You’re assuming that the scientists have figured out why this happens, rather than just that it happens.

There’s plenty of science out there which consists of “oh, hey, look what I just noticed!“ And is just a lot of watching something happen without any explanation for it. That’s why scientists will continue to study this phenomenon until they figure it out. Probably the company that is sponsoring them can profit from it in some way.

From the research paper (behind the paywall) it appears they only tested cancer cells, shown below, and on mouse models. It’s been awhile since I’ve studied this, so I don’t know if the proteins involved are specific to cancer cells or not. If not I’d assume it would kill all cells. With the mouse models I assume they injected directly into the tumor for targeted treatment, but I didn’t dive into it that deep.

Paper link: faseb.onlinelibrary.wiley.com/…/fj.202500412R?sam…

2.2 Cell Culture

Human monocyte-like THP-1 leukemia cells (THP-1, THP-1Asc-KO, THP-1Gsdmd-KO, THP-1-Null, THP-1-defCasp1, and THP-1-defNLRP3) [4, 21] were provided by Professor Li Sun’s lab (Institute of Oceanology, Chinese Academy of Sciences, Qingdao, China), and human liver cancer Huh7.5 cells were maintained in our lab. THP-1 cells and Huh7.5 cells were cultured in RPMI 1640 medium with 10% FBS, 100 U/mL penicillin, and 100 μg/mL streptomycin at 37°C in a 5% CO2 humidified incubator. All experiments were carried out with the same batch of cell lines between passages 2 and 8.

2.15 Xenograft Tumor Mouse Model

BALB/C nu-nu male mice, 4 weeks old, were obtained from Beijing Vital River Laboratory Animal Technology Co. Ltd. (Beijing, China). A total of 3 × 106 Huh7.5 cells were subcutaneously injected into the right fore flank of each nude mouse. The daily drug treatment began when the tumor size reached ~100 mm3 and continued for a further 2 weeks as follows: EPS3.9 (30 and 60 mg kg−1 d−1, intraperitoneal injection) dissolved in assisted solvent (PBS); Control groups were given the same volume of PBS. Body weight and tumor volumes were measured every day with a balance or with a vernier caliper. The tumor volume was calculated with the formula: 1/2 × [length × (width)2]. After treatment for 2 weeks, mice were sacrificed by decapitation and tumor tissues were collected for further analysis.

Pyroptosis is a fiery form of programmed cell death that helps the body fight infections and disease. Unlike regular cell death (apoptosis), pyroptosis is dramatic and explosive—cells swell, burst open, and release inflammatory signals that alert the immune system.

Originally discovered as a defense against bacteria and viruses, pyroptosis has recently become a hot topic in cancer research. That’s because triggering pyroptosis in tumor cells can not only destroy them directly but also rally the immune system to join the attack, essentially turning the tumor into a signal flare for immune response.

Maybe it’s something to do with this.

I imagine a lot of what we know now was learned after we realized the benefits of things. I’d give it a few years/decades for researchers to spend time to analyze the data and figure it out.

In the meantime, fuck cancer and hell yes to this deep sea sugar stuff!

It’s possible they haven’t discovered why yet.
So far, I’ve found two things.

• The pyroptosis pathway triggered is the typical one (lots of Caspase-1 proteins get assembled into a giant inflammosome complex and attack Gasdermin D, which then starts poking holes in the cell membrane).
• The EPS3.9 molecule has a high affinity for a five separate membrane lipids.

But without any formal biochemistry training, I am missing a lot of prerequisite knowledge.

Is that high affinity above normal? Does it need to bind all five to enter the cell, or just any of them? Are those lipids, or that combination of lipids, exclusive to tumor cells? I have no info on any of these questions.

It’s also entirely possible that it’s attacking healthy liver cells too, just at a reduced rate due to cancer cells being resource hogs.

It’s discussed elsewhere here, but to answer directly - as I understand it, cancer cells can only use energy from sugars. Cancer cells are also extremely energy hungry, since they spend so much energy growing. When a cell absorbs these particular sugars, it self-destructs in spectacular fashion.

It sounds like they’re expecting cancer cells to absorb the vast majority of these sugars, leaving just a few for healthy cells. Which sounds to me like a kind of chemotherapy, but more effective and with weaker side effects.

(Not a biologist, most of this is over my head!)

I was wading in here to post exactly that XKCD.

We discover hundreds of new compounds that kill cancer cells every year. Perhaps we should only be posting in uplifting news when new drugs are found effective.

You’re thinking too small. If we cure cancer, everyone can start smoking again. Asbestos is back in business. There are hundreds of industries that would take off immediately. W

The company that would truly suffer is the one that makes those little stickers in California.

Even if so… If this is as effective and safe as it seems then it will get leaked to the public or reversed engineered and then made public. The original paper’s abstract says “this active exopolysaccharide is ubiquitous among the genus Spongiibacter” which means it’s accessible.

The repression of such a boon could not last long. History has proven the human spirit is nothing if not irrepressible. There are plenty of people capable and motivated enough to run what little information we already have all the way to a consistent home manufacturing solution. Its publication and distribution is another game entirely but I’d bet on the public there as well.

Take a look at the Four Thieves Vinegar Collective for some tangible encouragement. Knowledge is power. Together we can be powerful enough to create what we need to survive. Government buy-in encouraged but optional.

Cancer cells often times lose their ability to perform oxidative phosphorylation. This means they can only rely on glycolysis as a sole source of ATP… This makes them EXCESSIVELY glucose hungry.

It’s called the warburg effect. I’d have to read up on it and brush up on biochem, but that’s the basic principle.

Essentially, cancer should soak up all the harmful sugar before it hits normal cells. This makes it even safer in theory than traditional chemo like methotrexate and such

Because they try to absorb extra sugars in many cases.

I have absolutely no medical knowledge besides a first aid course. Does that mean that, by not eating any sugars, I could starve cancer cells? So like during keto (I did that years ago before the boom) I actually could have starved a lot of cancer cells?