alt Hacker NewsSorry, as someone in this field, this is bullshit. It is in mice.
Several things trigger my bullshit meter. Quote:
"This dramatically surpasses the therapeutic efficacy of current standard treatments, including immune checkpoint inhibitors (anti-PD-L1 antibody) and liposomal doxorubicin (chemotherapy agents)"
PD-L1 monoclonal antibodies are only effective against cancers that are, you guessed it, PD-L1 positive. At high percentages, ranging from 1 to 50%. Are these authors even familiar with the state of the art when it comes to cancer medications? Mouse tumors do not equate to people tumors. Many tumor types are not PD-l1 positive.
Doxy is an ancient SOC chemo.
This is a nothing burger.
Give me phase II/III clinical trials, and then let me know what their PFS/OS was after 5 years. and what the medians were at 3- and 5-years. Also, ORR and CR and needed.
CAR-T is ahead of the game, and will be the ultimate winner here as it grows to scale.
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Seems like a very interesting approach, even if it’s early stage.
> Many tumor types are not PD-l1 positive. > Doxy is an ancient SOC chemo. This is a nothing burger.
Meh the research didn’t say those were state of the art, but that they were “common” treatments. In other words a baseline for a presumably cheap and well studied animal surrogate.
> CAR-T is ahead of the game, and will be the ultimate winner here as it grows to scale.
Last I read up on it last year CAR-T treatments struggled with solid mass tumors.
Many cancers don’t have unique proteins for CAR-T to target (similar to the pd-l1 issue).
Then CAR-T struggles getting the modified T cells into the solid mass tumors en masse. Interestingly this approach actually makes use of the tumor environment rather than be hindered by it.
> Sorry, as someone in this field, this is bullshit. It is in mice.
Nice to hear an expert opinion. Let's hope your comment goes back to black. I have a lot of question!
> This is a nothing burger.
Is it enough for a bread-mayo-bread sandwich? Lettuce?
IIUC the bacteria makes the cancer disappear for two weeks, until they end the study and kill the mice. (IIUC this is timeline is usual for very early studies.) They tried other bacterias and one of them made the cancer disappear for a few days, so I'm worried about the long time efficiency of this method.
Is injecting the bacterias a second time as efficient as the first time, or the inmune system kills the bacteria before they hurt the cancer?
What happen in case of metastasis? Each one must be injected with the bacterias or they will jump and make all of them disappear?
Does the bacteria infect other organs and kill you? Is there a good antibiotic in case the bacteria cause problems?
They used cancers that were 200mm3 (i.e. like a sphere of 7mm = 1/4 inch). What happens in bigger cancers? Does bigger cancer have better irrigation and make it more difficult for the bacteria to survive? What happens to tiny hidden metastasis (that probably still have good enough irrigation)?
In my dad’s case- he had gastric melonama. We surgically removed it and as consolidation We administered pd-L1 Immune checkpoint inhibitor. Melonama recurred again in 6 months time. This time in esophagus.
As an engineer I think all drugs tested and efficacies studied are on statistically not so significant data points. Given the permutations and combinations far exceed the clinical trials available and hence everything post clinical trial is also just an extended trial.
Wonder How to fix this? I am assuming heLa cells etc are also not the right test setup to have better test results.