Joining the scores of scientists who are moving to what will hopefully be a much better, safer space (and is not controlled by an evil man). See you on the other side!

RT @ELogarinho: Join us in Stresa, Italy for the amazing @embo Chromosome Segregation and Aneuploidy organized by @SteSantaguida @Fachinet….

Introducing Grok Imagine.

RT @SteSantaguida: We are very excited to open the registration for the upcoming @EMBOevents on Chromosome Segregation and Aneuploidy in be….

RT @STOPlabPI: Great morning session with novel insights into cancer biology from Hind Medyouf, George Davey Smith @mendel_random @gou_koh….

Our Review on “Aneuploidy as a driver of human cancer” is out in Nature Genetics. Check it out! 🎉. The Ben-David lab wishes everyone Shana Tova — may the new year be much better than the ending one, bringing peace and stability to all! 🙏.

RT @shouval: דברים חשובים ומרגשים שנשאה @MichalFeldman9 המוכשרת והמדהימה על מחקר ועשיה בעת הזו בארץ הזו.

RT @SteSantaguida: Fantastic FASEB aneuploidy meeting in sunny Melbourne!! Great science with a terrific group of scientists and friends😎🧬🔬….

A great opportunity for a postdoc in Israel, with a lucrative fellowship to become a member of the supportive Azrieli community. If you’re looking for a postdoc in cancer genetics, check out our lab at:

RT @SteSantaguida: Very happy to share our latest papers on the identification of novel dependencies of aneuploid cells just published in @….

16/ We are thankful to our great collaborators @RalserLab @DrFranVazquez ​​@NCIEytanRuppin @francesconica13 and Talia Golan. And grateful to our funders and institutions @TelAvivUni @TAUMedFaculty @ERC_Research @EMBO_YIP @ICRF_Israel @AIRC_it @IEOufficiale @LaStatale @semm_it.

15/ Altogether, we propose that aneuploid cells increase CRAF/MEK/ERK pathway activity, which helps them overcome the elevated DNA damage. Inhibition of CRAF/MEK/ERK signaling could therefore sensitize aneuploid cells to DNA damage inducers.

14/ Finally, we analyzed data from pancreatic PDXs and breast cancer patients treated with olaparib and immunotherapy. Resistance was associated with high RAF/MEK/ERK pathway activity, especially in highly aneuploid tumors.

13/ We found that MEK overexpression reduced sensitivity to etoposide and olaparib. Moreover, trametinib sensitized highly aneuploid clones to etoposide, suggesting the potential benefits of combining MEK/ERK inhibitors with DDR inhibitors.

12/ As a result, these clones were more sensitive to MEK inhibitors (trametinib, selumetinib) and the ERK inhibitor ulixertinib, demonstrating dependency on the RAF/MEK/ERK pathway.

11/ CRAF downstream targets MEK and ERK also showed significantly higher activity in aneuploid clones, indicating elevated RAF/MEK/ERK signaling.

10/ Inhibiting CRAF with TAK632 sensitized highly aneuploid clones to DNA-damaging agents like etoposide and olaparib, confirming that CRAF activation helps aneuploid cells overcome DNA damage.

9/ Importantly CRAF activity is linked to the DNA damage response (DDR) and is activated in response to DNA damage. We found that etoposide increased CRAF activity in parental RPE1 cells, and higher CRAF activation correlated with resistance to DNA-damaging drugs in cancer cells.

8/ Additionally, highly aneuploid tumors in pediatric PDX models were more sensitive to RAF inhibitors. Thus, aneuploid cancer cells also activate CRAF.

7/ We investigated whether CRAF activity is linked to high aneuploidy in human cancer cells. Analysis of hundreds of cancer cell lines showed increased CRAF activity in highly aneuploid cells.

6/ We then tested whether the increased sensitivity to RAF inhibitors in aneuploid clones was due to higher CRAF activation and found that CRAF was consistently activated, and that this activation is required for the proliferation of highly aneuploid clones.