this post was submitted on 01 Jul 2026
105 points (97.3% liked)

Technology

85870 readers
4311 users here now

This is a most excellent place for technology news and articles.


Our Rules


  1. Follow the lemmy.world rules.
  2. Only tech related news or articles.
  3. Be excellent to each other!
  4. Mod approved content bots can post up to 10 articles per day.
  5. Threads asking for personal tech support may be deleted.
  6. Politics threads may be removed.
  7. No memes allowed as posts, OK to post as comments.
  8. Only approved bots from the list below, this includes using AI responses and summaries. To ask if your bot can be added please contact a mod.
  9. Check for duplicates before posting, duplicates may be removed
  10. Accounts 7 days and younger will have their posts automatically removed.

Approved Bots


founded 3 years ago
MODERATORS
top 6 comments
sorted by: hot top controversial new old
[–] abbadon420@sh.itjust.works 26 points 19 hours ago (3 children)

Tldr: The anticancer effects of PCAIs in pancreatic cancer cells involve MAPK and PI3K/AKT pathways hyperactivation

[–] rain_enjoyer@sopuli.xyz 11 points 19 hours ago

just give your cancer cancer ez gg

[–] PostProcess@lemmy.world 8 points 19 hours ago

AHH that old chestnut...

[–] heydo@lemmy.world 5 points 19 hours ago (1 children)

I need a THDU on that one...

Too hard, didn't understand.

[–] rain_enjoyer@sopuli.xyz 11 points 17 hours ago (1 children)

cells have different enzymes, enzymes do different things, to keep everything in order you need some way to control these enzymes. there are many, many ways in nature to do this, but the one relevant here is that some enzymes have tyrosine residue sticking out in a specific way. when phosphate is attached to them, extra charge appears, which can bend enzyme out of or into shape, switching it on or off or changing something about the way it works.

the job of flipping these switches belongs to tyrosine kinases, and in many cancers something is wrong about these. the ones relevant here are from RAS/MAPK pathway and PI3K/AKT/mTOR pathway, and these are involved in many things, but among them is cell growth and division. blocking one or other tyrosine kinase from working is something that many of anticancer drugs do, and it works pretty well, because overactive (for whatever reason) or mutated tyrosine kinase is often present. in many cancer cells, if for some reason MAPK is made to be more active, cancer cells might grow faster.

now the thing is, there is something peculiar about the specific way in which RAS/MAPK cascade is broken in that cancer type, that when it's cranked up cells stop spreading and break apart. this is something that this new drug seems to be doing (through a couple of layers of other enzymes), and it's weird, and unexpected, and in no way you'd get funding for that, but it works apparently

[–] heydo@lemmy.world 1 points 1 hour ago

That's a damn good explanation, thanks!