Reduction in cancer incidence associated with IGF-1/insulin signaling knockdown in C. elegans does not depend on FoxO3, unlike lifespan extension.

“and here's the thing about that data and this is what I think if you get rid of another gene that's homologous to fall so - Oh deaf sixteen is right that's too far completely obliterates the lifespan extension meaning it's the Fox o3 that seems to be really important for we have how many we have for foxes yeah you mean different fox genes okay yeah I don't know exactly how many but the Fox oh we have three we have one two and four was it one two and there was our one two four or five but but their analog is sixteen I remember that right there daf-16 is basically our Fox Oh Fox oh yeah so okay well anyways yeah I'm not sure I'm getting confused with you know this but what is interesting is that the lifespan extension was completely like ameliorated”

“the cancer reduction didn't depend on Fox or 3 only the lifespan extension”

“and daf ii ended up being the analog of the igf receptor and i think daf 16 was basically an analog of fox03a or 3b i can't recall yeah it wasn't quite the receptor it was the thing that the receptor turned on but it's one one step downstream one step downstream inside yeah”

“if you knocked out that Gene you could double the lifespan from roughly two weeks to four weeks or four weeks to eight weeks I forget what it was of uh C elegans this worm”

“when some very seminal and interesting work was published looking at the daf 16 mutation in or maybe it was daf2 I can't remember if it was daf2 first or daf 16 but it was the analog of the igf receptor and if you knocked out that Gene you could double the lifespan from roughly two weeks to four weeks or four weeks to eight weeks I forget what it was of uh C elegans this worm”