Pillar 1 - FTO (new thread), page-1390

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03/08/21

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Post #: 54977363
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Originally posted by Mason14: ↑

I think it is a little more complex than that, @LongTony.

My understanding is that the expression levels of FTO in a cancer cell is relative to a control or healthy cell. If the expression of FTO is greater in the cancerous tissue relative to the healthy tissue, then it is deemed 'FTO overexpressing' and vice versa. If you take a tumor sample but have no healthy sample to compare it to, how would you know that the cancerous cell has upregulated FTO expression? Is there a standardised expression level of FTO in normal human breast tissue? I don't know - probably not given intra-individual variance. I think it becomes even more challenging when we begin to consider the dynamic interaction between erasers (FTO & ALKBH5) and writers (METTL3/METTL14, for example) or even readers, and how they influence intracellular mRNA methylation and demethylation.

This is where I believe something like a senstivity assay could be a better alternative. Irrespective of FTO expression status or the complexities of intracellular methylation/demethylation, you could get very clear indication of whether inhibiting FTO influences cellular function for a given cancer sample. If the cancer is sensitive to Bisantrene, we could see a reduction in any of the common traits of cancer (upregulated growth, proliferation etc) which may then be an indication that the patient may benefit from a course of Bisantrene. Given the role of FTO in metastasis and therapy resistance, I suspect that patients with advanced cancers and/or resistant to therapy would be a good place to start.

There are three known MoAs @IndexInvestor

Telomerase inhibition: IC50 3.8 uM (1)

1 https://pubmed.ncbi.nlm.nih.gov/20206144/

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Isn't telomerase inhibition a property of all anthracyclines?

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