Justin Engel retweeted
3 papers in @Nature today reflecting large scale efforts at mapping dependencies and multimodal molecular profiling data from a large panel of patient-derived 3D cancer models. This is DepMap on steroids!
nature.com/articles/s41586-0…
nature.com/articles/s41586-0…
nature.com/articles/s41586-0…
Justin Engel retweeted
Sharing a new paper from the lab: How do ecDNAs segregate during cancer cell division?
ecDNA lacks a centromere and needs to attach to mitotic chromosomes to be distributed to daughter cells. The question is: HOW?
nature.com/articles/s41556-0…
-1/x
Justin Engel retweeted
ONLINE NOW in @Nature Cell Biology: ecDNA anchors to H3K27ac-marked active regions on chromosomes to survive normal mitotic cell division and persist into the next generation of daughter cells. Read more about the latest #relentlessdiscovery from CRI's Wu Lab ⬇️ cri.utsw.edu/mechanisms-for-…
@yipengxie_utsw, @YoonKimUTSW & @SihanSean
Justin Engel retweeted
Excited to share our latest paper, out today @CellCellPress. We found that large pieces of the human genome can transfer between cells upon direct contact, endowing recipient cells with heritable phenotypic changes. (1/7)
cell.com/cell/fulltext/S0092…
Justin Engel retweeted
Now online! Disrupted molecular glue complex drives RAS inhibitor resistance dlvr.it/TSPW45
Justin Engel retweeted
"In this study, we present a genome-scale map of genetic interactions in the human haploid cell line HAP1, based on CRISPR-based perturbation of ∼4 million gene pairs. The resulting network comprises ∼89,000 high-confidence gene-gene interactions"
doi.org/10.1016/j.cell.2026.…
Justin Engel retweeted
Just published with the #AACR26 New Drugs on the Horizon session: TNG961 Is a Selective Oral HBS1L Molecular Glue Degrader for the Treatment of FOCAD-Deleted Cancers - by Hilary Nicholson and colleagues aacrjournals.org/cancerdisco…
Justin Engel retweeted
What if a small molecule could activate a transcription factor program in one cell type and destroy the same pathway in another? In our new preprint, we describe one such story on bifunctional molecules that toggle between transactivation and repression.
In a phase 1 study of the oral p53 reactivator rezatapopt in heavily pretreated patients with TP53 Y220C–mutated solid tumors, the most common adverse events were nausea and vomiting, and the overall response was 20%. Full PYNNACLE study results: nej.md/3OIQC5P
Science behind the Study: Restoring Function to a Variant of p53 in Solid Tumors nej.md/3N0pQW8

ALT Panel A: A figure showing the change in the sum of diameters of the target lesions across tumor types. Panel B: A figure showing the overall duration of treatment and the time to first response observed in 46 patients treated with a dose in the observed efficacious-dose range who had wild-type KRAS.
Justin Engel retweeted
You can read more about the initial discovery and preclinical characterization of rezatapopt and the first examples of acquired on-target secondary p53 mutations in patients treated with rezatapopt in @CD_AACR:
doi.org/10.1158/2159-8290.CD…
doi.org/10.1158/2159-8290.CD…
When a phase 1 trial is published in @NEJM, you can bet it will be impactful. Here, the p53 reactivator rezatapopt showed an ORR 20% among 77 pts with TP53 mutant (Y220C) advanced tumors. Are we getting closer to drug the most undruggable of all mutations? nejm.org/doi/full/10.1056/NE…
Justin Engel retweeted
Delighted to share new work from our lab: CRISPR fusion proteins to boost PRECISE genome editing (TruEditors).
We wondered what if we could “turn on” and test every gene in the human genome to accelerate protein design?
Justin Engel retweeted
New preprint on technologies to scale up CRISPR screens.
We use them to map 665,856 pairwise genetic perturbations and outline a path to comprehensive interaction mapping in human cells.
We also introduce an approach for cloning lentiviral libraries with billions of elements.
Devastated to hear the news. Rest in peace, Ethan. Former research technician @CRI_UTSW @UTSWMedCenter
We lost someone extraordinary
Ethan Neumann, a PhD candidate in my lab, worked tirelessly to study #fibrolamellar carcinoma, the cancer that would ultimately claim his life
On the day before he died he officially became Dr. Neumann:
myarchoan.wixsite.com/yarcho…
Justin Engel retweeted
📢Awesome talk alert! A reminder that @McclellandLab will be giving a Chromosomal Instability lecture tomorrow👇Zoom link:
cam-ac-uk.zoom.us/j/84115680…
Meeting ID: 841 1568 0528
Passcode: 491672
Don't miss it- Sarah's lab work is terrific! @markowetzlab @DKFZ @emblebi @CRUKCamCentre
Justin Engel retweeted
#ResearchHighlight
Published in @CellCellPress, @PeterLyLab (@UTSWMedCenter) conducted a genetic screen in which they identified the Fanconi anaemia pathway as a driver of chromothripsis, complex genomic rearrangements & ecDNA generation.
📖👉go.nature.com/4ehX6j9
Justin Engel retweeted
📢 Apply Now—We are excited to announce that we are now accepting applications for the @UTSWGradSchool Postbaccalaureate to Ph.D. Program (PB2PHD). To learn more about PB2PHD, the areas of research, eligibility criteria, and how to apply, scan the QR code in the flyer below ⬇️
Thanks for sharing our work! – at Dallas, TX
This Post is from an account that no longer exists. Learn more
Justin Engel retweeted
Cancer cells appear to hijack a genetic pathway involved in DNA repair to drive malignancy and overcome treatment, a new UTSW study shows. The findings explain how chromosomes in some tumors undergo massive rearrangements and could lead to new strategies to avoid cancer drug resistance. @PeterLyLab
bit.ly/4gkXxLV
Justin Engel retweeted
Thank you @CD_AACR for highlighting our work on chromothripsis! 🙏
Read Cancer Discovery's #ResearchWatch: The Fanconi Anemia Pathway Mediates Chromothripsis and Resistance to Cancer Therapy. bit.ly/4d350MW
Justin Engel retweeted
Grad students and postdocs!!
Please join us at the 2025 @GordonConf
GRS on Mammalian DNA Repair on Feb 1-2 with @LabLegube as our keynote speaker!
Talks selected from submitted abstracts
Register here: grc.org/mammalian-dna-repair…




































