RT @NKI_nl: 📢 Applications for the NKI PhD program open from Jan 1 - Feb 28. Join our international research community in Amsterdam, workin….

RT @deVisserKarin: 👇ready for the next step in your career? The NKI is recruiting a junior group leader! Don't miss this opportunity. The….

Thanks to all collaborators at @NKI_nl and @oncodeinstitute and the wonderful HAP1 cells for expressing SLFN11 (which is inactivated in most used cancer cell lines).

p53-independent apoptosis occurred through a ribotoxic stress response. The @Snippertlab and @Schumacher_lab showed that ribosome stalling occurred in patient-derived organoids and healthy human T cells. This highlights ribosome stalling as a new signaling event upon DNA damage.

A screen in haploid cells discovered SLFN11 and GCN1/2 as needed for translation inhibition. Although both affected translation SLFN11 was critical for stalling. This may relate to the strong link between SLFN11 expression and chemotherapy response first described by Yves Pommier

When cells were exposed to DNA damage Nicolaas noticed that translation was inhibited, associated with apoptosis and independent of p53. Ribosome profiling in collaboration with @AgamiLab showed that DNA damage triggered ribosome stalling at the rare Leucine codon (UUA).

How does DNA damage cause apoptosis when p53 is mutated? Critical to understand treatment of many tumors. Excited that ‘DNA damage induces p53-independent apoptosis through ribosome stalling’ by Nicolaas Boon and collaborators is out:

Happy and proud to be elected as member of the Royal Netherlands Academy of Arts and Sciences!.

RT @IRBBarcelona: 📢Registrations are open for the #BarcelonaBiomed #Conference "Molecular Determinants of #Cancer Therapy Resistance"!. 👉18….

I am very excited, what an honour!.

RT @NKI_nl: NKI researchers have compiled a detailed catalog of bacteria living in cancer metastases. They shed light on their diversity an….

RT @LaskerFDN: Congratulations to Piet Borst, 2023 #LaskerAward winner! – “for an exceptional 50-year career of scientific discovery, mento….

@glmclelland Thanks to collaborators, internship students, @NKI_nl, @Oncodeinstitute and Jean Schaffer for a nice N&V!.

@glmclelland When would this be important? DIESL helps cells to survive in nutrient-poor conditions and supports the rapid postnatal growth of mice, especially when they transition from nutritious milk to solid food.

@glmclelland How would TMX1 mutants generate triglycerides? Time for a genetic modifier screen! Mutagenesis of TMX1 knockouts pointed out DIESL, a parallel TAG synthesis pathway normally in complex with TMX1 at the endoplasmic reticulum. DGATs and DIESL act under different conditions.

DGAT-deficient cells showed no sign of triglyceride synthesis: no additional pathway??? Unstoppable @glmclelland mutagenized the cells and found mutants in TMX1…that accumulate triglycerides!

Thinking that humans may have additional pathways to synthesize triglycerides @glmclelland stripped away the known triglyceride synthesis pathway in haploid human cells by mutating DGAT1 and DGAT2.

If you like #genetics in human cells you may enjoy our latest paper by @itsgianluca and collaborators. A ‘fishing expedition’ using logic as our guide by Gian-Luca McLelland to study triglyceride synthesis. After some plot twists it yields DIESL!.

Are you interested in doing a PhD in our lab in Amsterdam to discover ‘hidden’ biology using #genetics? The application deadline of the #PhDprogram at the Netherlands Cancer Institute ends on the 3rd of September!

Are you interested to join our laboratory at the Netherlands Cancer Institute to discover exciting ‘hidden’ biology using #genetics? Then look no further and apply for our #PhDprogram at