Where’s the fish? lol

There are entire institutions that don’t count Scientific Reports papers in considerations for promotion/graduation. It’s widely seen in my field as a dumping ground for papers that can’t get accepted anywhere else.

That’s not to say that there’s no great papers in there. There are. Just on average not.

Scientific Reports is one if the lowest tiers of journals. That doesn’t mean that there isn’t good work that comes out in it, but on average the work is not highly impactful.

This illustrates the disconnect between science and mainstream: the articles that are exciting to researchers rarely make it to the mainstream, whereas less interesting work to researchers often make it to the press based on an exciting title.

And glass

Bivalent produces good neutralizing antibodies against xbb

https://www.nejm.org/doi/full/10.1056/NEJMc2214293

How did they control for community-associated dietary/exercise differences?

Seinfeld

I remember when Vinnie Testaverde (44) and Brett Favre (38) played a game in 2007 and they called it the senior bowl. Lol times have changed.

I was still defending Dave a little until that

Oh no. I remember her from Ed as Carol’s little sister. RIP.

By now we have hundreds of thousands of people’s full (whole genome) DNA sequences. Iceland alone has a project to sequence its population, for example. Many cancer sequencing projects sequence normal tissue as well.

Human DNA is so similar it’s enough to publish a few genomes and then simply annotate the differences (e.g. single nucleotide polymorphisms). All major genome webportals include these data.

They’re streets behind

Could be anything

While there are drugs that target epigenetic regulators (e.g. Ezh2 inhibitors), it’s not clear yet how the new data would take advantage of them (if they can at all). While some of these drugs have shown promise, all of them have some drawbacks because they affect so many genes, often leading to unwanted toxicities. But hopefully this type of new data may help refine when to use which epigenetic drugs in which combinations.

Even so, epigenetic drugs may not always be the best answer to epigenetic dysregulation in cancer cells - remains to be seen though.

Directly? Probably not much.

But indirectly, it can change the way other researchers approach their projects - by more carefully paying attention to epigenetic marks etc and changing the way they might model their hypotheses. It also has implications about the evolution of drug resistance, metastasis, and more. So I think this will help more researchers appreciate and incorporate non-genomic mechanisms in their thoughts - many already do, of course, but more would be better.

What’s novel is that the papers attribute cell-to-cell variation within a tumor to a larger degree of epigenetic regulation compared to genetic variation (i.e. mutations) than previously demonstrated. In other words, cells that look and behave different from each other within the same tumor are less so as a product of different mutations, than as a function of their epigenetic “plasticity” - suggesting more than previously shown that cells can readily change their phenotype without necessarily changing their genotype.

Which, some of us already thought so… but these papers use large datasets and brand new technology to measure it more finely than anyone has before.

It doesn’t look crushed to me