I was browsing Twitter while deciding if I’d get out of bed or not and ended up re-reading the 2020 Prof. Chen COH paper in which CS1 & CS2 were identified as the most efficient in suppressing FTO where FTO was present out of 260,000 compounds (2).
Why? I had a targeted twitter ad from Novartis about HR-MDS & AML (1)
https://twitter.com/tim3target/status/1428025611587571717?s=21
The articles within this link has some interesting reading for the AML thread and a comparison with what Novataris BP currently have to work with for AML patients. Leaving here as a lot of the FTO discussion has stemmed from the AML studies.
1. NOVATARIS direct LINK - Tim-3 (this is mostly AML, getting to the FTO on topic bit below)
https://www.tim3.com/hr-mds-aml-disease-complexity
2. COH Chen - Targeting FTO suppresses cancer stem cell maintenance and evasion.
https://www.sciencedirect.com/science/article/pii/S1535610820302166
There was a particular phrase that stood out to me, “(I) Confirming FTOH231A/E234A mutation via Sanger sequencing.” (3) partially as I’ve been craving a beachside sausage sanger, partially as measuring FTO levels in candidates, even in future the population would be of immense interest in preventative medicine if you know what you are more likely to suffer from because of DNA and more effective targeted treatment.
While Sanger sequencing probably isn’t the way and I haven’t read a lot about it, it brought up the question again, “How do we measure potential for FTO in candidates?”
@RaceOncology what is the main challenge when it comes to measuring the genomics for FTO in people?
Simplified, how does Nucleics DNA sequencing compliment any of FTO measurements?
I'm sure that I have probable made a dog's breakfast of quite a lot within this one post, as started in bed half asleep on iPhone, then had to move to Mac later as HotCopper doesn't like copy n paste at all. How is FTO checked in cancer patients like the way blood glucose is checked in diabetics? Alright, time for coffee, moka pot strength needed today.
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