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Jason Sheltzer Profile picture
@JSheltzer
May 25, 2016 • 4 tweets • 1 min read • Read on X
tfw when you can't remember which of the students youre harassing "caused" your heart attack huffingtonpost.com/entry/thomas-p… Image
He claims that student 1's investigation caused his heart attack, while student 2 (that he had an affair with) says that he claimed that...

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More from @JSheltzer

Jason Sheltzer Profile picture
Jul 6, 2023
Check out our new study in @ScienceMagazine, where we take on a 100-year-old debate: what’s the role of aneuploidy in cancer?

We discovered that genetically removing extra chromosomes blocks cancer growth - a phenomenon we call “aneuploidy addiction”. science.org/doi/10.1126/sc…
In the 19th century, pathologists observing cancer cells under a microscope noticed that they frequently underwent weird mitoses. The chromosome bodies visible in these cells were not equally divided between daughter nuclei - in other words, they were aneuploid. Image
Early pathologists like Theodor Boveri proposed that it was this aneuploidy that actually caused cancer. But, there was no way to test it. Eventually, this theory fell out of favor - researchers discovered oncogenes and showed the impact that point mutations could have in cancer.
Read 16 tweets
Jason Sheltzer Profile picture
Jan 10, 2023
Very excited to share a new paper from my lab: using a set chromosome-engineering tools, we show that cancers are “addicted” to aneuploidy. If you genetically eliminate single aneuploid chromosomes, cancer cells totally lose their malignant potential!
biorxiv.org/content/10.110…
To back up, for many years researchers have used the standard tools of molecular genetics to learn about the function of individual oncogenes and tumor suppressors. We can easily over-express, mutate, or knockout genes like KRAS and TP53 to study their biology.
Chromosome gain events are exceptionally common in cancer, but the genetic tools that allow us to manipulate individual genes don’t work for these chromosome-scale copy number changes. You can’t package a whole chromosome in a lentivirus to over-express it.
Read 13 tweets
Jason Sheltzer Profile picture
Nov 28, 2022
If you choose to transfer a manuscript between Nature-family journals, you can consult a web page that lists the acceptance rates for 124 journals published by the Springer Nature Group.

I haven’t seen this data circulated before, so I copied it to share here:
According to this data, "Nature" is not actually the most selective journal. Nature Med, Cancer, and Human Behavior all have lower acceptance rates.
This could be Simpson’s paradox. Maybe a cancer paper has a 2% acceptance rate at Nature and a 4% acceptance rate at Nature Cancer, but Nature also loves to accept ML papers, which increases the overall acceptance rate?
Read 6 tweets
Jason Sheltzer Profile picture
Nov 1, 2022
Interesting new paper with an important message - normal clone-to-clone variability is an important confounder in CRISPR experiments.

nature.com/articles/s4159…
Westermann and colleagues were studying a gene believed to regulate YAP1 expression. They made two CRISPR knockout clones in the gene. Unexpectedly, they found that one KO clone upregulated YAP1 while one downregulated YAP1! Image
They then proceeded to assess YAP1 expression across a panel of wild-type clones that were not modified with CRISPR, and they saw similar variability. Image
Read 10 tweets
Jason Sheltzer Profile picture
Oct 17, 2022
New from my lab: we show that a clinical-stage oncology drug from Eli Lilly is mischaracterized, and its true anti-cancer target is EGFR. We also show how in vitro drug assays can be misleading - cellular+genetic methods are needed to determine drug MOAs.
biorxiv.org/content/10.110…
Ralimetinib (LY2228820) was developed by Eli Lilly as a p38a inhibitor. Thus far, it has performed poorly in clinical trials, with basically no tumor regressions attributed to its effects:
We used CRISPR to delete MAPK14, the gene that encodes p38a, and we found that ralimetinib still kills p38a-knockout cancer cells. This demonstrates that ralimetinib’s anti-cancer effects result from some other cellular target.
Read 13 tweets
Jason Sheltzer Profile picture
Mar 29, 2022
Out now from @joans and me - (nearly) everything you know about survival analysis in cancer is wrong.

cell.com/cell-reports/f… Image
We conducted a comprehensive analysis of genetic, epigenetic, and transcriptional features linked with patient outcomes across 10,000 patients and 32 cancer types.

A web portal for exploring this resource is here: tcga-survival.com Image
Why the clickbaity headline? It’s extremely common to infer the functional importance of genetic alterations based on cancer survival data. For instance, showing that a “cancer driver” is associated with patient death.
Read 10 tweets

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