA data. Here’s a breakdown of our findings. Important work spearheaded by the talented PhD candidate Joana Marques. Check it out here: www.biorxiv.org/content/10.1... (1/8)🧵

Cancer type-specific association of p53 deficiency with aneuploidy and chromosome losses

Aneuploidy and mutations in the TP53 tumor suppressor gene are among the most frequent genetic alterations in cancer, and p53 inactivation is considered an important contributor to the emergence of cancer aneuploidy. It is unclear, however, if p53 protects against particular forms of copy number alterations and whether it does so universally across cancer types. By analyzing p53 status and various aneuploidy features in 31 cancer types in the TCGA database, we verify that on a pan-cancer level p53-deficient cancers tend to have a higher degree of aneuploidy. However, for many cancer types, the average degree of aneuploidy is similar in p53-proficient and -deficient samples, and a substantial degree of aneuploidy can accumulate with intact p53 in almost all cancer types. Neither arm-level nor whole chromosome aneuploidy but rather chromosome loss events distinguish p53-deficient from proficient cancers. p53 inactivation is therefore neither sufficient nor necessary for the emergence of cancer aneuploidy, but is associated with the degree of aneuploidy in a subset of cancer types and more universally with chromosome losses. Our findings underscore the poorly understood nature of aneuploidy emergence in cancer and shed new light on the role of p53 therein. ### Competing Interest Statement The authors have declared no competing interest. Dutch Cancer Society (KWF Kankerbestrijding) European Research Council, ERC-SyG 855158

biorxiv.org

An amazing inaugural Hubrecht Symposium on Developmental Biology, bringing the Dutch community together and getting inspired by amazing science! A big thank you to the speakers, the organizing committee and the many dedicated Hubrechters who made it happen.

Hubrecht Institute@hubrechtinstitute.bsky.social · last yr.

We closed today with a great keynote by @embo.org director Fiona Watt, highlighting how spatial maps of epidermal cell populations have allowed the generation and testing of new hypotheses. Thanks for joining the #HubrechtSymposium2025! We hope you leave with fresh insights and new connections.