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vrendo.bsky.social
Veronica Rendo
@vrendo.bsky.social
68 followers 81 following 26 posts
Group Leader, Uppsala University 🇸🇪 | Studying brain tumor evolution and treatment resistance
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · May 6
Better late than never! The Rendo Lab website is officially up and running 🧠 🧬 Read about our ongoing research and the wonderful team that makes it happen!
rendolab.org
Rendo Lab
rendolab.org
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Reposted by Veronica Rendo
marta-shahbazi.bsky.social
Marta Shahbazi @marta-shahbazi.bsky.social · Apr 29
Working hard with @mllthingsdna.bsky.social @katemiro.bsky.social @ms01.bsky.social and @vrendo.bsky.social @embo.org #ChromoPloidy25
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Reposted by Veronica Rendo
bendavidlab.bsky.social
bendavidlab.bsky.social @bendavidlab.bsky.social · Apr 27
Excited to get the #EMBOChromoploidy meeting started! 3 days of fantastic science and fun in beautiful Stresa are beginning now!

meetings.embo.org/event/25-ane...
Chromosome Segregation and Aneuploidy
Aneuploidy is a hallmark of cancer and developmental disorders such as Down syndrome. Understanding how cells accomplish faithful chromosome segregation and how chromosomal instability (CIN) impacts …
meetings.embo.org
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Mar 19
Thanks so much! 🙏🏻
vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Mar 19
5/5 Thank you to all the funding agencies that made this research possible, in my case @vetenskapsradet.bsky.social, Cancerfonden, and the Berth von Kantzows Foundation.
vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Mar 19
4/5 Thank you @rameenberoukhim.bsky.social and @bandolab.bsky.social for your constant trust, mentorship and support, let's hope this is the first of many more papers to come!
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Mar 19
3/5 Words cannot describe how thrilled I am to see this paper out! It's not only my first publication as a senior author, but also the result of a wonderful collaboration with the dream team Jeremiah Wala, Simona Dalin, Sophie Webster, and others! 🤩
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Mar 19
2/5 We mimic BRD4 focal deletions using CRISPR-Cas9 technology and show that these focal deletions rescue ovarian cancer cells from toxicity associated with BRD4 overexpression, suggesting that BRD4 levels must be fine-tuned for cancer cell proliferation.
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Mar 19
1/5 In this case, we describe breakpoints in the BRD4 locus, which rescue gene overexpression toxicity in breast and ovarian cancers with chromosome 19 gains.
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Mar 19
📣 Online now! Our study shows how recurrent focal deletions constitute a mechanism by which cancer cells can dampen toxicity due to gene amplification.

www.cell.com/cell-genomic...

🧵👇:
Recurrent breakpoints in the BRD4 locus reduce toxicity associated with gene amplification
Wala et al. identify recurrent focal BRD4 deletions in tumors harboring larger amplifications, suggesting that these deletions may serve to limit toxic BRD4 overexpression. A CRISPR-Cas9 cell line mod...
www.cell.com
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Feb 27
Thanks Mimi, so grateful for your mentorship. Cheers to all the collaborations ahead!
vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Feb 27
That's so kind of you! Thank you for a brilliant seminar today, and welcome to Uppsala! 😊
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Feb 27
Today we celebrated my official Group Leader appointment and paper publications with bubbles and prinsesstårta, the Swedish way! 🍰🥂🍾 Skål!
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Feb 19
Thanks so much, John! 🙏🏻❤️
vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Feb 19
So excited to see this paper out! An example of how window of opportunity trials can help dissect the mechanisms of response and resistance associated with targeted therapies in glioblastoma 🧠
www.science.org/doi/10.1126/...
Thanks to the patients and scientific team who made this study possible.
A window-of-opportunity trial reveals mechanisms of response and resistance to navtemadlin in patients with recurrent glioblastoma
In patients with glioblastoma, navtemadlin resistance is not mediated by TP53-inactivating mutations, and combination with TMZ may improve efficacy.
www.science.org
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Jan 27
12/ A big acknowledgement to all of our collaborators, as well as the different institutions and foundations who supported our research, including @ec.europa.eu @braintumourcharity.bsky.social @vetenskapsradet.bsky.social @ercresearch.bsky.social
vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Jan 27
11/ Overall, our study establishes a compendium of genes compensated across human cancers, with functional evidence for toxicity effects associated with gene overexpression in the context of this disease. Many targets to explore pan-cancer and in specific tumor types!
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Jan 27
10/ RBM14 amplification (which occurs in the CCND1 locus) is clinically actionable! We find that RBM14 amplification status is correlated with survival in a recently published cohort of >1000 colorectal cancer patients treated with irradiation as standard of care.
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Jan 27
9/ We additionally find that RBM14 overexpression can induce an innate immune response, activating the STING-STAT3 axis (we interpret changes in STING perinuclear localization as a marker of pathway activation) and rendering cells more sensitive to STAT3 inhibition.
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Jan 27
8/ Given its role in c-NHEJ-mediated DNA repair, we evaluated the effects of RBM14 overexpression in DNA damage response. We found that gene overexpression increases reliance on DNA repair by c-NHEJ (an error-prone process) over HR, increasing the rate of aberrant cell divisions.
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Jan 27
7/ We observe a similar effect with RBM14, encoding a member of the family of RNA binding proteins and the HDP-RNP paraspeckle complex. RBM14 is focally amplified on chromosome 11 and results toxic to breast and lung cancer cells when overexpressed.
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Jan 27
6/ The well-known cell cycle inhibitor CDKN1A (p21) is an ARGOS gene amplified at the arm-level in chromosome 6p. By creating inducible cell line models, we show that overexpression of CDKN1A impairs the growth of breast cancer cells.
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Jan 27
5/ The overlap between “compensated” and “toxic” genes identified eight ARGOS gene candidates across cancers, from which we selected CDKN1A and RBM14 for follow-up validation.
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Jan 27
4/ By analyzing data from 17 ORF screens conducted by many of our wonderful collaborators and co-authors
@broadinstitute.org, we identify many genes that result detrimental (i.e. cause growth inhibition or cell death) to cancer cells when overexpressed. We term these “toxic genes”.
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vrendo.bsky.social
Veronica Rendo @vrendo.bsky.social · Jan 27
3/ The expression of these collaterally altered genes should scale with their copy number. However, by integrating data from >8000 tumors in TCGA & CCLE, we identify amplified genes that are consistently expressed at lower levels than expected, and term them “compensated genes”.
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