Dr. Omene MD, PhD

Neurologist → Neuro-oncologist | Prof @UAlberta | Neuroscience x Oncology x AI | Cancer metabolism • Clinical trials • Some pop culture & millenial nostalgia

[Dr. Omene MD, PhD @DoctorOmene]

https://t.co/M6AcRrEqCJ

[Dr. Omene MD, PhD @DoctorOmene]

The pod was amazing! I think it's wise to be cautious generally, agreed.
One thing that isn't intuitive to me is why VEGF gets the spotlight. There are several hallmarks of cancer and BPC-157 may positively augment many of them.

(Also does BPC-157 indiscriminately upregulate VEGF or is it angiomodulatory in a context dependent manner?)

We know VEGF isn't the entire story for targeting cancer. For example, bevacizumab, which blocks VEGF, has no survival benefit in GBM and a weak signal of worsening outcomes in some studies.

You could make the case that the local anti-inflammatory effect from BPC-157 should do more to prevent tumor growth than its VEGF effect would do to foster it. Etc.

From my imagination of the tumor microenvironment I think equipoise is the right stance on the topic versus abundance of caution.

That is - "we don't know, could be good or it could be bad we need to study it" vs. "we think it could be bad so be cautious"

[Aakash Gupta @aakashgupta]

This is what a brain looks like with no priors.

Your brain is a prediction machine. Every sensory input gets compared against an expected input built from prior experience. When reality matches your model, you feel nothing. When reality breaks your model, you feel wonder.

She's around two. Her model of the world is microscopic. A train is 200 tons of metal moving 50 mph through her field of view, and her brain has no template that fits. The prediction error is so large her face becomes the prediction error.

This is Karl Friston's free energy principle in real time. The brain minimizes surprise by updating its model. Children update constantly because almost everything is new. Adults update almost never because almost everything matches a prior.

That's why adults can stand next to the same train and feel nothing. Their model already contains it. The signal gets predicted away before it reaches conscious awareness.

The wonder window narrows as priors fill in. After that, you have to manufacture novelty. She still gets it for free.

You used to react to everything this way. Then your brain finished its training run.

[Dr. Omene MD, PhD @DoctorOmene]

@MichaelRedd_ 🎯🎯🎯

[Dr. Omene MD, PhD @DoctorOmene]

@EricTopol @NatureCancer This is promising. However, up to 60% of cells in the GBM TME are immunosuppressive myeloid cells, mostly macrophages. Amplifying T-cell response against this brick wall isn't going to cut it. That's why the median survival data is barely better than standard of care.

[Dr. Omene MD, PhD @DoctorOmene]

@tomhaberstroh @YahooSports How could Cleveland 2 have only 50.5% probability. Something is broken in the model sir.

[CopyRebeldia @CopyRebeldia]

La biología en PDF acaba de morir.

Un tío hizo una app donde exploras estructuras 3D como un videojuego.

UI: GPT Images 2. Código: Gemini 3.1 Pro.

Los libros de texto ya no sirven.

[All day Astronomy @forallcurious]

🚨: Neuroscience considers metacognition the highest form of intelligence..... "the ability to think about your own thinking."

[Dr. Omene MD, PhD @DoctorOmene]

@YannickBuccella Wait you are reporting on this but not on the vitamin C study? Or did I miss it?

[Dr. Omene MD, PhD @DoctorOmene]

@bobvarkey CAR-T likely unwise in GBM:

https://t.co/oGILYfa1ls

[Dr. Omene MD, PhD @DoctorOmene]

https://t.co/CGy1WCo0LD

[Dr. Omene MD, PhD @DoctorOmene]

@AlexanderMWolf7 @Outdoctrination It's a logical consequence of the mechanism. The link between AGE and aging is in the literature. On what grounds do you think they don't contribute to aging?

You are basically claiming "absence of evidence" but no affirmative mechanism. Also, evidence isn't absent.

[Dr. Omene MD, PhD @DoctorOmene]

@AlexanderMWolf7 @Outdoctrination Yes we see the water makes the steel rust but we have no idea whether or not it causes wear and tear 😂😂

[Dr. Omene MD, PhD @DoctorOmene]

@5_utr @RWJE_BA LOL

[Dr. Omene MD, PhD @DoctorOmene]

Yes but not both at once and not multi-agent across transporters and receptors. Glutamine blockade by itself will fail. Glucose blockade by itself will fail.

I am aware of all the DON pro-drugs and some glycolytic drugs. The DON pro-drugs limit toxicity though I'd argue the GI toxicity from DON isn't terrible compared to chemo.

Also there seems to be little attention paid to ketosis mitigating toxicity.

[Dr. Omene MD, PhD @DoctorOmene]

@teamoncology I don't see any coherent story here other than different sets of mutations for different clones. What was your takeaway?

[Dr. Omene MD, PhD @DoctorOmene]

@AlexanderMWolf7 @Outdoctrination If you look at how AGEs work its a problem of radicals ultimately.

[Dr. Omene MD, PhD @DoctorOmene]

@AlexanderMWolf7 @Outdoctrination Cell proliferation in and of itself would not drive aging. Byproducts of proliferative metabolism would. There's no free lunch. Consider that glucose is a primary proliferative substrate then consider AGEs. I still suspect that net excess electrons are going to be the driver.

[Dr. Omene MD, PhD @DoctorOmene]

Precisely. In a general sense, halting the proliferation of a tumor isn't the same as getting rid of the tumor.

However, if you stop growth clinically you have "stable disease". This is a worthy goal and should be achievable by blocking proliferative biosynthesis. That means blocking glucose and glutamine.

The next step is getting rid of the tumor entirely. Surgery does a great job. Radiation is not bad. Cytotoxic chemo is ok. I would prefer to use cytotoxic T cells.

It just so happens that blocking glucose an glutamine metabolism might allow T-cells to breakthrough in the tumor microenvironment.

[MF DOOM Insider @mfd00mbr]

May the 4th