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I’ll try. It will help if I have insomnia tonight, because that’s when I can review things.
A decision could come sooner than those dates, for reasons I’ve previously listed; but if so, it would be thanks to all the preparation and improvements made on both sides.
Where have you been hearing about a leukapheresis center shortage?
It’s also four business days since the new board member announcement.
Now
BEST BID
0.645 x 9000
BEST ASK
0.6466 x 1600
March 18: First India DCVax-Direct patent grant.
March 21: Citizen and undergraduate from India (with American graduate degrees) is announced as new NWBO board member. Venture Capitalist.
March 27: Second India DCVax-Direct patent grant.
No news is good news at this point, imo. The conservative guess is that we are now also 80 days (or more) from a possible or likely January 4 (or earlier) validation date.
Thanks. My very humble thought is that most traders notice today marks four business days from/after a possible chm meeting on March 21 and tomorrow marks four days from the second meeting day of March 22, and we haven’t received a negative PR thus far and perhaps it is getting more likely we will not receive one during this process.
Could you provide that double pennant chart again with this morning’s data included?
Question. Now that we have two patents for DCVax-Direct in India that go out to 2036, and knowing that India already allows Intratumoral dendritic therapy (albeit an arguably substantially inferior product), while also knowing DCVax-Direct is incredibly safe, and knowing DCVax-Direct had a strong phase 1 survival record in treating inoperable tumors, and knowing these patents are for treating inoperable advanced cancers, plus understanding these people are in emergency situations, while also understanding most of the world would be obliged to using real world data studies, is it possible there is an accelerated pathway for DCVax-Direct in India?
So if you look at what the car-t people did (which didn’t help survival but gave transitory (very temporary tumor regression) response.
they
1. Initially experimented with car-t to target egfrviii. The question is why? There are so many ways to do this cheaper, and either way, it doesn’t help survival.
2. Next, they tried to improve it by still targeting egfrviii, but also targeted normal cells that have normal egfr wildtype. At least we know why they used car-t for this part. It’s because the human immune system would not allow it, nor would DCVax-l, because our immune systems are evolutionarily designed not to attack normal cells. Car-t is useful only if it attacks what our body would not attack — if necessary. The trick is, what will it do to all the normal cells in the body, will it actually help stop the cancer, and what durability.
Let’s skip safety considerations for now. What we do know is normal egfr wildtype cells do not promote insane tumor growth like the variant egfrviii. We know that even getting rid of egfrviii and egfr wildtype, provides no durability as a monotherapy.
It’s therefore incredibly expensive as an adjuvant, but they could make it less expensive by simply targeting egfr wildtype (normal cells) and then run a trial to see if it could help DCVax-l. I sorta doubt it would help, but DCVax-l doesn’t attack normal cells, and since GBM has “normal” egfr often expressed as well as mutated, it might help DCVax-l do something it couldn't otherwise do.
However, again I haven't even gone into safety considerations, cost, and finally what Dr. Prins tried to teach the public a while back.
That is, it’s not the silver bullet antigen you must target when fighting heterogeneous solid tumor cancer, it is a quantitative solution. In other words, you must get all or as many cancer antigens as you can, because what we’ve learned from the hallmarks of cancer is that once it rears its ugly head, it has already developed many ways to duck a suppressed immune system.
Or as Senti might put it, you don’t take a rifle to a machine gun fight.
Finally, just a response to your stem cell point, and that is, yeah, sometimes what I analogize as dormant seeds that flower again once whatever therapy is gone, and certainly, that’s a problem, but with a vigilant and broad spectrum trained by DCVax-l, you have generational memory that recognizes those cancer cells when the seeds bud out. And because DCVax-l is not toxic, you can also indefinitely boost that memory with guardian vaccinations.
LearningCurve, I want to qualify my previous response. DCVax-l should/would target EGFRviii if it is present in the tumor cell.
However, car-t that target egfr wildtype are targeting normal cells with normal antigens, so I don’t believe DCVax-l would target them. They are important for normal cell function throughout the body.
Car-t isn’t necessary to target the former EGFRviii, (see first paragraph), imo. There are many less expensive ways.
Since the results of only targeting these two antigens provides very temporary results, the experimental therapy is useless as a monotherapy. Imo. Moreover, added chemo will reduce immune system response, and will not tackle the issue of tumor escape.
Do you suffer from amnesia? If you’re not certain, look at the note in your shirt pocket.
I would say yes, if the tumor has it, but your question is very specific, so you’d need to ask someone like Dr. Bosch.
No, DCVax-l was intentionally constructed to
work within the natural framework of the immune system, and as used in the DCVax-l trial, it stops progression and kills the remaining tumor cells. That’s why stabilization signifies response. DCVax-l targets hundreds of antigens to reduce the likelihood of tumor escape.
Car-T, even when used with chemo, aggressively ‘blows apart’ tumors which spread nonresponding cancer cells throughout the body, and because it only targets one or two antigens, easily allows the cancer cells to escape. That’s why partial or complete tumor response (transient) deceives the patient and apparently the researchers.
DCVax-l target hundreds of different antigens, whereas that Car-T therapy, as shown in the quote below, only targets two. That is why Car-T is “transient.” Tumor escape. The Car-T cynical response is to say oh well, let’s just add chemo now. So essentially, the Car-T spreads the cancer cells with non-responding antigens. The cynical approach of just divvying up antigens for various companies to make money without curing the problem is the problem.
Perhaps as little as a week or two after defendant’s reply due June 14. Maybe more, but not much, imo. Hopefully the magistrate will deny any requests for oral arguments this time.
Hey dufus, you thought he wasn’t independent if he owned shares before becoming a director. Once corrected on that, you ask another answerable question. Hint, look in next quarterly and/or proxy statement.
See post 681160.
Quit threatening learning curve.
ChatGPT:
Thank you.
You are, you are the dufus that made/makes a big deal out of Dr. Malik having sold a Smidgeon of his shares in 2023 to pay his taxes.
Aren’t you the dufus that made a big deal regarding Dr. Malik selling a smidgeon of his shares to pay his taxes?
Would it take another 45 days for a magistrate to decide if he received what he asked for?
I don’t think so.
What are you talking about? I was just noticing some dates.
BTW, India, like every other country, is important.
You are dope on a rope.
Is one H2O molecule in a water cycle, “independent”?
MAA was filed on December 20, in UK, which was December 21 in India.
Just noticing.
Which was March 19, 2024 in India.
Just noticing.
165th day (6/14) + 45 days (last decision wait)
150th day (5/30) (accelerated) + 60 days (clock off)
Just noticing 210th.
7/29
“All the world’s a stage….”
Could you please use a paragraph break on occasion?
No, aspirin would not, and aspirin would not create hundreds of different t-cell clone types that target hundreds of different antigens after multiplying into the hundreds of millions. Also, aspirin has dozens of potential side effects, cannot be used in adolescents safely and cannot be used in certain other populations.
Your Journal has an impact factor of under 6. JAMA Oncology has an impact factor of 33. The points regarding PFS you made are moot due to pseudo progression. Moreover, your Journal’s hand waiving at externally controls goes wanting and has been discussed here countless times.
Ultimately, you and your biased friends are thankfully not regulators.
Just like your unlearned statement that aspirin is really safe, your inane argument calling into question the JAMA conclusion of efficacy for DCVax-l against GBM is wrong.
Just a noticing. June 14th is the 165th day of the year.
Aspirin can be very toxic to certain populations, cannot be administered safely to adolescents and can be deadly in slightly elevated doses.
https://www.cancertherapyadvisor.com/home/decision-support-in-medicine/hospital-medicine/aspirin-toxicity/
It also isn’t proven to increase long term survival in GBM patients.
You pretended the judge hadn’t seen what Defendants were intending to request. He did, and he shortened it from July 12 to June 14.
Marzan, you wouldn’t know one way or the other.
Crickets.