General / Off-Topic A way to fix Cancers?

[Robin of Spiritwood]

Hello everyone. I've stumbled upon something.

A large number of cancers happen when a gene stops working. This gene is BRCA1.
If we could get it to work again, we might be able to help out the people with cancers related to the dysfunction.

*Angelina Jolie is a person with a BRCA1 mutation, leading her to do pre-emptive surgeries. Unfortunately, this below is insufficient to address that problem, but might work in people with a normal BRCA1 gene.

Spoiler: Simplified pathway

Basically, if the gene isn't mutated or damaged, but just switched off, we can switch it on again, for pennies.

The body has a built in feedback system that gave me the clue. For some reason, switched off BRCA1 switches ON NNMT, another gene, which helps get rid of excess vitamin B3.
This makes no sense at first reading. Why would the body do that??

Spoiler: NNMT is kind of an important thing

NNMT as a gene is found in animals from worms to humans. 85% of the gene code is preserved between various species. Nature does NOT do things like that without a very Good Reason.

Well the answer is in the processes.

If you go about chowing down on tons of animal protein, you'll take in loads of branched chain amino acids. One of those is Methionine.
Loads of Methionine will churn the Methionine-Homocysteine cycle shown above.
That cycle tries to stick methyl groups onto other substances, such as the histone proteins that turn genes on and off.

Ok. If the BRCA1 gene gets switched off because the histone on its promoter region is methylated by the cycle, we go on to developing some cancers. But the body tries to fix it by activating NNMT gene, using surplus vitamin B3 to mop up the methyl groups.

In other words, if we supply enough vitamin B3, we can stop the whole process. Vitamin B3 is nicotinamide. Take enough, and there won't be surplus methyl groups to spoil the BRCA1 gene from working. Methylating nicotinamide is a one-way process, causing methyl groups to be lost.

Is this hypothesis correct? If so, giving Vitamin B3 would stop cancers.

Nicotinamide in the prevention of breast cancer recurrences? - PMC

www.ncbi.nlm.nih.gov

a recent phase III clinical trial investigating the effects of nicotinamide (vitamin B3, the physiological inhibitor of SIRT1) in non-melanoma skin cancer demonstrated the ability of this vitamin to reduce the rates of new tumorigenic events in high-risk patients

The Role of Nicotinamide in Cancer Chemoprevention and Therapy - PMC

Nicotinamide (NAM) is a water-soluble form of Vitamin B3 (niacin) and a precursor of nicotinamide-adenine dinucleotide (NAD+) which regulates cellular energy metabolism. Except for its role in the production of adenosine triphosphate (ATP), NAD+ ...

www.ncbi.nlm.nih.gov

In animal studies, nicotinamide suppresses cancers in:

• Bladder
• Lung
• Liver
• Kidney

as well as Leukaemias.

As a corollary, we can ask the other obvious question. What happens if we restrict the methionine?

Methionine restricted (MR) diets have been shown to slow tumor growth in late stage cancer patients1, 2. More recently it has been shown that methionine restriction helps weight loss in obese animals and humans

I know why the obesity is going on too.

 

[Patrick_68000]

It seems that in the future, Messenger RNA technology will reduce significantly all the cancers.

 

[Robin of Spiritwood]

The methylation of cancer suppressing genes is much bigger a problem than it seems.
There are at least 20 of them that can get switched off by the same chemistry.

And all of them would benefit from supplying enough nicotinamide to run the NNMT enzyme that gets upregulated in a number of cancers.

Egs: p53, p16, Nrf1, Nrf2, VHL, APC, CADM2...

Mutation of p53 and its dysfunction is needed in about half of the cancers in solid tumors for them to grow. What's happening in the other half? Is p53 just being downregulated because the promoter got methylated? Likely so. What would happen if we switched that back to normal?

Here is a bit more too. We need Vitamin B3 as raw material to make NAD+ . That gets used by PARP enzyme systems to fix DNA breaks. Supplying it seems a logical thing to do to inhibit cancer.

Going by published trials: NAM is NicotinAMide.
"Accumulating evidence suggests that NAM plays a role in cancer prevention and therapy. Phase III clinical trials have confirmed its clinical efficacy for non-melanoma skin cancer chemoprevention or as an adjunct to radiotherapy against head and neck, laryngeal, and urinary bladder cancers. Evidence for other cancers has mostly been collected through preclinical research and, in its majority, is not yet evidence-based. NAM has potential as a safe, well-tolerated, and cost-effective agent to be used in cancer chemoprevention and therapy. However, more preclinical studies and clinical trials are needed to fully unravel its value."

... it seems nobody has published this mechanism of action.

I had this ad site pushed at me today:

For Authors & Referees | British Journal of Cancer

For Authors & Referees

www.nature.com

Asking for papers on cancer.
Looks like the algorithm found the OP.