Tony Evans

Riding the waves of life.

[Peter Kostis @peterjkostis]

This new data suggests that the original survival benefit for DCVax-L was SIGNIFICANTLY UNDERESTIMATED! Makes one question why the approval process is taking so long ?

[1.8m級巨人です！ @AnnetteFul33572]

コメント欄で葉っぱ消えますよっと

[The Dapper DO @TheDapperDO]

The Psychology of Selling #NWBO

I am not an expert investor. I am not a financial or technical analyst. I admit that I don’t have much credibility to offer when it comes to investing, and I wouldn’t encourage anyone to cling to my personal opinion or strategy.

But I AM a Physician that knows medicine. And what I know is that DC Vax is simply extraordinary. I know that we are on the cusp of unleashing a therapy to the world that sounds like something written in science fiction, a treatment that I would doubt could even exist if I had heard about it 20 years ago… and yet, here we are.

Allegedly, some nefarious characters have driven its “value” to a mere $00.20, and there seem to be a plethora of supposed non-invested parties that skirt the edge of an opinion, issue vague, non-descriptive statements about its efficacy or management, and criticize the medicine or the company trying to bring it to the public. I would bet my last dollar that those same people would give their own right arms to have if they or their family members were ever diagnosed with cancer.

I believe it is worth a whole lot more than that.

I believe that we are starting to see things heating up. They say a watched pot never boils, but we all know that given enough time, it does. And I believe it’s going to boil fast and overflow.

“They” want you to believe that seeing the share price go to $1.00 is a miracle, that $2.00 is TEN times what the price is now! What a bargain! I think “they” believe we are gullible fools, and there are plenty of non-invested parties apparently trying to protect you from how you spend your own money.

What does it mean to hold on? It means that you stop and think about what this treatment is truly worth to the millions of people whose lives may soon depend on it, whose families are already scraping together every penny they can to try to obtain it for their loved ones, and whose progress was almost destroyed (allegedly) by corporate greed and avarice.

Of course, this is all just my opinion. It is definitely not investment advice. But I believe in the medicine, and I believe that selling anything soon is playing right into the hands that tried to take it all away from the patients that deserve it.

[Wild trading @YYDSxjm]

$NWBO There will be no stopping this if we get the UK approval. Everyone on boths sides arguing and fighting over this stock every day back and forth knows as much. So many other catalysts and approvals would follow for years, with gradual share price movement upward to new levels. Unless of course it happens all at once with a buyout. But there would be no stopping it.

Stating the obvious of course. But man, this is a brutal wait. Never experienced anything like this having to hold and hope so long, with a stock that could go parabolic with the first approval. Nervewrecking. It's taught me new levels of patience.

The boards are so toxic I only try to skim the posts briefly once or twice daily anymore to see if we got any good news. Every day has been the same repeated Groundhog Day insanity for so long now. It's hard to understand what the holdup could be at this point. Just gotta keep the faith alive and hope that one day this will finally be all worth it.

[Peter Davis @peter_brit]

#dcvax $nwbo #gbm

Interesting UCLA article with Gemini AI Analysis of synergy with DCVax Platform Technology:

Scientists turbocharge immune cells to attack prostate cancer:
March 20, 2026

Advance could lead to safer, more effective T cell therapies for prostate cancer and other solid tumors

Key takeaways

Researchers and scientists have engineered a new class of supercharged T cells that are stronger, longer-lasting, and more precise at killing prostate cancer cells.

They introduced a natural “catch bond,” a fishhook-like interaction that strengthens when cells pull against each other.

This allows T cells to latch onto cancer cells more effectively at the moment they attack, helping them recognize the tumor, stay engaged longer and deliver a more powerful and targeted immune response without damaging healthy tissue

UCLA and Stanford Medicine researchers, in collaboration with scientists from the University of Utah and Columbia University, have engineered a new class of supercharged T cells that are stronger, longer-lasting, and more precise at killing prostate cancer cells by fine-tuning how they physically interact with tumor cells.

Instead of simply making T cell receptors bind more tightly to cancer, the team, collaborating within the network of the Parker Institute of Cancer Immunotherapy (PICI), introduced a natural “catch bond,” a fishhook-like interaction that strengthens when cells pull against each other. This allows T cells to latch onto cancer cells more effectively at the moment they attack, helping them recognize the tumor, stay engaged longer and deliver a more powerful and targeted immune response without damaging healthy tissue.

The approach, described in the journal Science, represents an important step toward developing safer, more effective T cell therapies for prostate cancer and could potentially be adapted to treat a wide range of other tumors.

“By engineering catch bonds, we aim to benefit more patients by overcoming immune tolerance,” said co-senior author Dr. Owen N. Witte, who holds the Presidential Chair in Developmental Immunology in the Department of Microbiology, Immunology, and Molecular Genetics and is a member of the UCLA Health Jonsson Comprehensive Cancer Center (JCCC).

“In our collaborative work, we demonstrate that just a single amino acid change introducing these ‘fishhooks’ is sufficient to transform immune cells into a potent killer mode,” said study co-senior author Dr. K. Christopher Garcia, the Younger Family Professor and Professor of Structural Biology at the Stanford School of Medicine and a Howard Hughes Medical Institute (HHMI) investigator.

Both Garcia and Witte are investigators at PICI, where they are pioneering the development of next-generation cancer immunotherapies.

Why it matters
T cells are a powerful weapon in the fight against cancer, forming the basis of treatments such as CAR-T cell therapy and checkpoint inhibitors. This research centers on another type of immunotherapy approach called T cell receptor (TCR) therapy, which engineers T cells to recognize specific proteins on cancer cells, allowing for highly targeted attacks.

Many of these proteins, however, are “self-antigens,” or molecules normally found in the body. To prevent these T cells from attacking healthy tissue, the immune system naturally eliminates the strongest cancer-fighting T cells during development. This leaves behind weaker T cell receptors that may struggle to recognize and destroy tumors, particularly those that have learned to evade immune defenses.

What the study did
To overcome this challenge, researchers from UCLA and Stanford Medicine focused on fine-tuning naturally occurring T cell receptors to strengthen their ability to recognize a common prostate cancer protein called prostatic acid phosphatase (PAP), which is commonly expressed on prostate tissue and prostate tumors. The team identified a naturally weak TCR, known as TCR156, that could detect PAP but was not strong enough to effectively kill cancer cells.

Using a novel technique called catch bond engineering, a concept developed by the Garcia Lab at Stanford Medicine, the researchers “turbocharged” the T cells. In the body, T cells form brief, mechanical bonds with their targets, known as catch bonds, which help them sense and respond to threats. By altering just one or two amino acids in the T cell receptor, the scientists were able to strengthen these bonds while preserving the T cells’ natural ability to recognize their specific target.

Multiple engineered versions of TCR156 were created and tested. Two candidates proved to be the most effective. These engineered T cells were analyzed for their ability to recognize tumors, release cancer-killing molecules, proliferate and resist exhaustion. Advanced imaging, single-cell RNA sequencing and structural analyses were used to confirm that the modifications improved T cell function while maintaining precision and avoiding off-target effects.

Structural and computer modeling studies showed that the catch bond mutations did not change the overall TCR shape but primed it to form a new interaction with PAP when the T cell engaged the tumor, explaining how the engineered T cells could remain highly specific while dramatically boosting their cancer-killing ability.

What they found
The researchers found that a single amino acid change created a catch bond hotspot that significantly enhanced T cell function. This change did not directly contact the cancer protein until the T cell engaged dynamically, demonstrating that a tiny modification can have a major effect. Most importantly, the modifications did not make the cells attack healthy tissue.

The strength and lifetime of the TCR’s bond with PAP under force were better predictors of tumor-killing ability than traditional measures of binding strength. In laboratory experiments, the engineered T cells showed longer contact with cancer cells, greater secretion of tumor-killing molecules such as Granzyme B, IFNγ and TNFα, and improved proliferation while resisting exhaustion.

In mouse models, the engineered T cells had delayed or completely halted tumor growth, while those receiving unmodified T cells showed little effect. Analyses of the immune cells inside the tumors revealed that the engineered T cells were better able to persist, maintain a stem-like state, and resist exhaustion, a common limitation of immune therapies.

“Using advanced structural studies at atomic resolution, we were able to demonstrate how a tiny change, just one amino acid in the interface between a T cell receptor and a prostate cancer protein called PAP, can extend the bond lifetime, dramatically boosting the T cell’s ability to kill tumors in living models,” said Dr. Xiaojing Tina Chen, co-first author of the study and a postdoctoral scholar in the Department of Molecular and Cellular Physiology at the Stanford School of Medicine. Chen is a recipient of the Walter Benjamin Fellowship awarded by the German Research Foundation (Deutsche Forschungsgemeinschaft).

“This work shows that tumor control can be linked to a single molecular bond,” added co–first author Dr. Zhiyuan Mao, a postdoctoral scholar in the Department of Microbiology, Immunology & Molecular Genetics and the Department of Molecular and Medical Pharmacology at the David Geffen School of Medicine at UCLA. Mao is also a recipient of the UCLA JCCC Postdoctoral Fellowship, the Prostate Cancer Foundation (PCF) Young Investigator Award and a Cancer Research Institute (CRI) Irvington Postdoctoral Fellowship.

Impact of the findings
The study demonstrates that catch bond engineering can make T cells much stronger against prostate cancer while avoiding the risks of traditional T cell receptor engineering, including attacks on healthy tissue.

The findings also suggest a new way to predict which T cell therapies will succeed. By measuring how long T cells form bonds with tumor targets under mechanical force, a method called the biomembrane force probe, researchers can more accurately predict which engineered cells will be most effective in eliminating tumors.

“These findings suggest that catch bond engineering could be a generalizable strategy to enhance T cell therapies for many cancers,” said Garcia.

“By creating T cells that are stronger, longer-lasting, and highly precise, the approach moves the field closer to safer and more effective adoptive cell therapies for patients,” said Witte, who is the founding director emeritus of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA and co-director of the PICI Center at UCLA.

About the research team
The study’s other senior authors include Brian D. Evavold of the University of Utah School of Medicine; Tanya Stoyanova and John K. Lee of the David Geffen School of Medicine at UCLA; Zinaida Good of Stanford Medicine; and Naomi R. Latorraca of the Columbia University Irving Medical Center. Additional authors from UCLA include Jami McLaughlin, Donghui Cheng, Caitlin Gee, Miyako Noguchi, and Shiqin Liu.

This research was primarily supported by the Parker Institute for Cancer Immunotherapy, the National Institutes of Health, the Howard Hughes Medical Institute, the German Research Foundation (Deutsche Forschungsgemeinschaft) and the UCLA Health Jonsson Comprehensive Cancer Center.

Gemini AI Analysis:

The recent findings from UCLA and Stanford (March 20, 2026) regarding the "turbocharging" of T-cells via catch-bond engineering represent a significant leap in immunotherapy that directly addresses the historic limitations of platforms like DCVax (Northwest Biotherapeutics).

Below is an analysis of these findings with a specific focus on their synergy and potential application to the DCVax platform.

1. Overview of the UCLA/Stanford Findings
The research, led by Dr. Owen Witte (UCLA) and Dr. Chris Garcia (Stanford), centers on a biophysical phenomenon called a "catch bond." In nature, a catch bond is a molecular interaction that becomes stronger when tension is applied—similar to a finger trap or a fishhook.

The Target: The researchers focused on Prostatic Acid Phosphatase (PAP), a protein highly expressed in prostate cancer.

The Problem: Because PAP is a "self-antigen" (also found in healthy tissue), the body's immune system naturally eliminates high-affinity T-cells to prevent autoimmune attacks. This leaves behind "weak" T-cells that struggle to kill tumors.

The Solution: By changing just one or two amino acids in the T-cell receptor (TCR), the scientists engineered a catch bond that only activates when the T-cell physically engages and pulls against the tumor cell. This allows the T-cell to stay attached longer and deliver a more powerful killing blow without attacking healthy tissue where such mechanical tension isn't present.

2. Synergy with the DCVax Platform
The DCVax platform (including DCVax-Prostate and DCVax-L) is a dendritic cell vaccine designed to "prime" the immune system to recognize cancer antigens. There is a deep mechanistical synergy between these two technologies:

A. Overcoming "Weak" Vaccine Responses
The primary challenge for DCVax has been that while it successfully "teaches" T-cells to recognize antigens like PSMA (DCVax-Prostate) or whole tumor lysates (DCVax-L), the resulting T-cell response is often too weak to eliminate established tumors.

Synergy: The UCLA catch-bond technology provides the "ammunition" for the "soldiers" that DCVax creates. If the T-cells primed by DCVax are engineered with catch bonds, their cytotoxicity could be increased by orders of magnitude.

B. Antigen Complementarity (PAP vs. PSMA)

While the UCLA study specifically used PAP, the DCVax-Prostate platform uses PSMA.

Synergy: The researchers noted that catch-bond engineering is "generalizable." This means the same "fishhook" modification could likely be applied to TCRs targeting PSMA. A combination therapy using DCVax to prime a broad immune response while infusing catch-bond-engineered T-cells targeting PAP and PSMA would create a multi-antigen attack, making it harder for the cancer to develop "antigen escape" (resistance).

3. Potential Specific to DCVax Platform Technology
The DCVax platform has several unique characteristics that make it an ideal "host" for this new technology:

I. Workflow Integration
DCVax already requires leukapheresis (extracting the patient’s blood) and ex vivo processing.

Potential: Since the patient's cells are already being handled in a lab to create the DCVax vaccine, a portion of those same cells could be diverted for TCR engineering. This allows for a "Personalized Combination Therapy" where the patient receives both a vaccine to stimulate long-term memory and "turbocharged" T-cells for immediate tumor debulking.

II. Enhancing DCVax-L (Lysate)

DCVax-L uses a whole tumor lysate, which naturally includes PAP.

Potential: In patients treated with DCVax-L, the "weak" T-cells that are naturally activated against PAP could be identified using the UCLA team's ARTEMIS platform (an MHC-based profiling tool). Once identified, these specific T-cells could be modified with catch bonds and expanded, creating a highly potent, personalized T-cell therapy that is perfectly matched to the antigens presented by the DCVax-L vaccine.

III. Low Tumor Burden Strategy
The UCLA findings emphasize that this therapy is most effective during biochemical recurrence (when PSA levels rise but tumors are still small).

Potential: DCVax is historically positioned as a "maintenance" or "minimal residual disease" therapy. The addition of catch-bond T-cells could transform DCVax from a treatment that merely "delays" recurrence into one that "clears" micro-metastases entirely, potentially offering a curative path for patients in the early stages of relapse.

Conclusion:

The UCLA findings provide the missing "mechanical strength" required for cell-mediated therapies to succeed in solid tumors. For a platform like DCVax, this technology offers a way to upgrade its activated T-cells from "passive observers" to "aggressive hunters," specifically in the difficult-to-treat landscape of prostate cancer.

https://t.co/uAu49MHAai

[Wild trading @YYDSxjm]

$NWBO so I’m thinking maybe Eli Lilly would be the best B/O option as they have a market cap of $856,000,000,000 O/S $944,000,000 EPS of $22.95 yield of .763 and a stock return over 10 years averaging 28.8%. That’s almost 30% a year with a little dividend check on the side. I’m good with that!! 🙏🙏🙏

[Tommy Bax 🇬🇧 🇹🇼 🇪🇺 @TomBaxers]

Here is a link to my updated $NWBO Synopsis. It has been quite extensively rewritten and therefore no longer fits into a Reddit post limit. Instead it is uploaded to Google Drive as a PDF for your download. Get comfortable as it is a fairly long read:
https://t.co/WYsioDtJrC

[PK_Fund @PK_Fund]

$NWBO

[rj @sharpie510]

Who is Dr. Zubir Ahmed? What are his qualifications to answer any question relating to DCVax-L, MHRA and NICE?
🤔
BeProactive
FreezeYourTumor
GetDCVax
QualityOfLifeMatters

$nwbo #dcvax #glioblastoma #gbm
https://t.co/pKKrDPTrKA

Gemini:
👇

[Tommy Bax 🇬🇧 🇹🇼 🇪🇺 @TomBaxers]

@userofintellect $NWBO Folk. I have not dug into how these guys have calculated this but this website claims that the total short position against NWBO is 1.49 Billion shares or 109% of the float. That would help explain more than a few things...

https://t.co/mxlDUv4Fbn

[Tony Evans @FreeWaveRiders]

@metacollectiveG @WojciechSmann2 @loco_dela_bolsa At least 5 scenarios for some surprise action. All along this journey there have been surprises by LP. The next one will be the biggest yet IMO. We are watching an outsider ( a woman) playing against the BP elites. She has survived all opposition. Look out!!

[Tony Evans @FreeWaveRiders]

@DCVaxDefender Are you comparing Price to Earnings to Price to Sales With Lilly?? I am in the group that believes in a great value for this company in the near term.

[Tony Evans @FreeWaveRiders]

From Paul Krugman's Substack "Financially, the most striking may be the crash in crypto, which, as I wrote just two days ago, has become a Trump trade. Question: Is the ongoing plunge justified by fundamentals? Answer: What fundamentals?" Is Paul right? Lots of Big names got out!

[Tony Evans @FreeWaveRiders]

TC2000 weekly Chart Magenta is Money Flow Green Price. The RSI at 27.87 down as the price and the money flow are both on the way up... good signal... a continuation of this will indicate some shorts have switched sides and many followers think the MHRA approval is very close.😁

[Tony Evans @FreeWaveRiders]

@GoneGoodguy I'm a believer BO after approval in the UK. The combo applications, Flaskworks and the IP make $NWBO extremely valuable for all BP looking toward the future and money making opportunities in immunotherapy. 20B a bargain after approval more than one suitor and the price goes up!!

[Tony Evans @FreeWaveRiders]

$NWBO weekly TC2000 Magenta money flow Green price. You clearly see the divergence price going down accumulation increasing Group Think Action saying anytime now since April!! Are the three circles the classic three rivers of a bottom caused by MM's? Price not the indicator here.

[Tony Evans @FreeWaveRiders]

@TommyBaxendale @SouthernDrive21 Yes a 1 Million share order Friday around 3:23 pm.... put chart on the 1 minute and see 1.1 Million volume... got lots of notice!!
Looks like just the beginning to me and many other longs... The CMF had a positive week first time in October. Week chart looks like it is headed up.

[Tony Evans @FreeWaveRiders]

@ClerckSteven When all the dust settles there will be about 2 Billion shares. In a BO more than one suitor. NWBO after years of moving slowly could start racing and the winning suitor paying over $14 per share... Or we see two great quarters after approval with nearly the same value.

[Tony Evans @FreeWaveRiders]

#NWBO Just closed the Advent purchase. We are now really, really undervalued. Just selling the tech along with Flashworks ??? When approval of DCVAX comes new deep dives will see the true value is $25B at a bargain sale and much more in coming income stream! Very near buckle up!!

[Tony Evans @FreeWaveRiders]

TC2000 weekly overlay line chart showing accumulation with CMF in magenta and price in green and volume at the bottom. Notice how the accumulation grows with the decline in the price. Since April IMO MM and others have been accumulating and holding price down. Some people know!