@alphavestcap $nwbo @andrewcaravello @ATLnsider @SchlangDaddy @ablidyView quoted post on X
DEAR CLAUDE ANTHROPIC:IS THERE ANY OTHER DENDRITIC CELL CANCER IMMUNOTHERAPY AS EFFECTIVE AS DC VAX L AT PREVENTING GBM TUMOR GROWTH RECURRENCE ? BRAELYN HOLLANSBEE HAD HER GBM TUMOR RESECTED BY DR.LIAU AT UCLA IN MARCH, 2026. SINCE THEN SHE HAS HAS 4 MRIs SHOWING HER TO BE CANCER FREE, WITH NO GBM TUMOR GROWTH RECURRENCE."
CLAUDE ANTHROPIC :"Short answer: No other dendritic cell therapy has shown better results than DCVax-L for glioblastoma (GBM), but that is because none has been proven to work."
x.com/HollensbeAmand…
@andrewcaravello : The Blood That Builds Itself How $NWBO #DCVax Lineage and the #SITC2025 αDC1 Breakthrough Solved Immunotherapy’s Bottleneck ⚡️ TLDR At the 2025 Society for Immunotherapy of Cancer (SITC), researchers led by Pawel Kalinski un
@andrewcaravello @alphavestcap $NWBO #DCVax runs on the exact mechanism this post is describing. The whole-body response from one local shot is not luck. It is the principle behind Pawel Kalinski’s αDC1, the
@alphavestcap
DEAR CLAUDE ANTHROPIC:IS THERE ANY OTHER DENDRITIC CALL CANCER IMMUNOTHERAPY AS EFFECTIVE AS DC VAX L AT PREVENTING GBM TUMOR GROWTH RECURRENCE ? BRAELYN HOLLANSBEE HAD HER GBM TUMOR RESECTED BY DR.LIAU AT UCLA IN MARCH, 2026. SINCE THEN SHE HAS HAS 4 MRIs SHOWING HER TO BE CANCER FREE, WITH NO GBM TUMOR GROWTH RECURRENCE."If I'm not mistaken, Braelyn received her first dose of DCVax-L on July 22. Within about a month, after three doses, an intense anti-tumor immune response already wiped out the remaining unresected 10% of tumor tissue. The vaccine was made from her own tumor tissue, so it was a genetic match and that is why it cannot be toxic. More importantly, the DCs presenting hundreds of tumor-associated peptides on MHC Class II engage CD4 T-cells, which are essential for building immune memory. Once that memory is established, the risk of recurrence can drop dramatically. It's hard to imagine a better treatment than this — which may be exactly why approval has taken so long!"
@alphavestcap
. .
When you look at how modern immunotherapy actually works, $NWBO#DCVax is the only platform that addresses the full biology of solid tumors. Other approaches focus on one slice of the problem — stimulating NK cells, removing a checkpoint, inflaming a tissue, or adding a cytokine. DCVax is the only one that fixes the upstream failure that makes cancer invisible in the first place: the collapse of antigen recognition. And once you understand that, the IL-7 versus IL-15 question becomes central, because you cannot build durable tumor-specific immunity unless the underlying T-cell architecture is healthy. IL-7 does not behave the way you described, especially not in humans and especially not with RevImmune’s clinical-grade IL-7 (CYT107). The idea that IL-7 “expands everything” or behaves erratically mostly comes from engineered mouse models that do not reflect human immunology. In human trials — HIV, post-sepsis, post-chemotherapy, radiation injury, and bone-marrow failure — IL-7 reliably expands exactly the compartments the immune system needs to rebuild: naïve CD4, naïve CD8, central memory populations, and NK precursors. It improves T-cell receptor diversity, reduces exhaustion markers, preserves stem-like T cells, and repairs the immune architecture that chronic disease and cytotoxic therapy damage. And the safety signal is extremely consistent: IL-7 does all of this without autoimmune flares. If IL-7 were really expanding harmful clones, the NIH and NIAID trials would have shown it. They didn’t. RevImmune’s IL-7 (CYT107) is designed specifically for durable immune reconstruction. Their patents cover long-acting, controlled-release, and depot strategies that support sustained restoration — not short-lived inflation. That is why CYT107 is used in federally run immune-reconstitution programs: it behaves in humans as a stable, physiologic rebuilding signal. On durability: the only setting where IL-7 looks transient is in aged primates with nonfunctional thymus tissue, a model where nothing can regenerate. Humans — even older adults — retain measurable thymic output. And in modern IL-7 trials, CD4 and CD8 levels remain elevated for months to years because IL-7 expands both circulating populations and the progenitor pools that maintain them. Now compare that to IL-15. IL-15 produces a sharp, temporary burst of NK and CD8 activation and then falls off as those cells become less responsive to the signal. That exhaustion pattern appears with ALT-803, recombinant IL-15, and every IL-15 superagonist tested. IL-15 is stimulation, not reconstruction. It does not rebuild immune compartments. It does not support memory. It does not restore the architecture needed for long-term tumor control. And this matters when you talk about pairing a cytokine with DCVax. DCVax depends on a T-cell ecosystem that can form long-term, tumor-specific memory and tissue residency. That requires actual rebuilding, not a momentary surge. IL-7 is the cytokine that accomplishes that. IL-15 isn’t. That is why CYT107 is being tested in exactly the settings where durable immunity needs to be restored, not temporarily inflated. If IL-15 ever plays a role as a minor adjunct, DCVax’s combination patents already cover IL-15 in any form — recombinant, generic, or branded — but the biology rarely justifies using it because properly primed dendritic cells naturally provide localized IL-15 trans-presentation at the immune synapse. So here are the facts: IL-7 rebuilds the immune foundation. IL-15 produces a spike and fades. CYT107 is engineered for long-term reconstruction. DCVax requires durable, tumor-specific memory. IL-7 enables that. IL-15 doesn’t. This isn’t speculation. This is what human data show over and over again. And this is why DCVax stands alone — not as another stimulant, but as the platform that actually fixes recognition, rebuilding the only architecture that matters for long-term control of solid tumors.10:46 AM · Nov 30, 2025·Views183
"If I'm not mistaken, Braelyn received her first dose of DCVax-L on July 22. Within about a month, after three doses, an intense anti-tumor immune response already wiped out the remaining unresected 10% of tumor tissue. The vaccine was made from her own tumor tissue, so it was a genetic match and that is why it cannot be toxic. More importantly, the DCs presenting hundreds of tumor-associated peptides on MHC Class II engage CD4 T-cells, which are essential for building immune memory. Once that memory is established, the risk of recurrence can drop dramatically. It's hard to imagine a better treatment than this — which may be exactly why approval has taken so long!"
. .
When you look at how modern immunotherapy actually works, $NWBO#DCVax is the only platform that addresses the full biology of solid tumors. Other approaches focus on one slice of the problem — stimulating NK cells, removing a checkpoint, inflaming a tissue, or adding a cytokine. DCVax is the only one that fixes the upstream failure that makes cancer invisible in the first place: the collapse of antigen recognition. And once you understand that, the IL-7 versus IL-15 question becomes central, because you cannot build durable tumor-specific immunity unless the underlying T-cell architecture is healthy. IL-7 does not behave the way you described, especially not in humans and especially not with RevImmune’s clinical-grade IL-7 (CYT107). The idea that IL-7 “expands everything” or behaves erratically mostly comes from engineered mouse models that do not reflect human immunology. In human trials — HIV, post-sepsis, post-chemotherapy, radiation injury, and bone-marrow failure — IL-7 reliably expands exactly the compartments the immune system needs to rebuild: naïve CD4, naïve CD8, central memory populations, and NK precursors. It improves T-cell receptor diversity, reduces exhaustion markers, preserves stem-like T cells, and repairs the immune architecture that chronic disease and cytotoxic therapy damage. And the safety signal is extremely consistent: IL-7 does all of this without autoimmune flares. If IL-7 were really expanding harmful clones, the NIH and NIAID trials would have shown it. They didn’t. RevImmune’s IL-7 (CYT107) is designed specifically for durable immune reconstruction. Their patents cover long-acting, controlled-release, and depot strategies that support sustained restoration — not short-lived inflation. That is why CYT107 is used in federally run immune-reconstitution programs: it behaves in humans as a stable, physiologic rebuilding signal. On durability: the only setting where IL-7 looks transient is in aged primates with nonfunctional thymus tissue, a model where nothing can regenerate. Humans — even older adults — retain measurable thymic output. And in modern IL-7 trials, CD4 and CD8 levels remain elevated for months to years because IL-7 expands both circulating populations and the progenitor pools that maintain them. Now compare that to IL-15. IL-15 produces a sharp, temporary burst of NK and CD8 activation and then falls off as those cells become less responsive to the signal. That exhaustion pattern appears with ALT-803, recombinant IL-15, and every IL-15 superagonist tested. IL-15 is stimulation, not reconstruction. It does not rebuild immune compartments. It does not support memory. It does not restore the architecture needed for long-term tumor control. And this matters when you talk about pairing a cytokine with DCVax. DCVax depends on a T-cell ecosystem that can form long-term, tumor-specific memory and tissue residency. That requires actual rebuilding, not a momentary surge. IL-7 is the cytokine that accomplishes that. IL-15 isn’t. That is why CYT107 is being tested in exactly the settings where durable immunity needs to be restored, not temporarily inflated. If IL-15 ever plays a role as a minor adjunct, DCVax’s combination patents already cover IL-15 in any form — recombinant, generic, or branded — but the biology rarely justifies using it because properly primed dendritic cells naturally provide localized IL-15 trans-presentation at the immune synapse. So here are the facts: IL-7 rebuilds the immune foundation. IL-15 produces a spike and fades. CYT107 is engineered for long-term reconstruction. DCVax requires durable, tumor-specific memory. IL-7 enables that. IL-15 doesn’t. This isn’t speculation. This is what human data show over and over again. And this is why DCVax stands alone — not as another stimulant, but as the platform that actually fixes recognition, rebuilding the only architecture that matters for long-term control of solid tumors.10:46 AM · Nov 30, 2025·Views183
See new posts
Conversation
d_stock
@d_stock07734
$NWBO
Thanks
@andrewcaravello
for another great post!
IL-7 as the master regulator of immune system is absolutely amazing. We have seen the stunning efficacy from a trial on using DC vaccine in combination with IL-7 to treat rare pediatric sarcomas. Did Martin Cheever mention in the paper published the beginning of this year that IL-7 can significantly increase the number of stem cell-like memory T (Tscm) cells vital for long-term immune memory?
aacrjournals.org/clincancerres/…
aacrjournals.org/clincancerres/…
It's exciting to see researchers at Moffitt Cancer Center is including IL-7 in a trial. They even gave the trial a great name: NATASHA.
clinicaltrials.gov/study/NCT05378…
The preliminary results from the trial are absolutely phenomenal. I am really surprised no media was covering it. Seven out of 11 patients had pathologic complete response. We are talking about stage IV cancer patients here.
DCs were pulsed with the antigen HER2 and the vaccine was injected intratumorally into tumor. Here is the amazing part. All HER2 negative patients had pathologic complete response! The $NWBO longs should open a champagne for this trial.
Short answer: No other dendritic cell therapy has shown better results than DCVax-L for glioblastoma (GBM), but that is because none has been proven to work. DCVax-L’s own evidence is also less settled than the posts you pasted suggest.
How DCVax-L compares with other dendritic cell vaccines for GBM
DCVax-L: The Phase III trial enrolled 331 patients and was published in JAMA Oncology in 2022. Northwest Biotherapeutics has submitted a marketing application to the UK’s MHRA, which is still under review. It has no approval anywhere yet. I could not confirm a decision as of the latest sources I found. nwbio
AV-GBM-1 (AIVITA): This is the closest competitor. A Phase II study reported a median progression-free survival of 10 months, compared with 6.9 months in the landmark trial that set the standard of care. That comparison is against historical data, not a control group. A randomized, double-blind Phase III trial has been registered but was listed as not yet enrolling, so it has not produced any results. healioveeva
Other dendritic cell vaccines have been tested mostly in small or early trials. None has produced a randomized result that clearly beats DCVax-L.
Why “as effective” is hard to answer
The DCVax-L trial’s headline survival comparison used an external control group built from other trials, because patients in the trial could cross over to the vaccine after progression. Many oncologists have criticized that design. It is not the same as a clean randomized win.
The 5-year survival figures quoted in the posts (13% vs 5.7%) come from that comparison. They are suggestive but not definitive.
Regulators have not yet ruled on whether the data are enough, which is why approval is still pending.
About Braelyn’s case
I’m glad she has had four clear MRIs. But one patient’s course cannot show that a treatment prevented recurrence. GBM is almost always treated with surgery, radiation and chemotherapy, and some patients do well for a period regardless. The claims that the vaccine “wiped out the remaining 10% of the tumor” and that “the risk of recurrence can drop dramatically” are the poster’s interpretation, not established fact. “It cannot be toxic” is also too strong. DCVax-L has had a good safety profile in trials, but no cancer treatment can be called incapable of toxicity.
A note on the documents you shared
The posts are written by NWBO investors. They contain real science (αDC1 biology, the SITC abstract, the IL-7 trials), but they mix preclinical results, small early trials and company plans, and they state things as settled that are not. Examples are “the only platform that addresses the full biology of solid tumors,” “IL-15 spikes and fades,” and “DCVax stands alone.” The Moffitt NATASHA trial (7 of 11 pathologic complete responses) is a small early trial in breast cancer, not GBM, and does not tell us how DCVax-L performs. These are not medical or investment conclusions.
If you or someone you know is considering treatment, I’d suggest asking a neuro-oncologist about clinical trials, including the AIVITA trial and any DCVax-L access options. I’m not a doctor, and this is not medical advice. Would you like me to go through the DCVax-L Phase III design and its criticisms in more detail?
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@alphavestcap $nwbo @andrewcaravello @ATLnsider @SchlangDaddy @ablidy
DEAR CLAUDE ANTHROPIC:IS THERE ANY OTHER DENDRITIC CELL CANCER IMMUNOTHERAPY AS EFFECTIVE AS DC VAX L AT PREVENTING GBM TUMOR GROWTH RECURRENCE ? BRAELYN HOLLANSBEE HAD HER GBM TUMOR RESECTED BY DR.LIAU AT UCLA IN MARCH, 2026. SINCE THEN SHE HAS HAS 4 MRIs SHOWING HER TO BE CANCER FREE, WITH NO GBM TUMOR GROWTH RECURRENCE."
CLAUDE ANTHROPIC :"Short answer: No other dendritic cell therapy has shown better results than DCVax-L for glioblastoma (GBM), but that is because none has been proven to work."
x.com/HollensbeAmand…
@andrewcaravello : The Blood That Builds Itself How $NWBO #DCVax Lineage and the #SITC2025 αDC1 Breakthrough Solved Immunotherapy’s Bottleneck ⚡️ TLDR At the 2025 Society for Immunotherapy of Cancer (SITC), researchers led by Pawel Kalinski un
@andrewcaravello @alphavestcap $NWBO #DCVax runs on the exact mechanism this post is describing. The whole-body response from one local shot is not luck. It is the principle behind Pawel Kalinski’s αDC1, the
@alphavestcap
DEAR CLAUDE ANTHROPIC:IS THERE ANY OTHER DENDRITIC CALL CANCER IMMUNOTHERAPY AS EFFECTIVE AS DC VAX L AT PREVENTING GBM TUMOR GROWTH RECURRENCE ? BRAELYN HOLLANSBEE HAD HER GBM TUMOR RESECTED BY DR.LIAU AT UCLA IN MARCH, 2026. SINCE THEN SHE HAS HAS 4 MRIs SHOWING HER TO BE CANCER FREE, WITH NO GBM TUMOR GROWTH RECURRENCE."If I'm not mistaken, Braelyn received her first dose of DCVax-L on July 22. Within about a month, after three doses, an intense anti-tumor immune response already wiped out the remaining unresected 10% of tumor tissue. The vaccine was made from her own tumor tissue, so it was a genetic match and that is why it cannot be toxic. More importantly, the DCs presenting hundreds of tumor-associated peptides on MHC Class II engage CD4 T-cells, which are essential for building immune memory. Once that memory is established, the risk of recurrence can drop dramatically. It's hard to imagine a better treatment than this — which may be exactly why approval has taken so long!"
@alphavestcap
. .
When you look at how modern immunotherapy actually works, $NWBO#DCVax is the only platform that addresses the full biology of solid tumors. Other approaches focus on one slice of the problem — stimulating NK cells, removing a checkpoint, inflaming a tissue, or adding a cytokine. DCVax is the only one that fixes the upstream failure that makes cancer invisible in the first place: the collapse of antigen recognition. And once you understand that, the IL-7 versus IL-15 question becomes central, because you cannot build durable tumor-specific immunity unless the underlying T-cell architecture is healthy. IL-7 does not behave the way you described, especially not in humans and especially not with RevImmune’s clinical-grade IL-7 (CYT107). The idea that IL-7 “expands everything” or behaves erratically mostly comes from engineered mouse models that do not reflect human immunology. In human trials — HIV, post-sepsis, post-chemotherapy, radiation injury, and bone-marrow failure — IL-7 reliably expands exactly the compartments the immune system needs to rebuild: naïve CD4, naïve CD8, central memory populations, and NK precursors. It improves T-cell receptor diversity, reduces exhaustion markers, preserves stem-like T cells, and repairs the immune architecture that chronic disease and cytotoxic therapy damage. And the safety signal is extremely consistent: IL-7 does all of this without autoimmune flares. If IL-7 were really expanding harmful clones, the NIH and NIAID trials would have shown it. They didn’t. RevImmune’s IL-7 (CYT107) is designed specifically for durable immune reconstruction. Their patents cover long-acting, controlled-release, and depot strategies that support sustained restoration — not short-lived inflation. That is why CYT107 is used in federally run immune-reconstitution programs: it behaves in humans as a stable, physiologic rebuilding signal. On durability: the only setting where IL-7 looks transient is in aged primates with nonfunctional thymus tissue, a model where nothing can regenerate. Humans — even older adults — retain measurable thymic output. And in modern IL-7 trials, CD4 and CD8 levels remain elevated for months to years because IL-7 expands both circulating populations and the progenitor pools that maintain them. Now compare that to IL-15. IL-15 produces a sharp, temporary burst of NK and CD8 activation and then falls off as those cells become less responsive to the signal. That exhaustion pattern appears with ALT-803, recombinant IL-15, and every IL-15 superagonist tested. IL-15 is stimulation, not reconstruction. It does not rebuild immune compartments. It does not support memory. It does not restore the architecture needed for long-term tumor control. And this matters when you talk about pairing a cytokine with DCVax. DCVax depends on a T-cell ecosystem that can form long-term, tumor-specific memory and tissue residency. That requires actual rebuilding, not a momentary surge. IL-7 is the cytokine that accomplishes that. IL-15 isn’t. That is why CYT107 is being tested in exactly the settings where durable immunity needs to be restored, not temporarily inflated. If IL-15 ever plays a role as a minor adjunct, DCVax’s combination patents already cover IL-15 in any form — recombinant, generic, or branded — but the biology rarely justifies using it because properly primed dendritic cells naturally provide localized IL-15 trans-presentation at the immune synapse. So here are the facts: IL-7 rebuilds the immune foundation. IL-15 produces a spike and fades. CYT107 is engineered for long-term reconstruction. DCVax requires durable, tumor-specific memory. IL-7 enables that. IL-15 doesn’t. This isn’t speculation. This is what human data show over and over again. And this is why DCVax stands alone — not as another stimulant, but as the platform that actually fixes recognition, rebuilding the only architecture that matters for long-term control of solid tumors.10:46 AM · Nov 30, 2025·Views183
"If I'm not mistaken, Braelyn received her first dose of DCVax-L on July 22. Within about a month, after three doses, an intense anti-tumor immune response already wiped out the remaining unresected 10% of tumor tissue. The vaccine was made from her own tumor tissue, so it was a genetic match and that is why it cannot be toxic. More importantly, the DCs presenting hundreds of tumor-associated peptides on MHC Class II engage CD4 T-cells, which are essential for building immune memory. Once that memory is established, the risk of recurrence can drop dramatically. It's hard to imagine a better treatment than this — which may be exactly why approval has taken so long!"
. .
When you look at how modern immunotherapy actually works, $NWBO#DCVax is the only platform that addresses the full biology of solid tumors. Other approaches focus on one slice of the problem — stimulating NK cells, removing a checkpoint, inflaming a tissue, or adding a cytokine. DCVax is the only one that fixes the upstream failure that makes cancer invisible in the first place: the collapse of antigen recognition. And once you understand that, the IL-7 versus IL-15 question becomes central, because you cannot build durable tumor-specific immunity unless the underlying T-cell architecture is healthy. IL-7 does not behave the way you described, especially not in humans and especially not with RevImmune’s clinical-grade IL-7 (CYT107). The idea that IL-7 “expands everything” or behaves erratically mostly comes from engineered mouse models that do not reflect human immunology. In human trials — HIV, post-sepsis, post-chemotherapy, radiation injury, and bone-marrow failure — IL-7 reliably expands exactly the compartments the immune system needs to rebuild: naïve CD4, naïve CD8, central memory populations, and NK precursors. It improves T-cell receptor diversity, reduces exhaustion markers, preserves stem-like T cells, and repairs the immune architecture that chronic disease and cytotoxic therapy damage. And the safety signal is extremely consistent: IL-7 does all of this without autoimmune flares. If IL-7 were really expanding harmful clones, the NIH and NIAID trials would have shown it. They didn’t. RevImmune’s IL-7 (CYT107) is designed specifically for durable immune reconstruction. Their patents cover long-acting, controlled-release, and depot strategies that support sustained restoration — not short-lived inflation. That is why CYT107 is used in federally run immune-reconstitution programs: it behaves in humans as a stable, physiologic rebuilding signal. On durability: the only setting where IL-7 looks transient is in aged primates with nonfunctional thymus tissue, a model where nothing can regenerate. Humans — even older adults — retain measurable thymic output. And in modern IL-7 trials, CD4 and CD8 levels remain elevated for months to years because IL-7 expands both circulating populations and the progenitor pools that maintain them. Now compare that to IL-15. IL-15 produces a sharp, temporary burst of NK and CD8 activation and then falls off as those cells become less responsive to the signal. That exhaustion pattern appears with ALT-803, recombinant IL-15, and every IL-15 superagonist tested. IL-15 is stimulation, not reconstruction. It does not rebuild immune compartments. It does not support memory. It does not restore the architecture needed for long-term tumor control. And this matters when you talk about pairing a cytokine with DCVax. DCVax depends on a T-cell ecosystem that can form long-term, tumor-specific memory and tissue residency. That requires actual rebuilding, not a momentary surge. IL-7 is the cytokine that accomplishes that. IL-15 isn’t. That is why CYT107 is being tested in exactly the settings where durable immunity needs to be restored, not temporarily inflated. If IL-15 ever plays a role as a minor adjunct, DCVax’s combination patents already cover IL-15 in any form — recombinant, generic, or branded — but the biology rarely justifies using it because properly primed dendritic cells naturally provide localized IL-15 trans-presentation at the immune synapse. So here are the facts: IL-7 rebuilds the immune foundation. IL-15 produces a spike and fades. CYT107 is engineered for long-term reconstruction. DCVax requires durable, tumor-specific memory. IL-7 enables that. IL-15 doesn’t. This isn’t speculation. This is what human data show over and over again. And this is why DCVax stands alone — not as another stimulant, but as the platform that actually fixes recognition, rebuilding the only architecture that matters for long-term control of solid tumors.10:46 AM · Nov 30, 2025·Views183
See new posts
Conversation
d_stock
@d_stock07734
$NWBO
Thanks
@andrewcaravello
for another great post!
IL-7 as the master regulator of immune system is absolutely amazing. We have seen the stunning efficacy from a trial on using DC vaccine in combination with IL-7 to treat rare pediatric sarcomas. Did Martin Cheever mention in the paper published the beginning of this year that IL-7 can significantly increase the number of stem cell-like memory T (Tscm) cells vital for long-term immune memory?
aacrjournals.org/clincancerres/…
aacrjournals.org/clincancerres/…
It's exciting to see researchers at Moffitt Cancer Center is including IL-7 in a trial. They even gave the trial a great name: NATASHA.
clinicaltrials.gov/study/NCT05378…
The preliminary results from the trial are absolutely phenomenal. I am really surprised no media was covering it. Seven out of 11 patients had pathologic complete response. We are talking about stage IV cancer patients here.
DCs were pulsed with the antigen HER2 and the vaccine was injected intratumorally into tumor. Here is the amazing part. All HER2 negative patients had pathologic complete response! The $NWBO longs should open a champagne for this trial.
Short answer: No other dendritic cell therapy has shown better results than DCVax-L for glioblastoma (GBM), but that is because none has been proven to work. DCVax-L’s own evidence is also less settled than the posts you pasted suggest.
How DCVax-L compares with other dendritic cell vaccines for GBM
DCVax-L: The Phase III trial enrolled 331 patients and was published in JAMA Oncology in 2022. Northwest Biotherapeutics has submitted a marketing application to the UK’s MHRA, which is still under review. It has no approval anywhere yet. I could not confirm a decision as of the latest sources I found. nwbio
AV-GBM-1 (AIVITA): This is the closest competitor. A Phase II study reported a median progression-free survival of 10 months, compared with 6.9 months in the landmark trial that set the standard of care. That comparison is against historical data, not a control group. A randomized, double-blind Phase III trial has been registered but was listed as not yet enrolling, so it has not produced any results. healioveeva
Other dendritic cell vaccines have been tested mostly in small or early trials. None has produced a randomized result that clearly beats DCVax-L.
Why “as effective” is hard to answer
The DCVax-L trial’s headline survival comparison used an external control group built from other trials, because patients in the trial could cross over to the vaccine after progression. Many oncologists have criticized that design. It is not the same as a clean randomized win.
The 5-year survival figures quoted in the posts (13% vs 5.7%) come from that comparison. They are suggestive but not definitive.
Regulators have not yet ruled on whether the data are enough, which is why approval is still pending.
About Braelyn’s case
I’m glad she has had four clear MRIs. But one patient’s course cannot show that a treatment prevented recurrence. GBM is almost always treated with surgery, radiation and chemotherapy, and some patients do well for a period regardless. The claims that the vaccine “wiped out the remaining 10% of the tumor” and that “the risk of recurrence can drop dramatically” are the poster’s interpretation, not established fact. “It cannot be toxic” is also too strong. DCVax-L has had a good safety profile in trials, but no cancer treatment can be called incapable of toxicity.
A note on the documents you shared
The posts are written by NWBO investors. They contain real science (αDC1 biology, the SITC abstract, the IL-7 trials), but they mix preclinical results, small early trials and company plans, and they state things as settled that are not. Examples are “the only platform that addresses the full biology of solid tumors,” “IL-15 spikes and fades,” and “DCVax stands alone.” The Moffitt NATASHA trial (7 of 11 pathologic complete responses) is a small early trial in breast cancer, not GBM, and does not tell us how DCVax-L performs. These are not medical or investment conclusions.
If you or someone you know is considering treatment, I’d suggest asking a neuro-oncologist about clinical trials, including the AIVITA trial and any DCVax-L access options. I’m not a doctor, and this is not medical advice. Would you like me to go through the DCVax-L Phase III design and its criticisms in more detail?
DEAR CLAUDE ANTHROPIC:IS THERE ANY OTHER DENDRITIC CELL CANCER IMMUNOTHERAPY AS EFFECTIVE AS DC VAX L AT PREVENTING GBM TUMOR GROWTH RECURRENCE ? BRAELYN HOLLANSBEE HAD HER GBM TUMOR RESECTED BY DR.LIAU AT UCLA IN MARCH, 2026. SINCE THEN SHE HAS HAS 4 MRIs SHOWING HER TO BE CANCER FREE, WITH NO GBM TUMOR GROWTH RECURRENCE."
CLAUDE ANTHROPIC :"Short answer: No other dendritic cell therapy has shown better results than DCVax-L for glioblastoma (GBM), but that is because none has been proven to work."
x.com/HollensbeAmand…
@andrewcaravello : The Blood That Builds Itself How $NWBO #DCVax Lineage and the #SITC2025 αDC1 Breakthrough Solved Immunotherapy’s Bottleneck ⚡️ TLDR At the 2025 Society for Immunotherapy of Cancer (SITC), researchers led by Pawel Kalinski un
@andrewcaravello @alphavestcap $NWBO #DCVax runs on the exact mechanism this post is describing. The whole-body response from one local shot is not luck. It is the principle behind Pawel Kalinski’s αDC1, the
@alphavestcap
DEAR CLAUDE ANTHROPIC:IS THERE ANY OTHER DENDRITIC CALL CANCER IMMUNOTHERAPY AS EFFECTIVE AS DC VAX L AT PREVENTING GBM TUMOR GROWTH RECURRENCE ? BRAELYN HOLLANSBEE HAD HER GBM TUMOR RESECTED BY DR.LIAU AT UCLA IN MARCH, 2026. SINCE THEN SHE HAS HAS 4 MRIs SHOWING HER TO BE CANCER FREE, WITH NO GBM TUMOR GROWTH RECURRENCE."If I'm not mistaken, Braelyn received her first dose of DCVax-L on July 22. Within about a month, after three doses, an intense anti-tumor immune response already wiped out the remaining unresected 10% of tumor tissue. The vaccine was made from her own tumor tissue, so it was a genetic match and that is why it cannot be toxic. More importantly, the DCs presenting hundreds of tumor-associated peptides on MHC Class II engage CD4 T-cells, which are essential for building immune memory. Once that memory is established, the risk of recurrence can drop dramatically. It's hard to imagine a better treatment than this — which may be exactly why approval has taken so long!"
@alphavestcap
. .
When you look at how modern immunotherapy actually works, $NWBO#DCVax is the only platform that addresses the full biology of solid tumors. Other approaches focus on one slice of the problem — stimulating NK cells, removing a checkpoint, inflaming a tissue, or adding a cytokine. DCVax is the only one that fixes the upstream failure that makes cancer invisible in the first place: the collapse of antigen recognition. And once you understand that, the IL-7 versus IL-15 question becomes central, because you cannot build durable tumor-specific immunity unless the underlying T-cell architecture is healthy. IL-7 does not behave the way you described, especially not in humans and especially not with RevImmune’s clinical-grade IL-7 (CYT107). The idea that IL-7 “expands everything” or behaves erratically mostly comes from engineered mouse models that do not reflect human immunology. In human trials — HIV, post-sepsis, post-chemotherapy, radiation injury, and bone-marrow failure — IL-7 reliably expands exactly the compartments the immune system needs to rebuild: naïve CD4, naïve CD8, central memory populations, and NK precursors. It improves T-cell receptor diversity, reduces exhaustion markers, preserves stem-like T cells, and repairs the immune architecture that chronic disease and cytotoxic therapy damage. And the safety signal is extremely consistent: IL-7 does all of this without autoimmune flares. If IL-7 were really expanding harmful clones, the NIH and NIAID trials would have shown it. They didn’t. RevImmune’s IL-7 (CYT107) is designed specifically for durable immune reconstruction. Their patents cover long-acting, controlled-release, and depot strategies that support sustained restoration — not short-lived inflation. That is why CYT107 is used in federally run immune-reconstitution programs: it behaves in humans as a stable, physiologic rebuilding signal. On durability: the only setting where IL-7 looks transient is in aged primates with nonfunctional thymus tissue, a model where nothing can regenerate. Humans — even older adults — retain measurable thymic output. And in modern IL-7 trials, CD4 and CD8 levels remain elevated for months to years because IL-7 expands both circulating populations and the progenitor pools that maintain them. Now compare that to IL-15. IL-15 produces a sharp, temporary burst of NK and CD8 activation and then falls off as those cells become less responsive to the signal. That exhaustion pattern appears with ALT-803, recombinant IL-15, and every IL-15 superagonist tested. IL-15 is stimulation, not reconstruction. It does not rebuild immune compartments. It does not support memory. It does not restore the architecture needed for long-term tumor control. And this matters when you talk about pairing a cytokine with DCVax. DCVax depends on a T-cell ecosystem that can form long-term, tumor-specific memory and tissue residency. That requires actual rebuilding, not a momentary surge. IL-7 is the cytokine that accomplishes that. IL-15 isn’t. That is why CYT107 is being tested in exactly the settings where durable immunity needs to be restored, not temporarily inflated. If IL-15 ever plays a role as a minor adjunct, DCVax’s combination patents already cover IL-15 in any form — recombinant, generic, or branded — but the biology rarely justifies using it because properly primed dendritic cells naturally provide localized IL-15 trans-presentation at the immune synapse. So here are the facts: IL-7 rebuilds the immune foundation. IL-15 produces a spike and fades. CYT107 is engineered for long-term reconstruction. DCVax requires durable, tumor-specific memory. IL-7 enables that. IL-15 doesn’t. This isn’t speculation. This is what human data show over and over again. And this is why DCVax stands alone — not as another stimulant, but as the platform that actually fixes recognition, rebuilding the only architecture that matters for long-term control of solid tumors.10:46 AM · Nov 30, 2025·Views183
"If I'm not mistaken, Braelyn received her first dose of DCVax-L on July 22. Within about a month, after three doses, an intense anti-tumor immune response already wiped out the remaining unresected 10% of tumor tissue. The vaccine was made from her own tumor tissue, so it was a genetic match and that is why it cannot be toxic. More importantly, the DCs presenting hundreds of tumor-associated peptides on MHC Class II engage CD4 T-cells, which are essential for building immune memory. Once that memory is established, the risk of recurrence can drop dramatically. It's hard to imagine a better treatment than this — which may be exactly why approval has taken so long!"
. .
When you look at how modern immunotherapy actually works, $NWBO#DCVax is the only platform that addresses the full biology of solid tumors. Other approaches focus on one slice of the problem — stimulating NK cells, removing a checkpoint, inflaming a tissue, or adding a cytokine. DCVax is the only one that fixes the upstream failure that makes cancer invisible in the first place: the collapse of antigen recognition. And once you understand that, the IL-7 versus IL-15 question becomes central, because you cannot build durable tumor-specific immunity unless the underlying T-cell architecture is healthy. IL-7 does not behave the way you described, especially not in humans and especially not with RevImmune’s clinical-grade IL-7 (CYT107). The idea that IL-7 “expands everything” or behaves erratically mostly comes from engineered mouse models that do not reflect human immunology. In human trials — HIV, post-sepsis, post-chemotherapy, radiation injury, and bone-marrow failure — IL-7 reliably expands exactly the compartments the immune system needs to rebuild: naïve CD4, naïve CD8, central memory populations, and NK precursors. It improves T-cell receptor diversity, reduces exhaustion markers, preserves stem-like T cells, and repairs the immune architecture that chronic disease and cytotoxic therapy damage. And the safety signal is extremely consistent: IL-7 does all of this without autoimmune flares. If IL-7 were really expanding harmful clones, the NIH and NIAID trials would have shown it. They didn’t. RevImmune’s IL-7 (CYT107) is designed specifically for durable immune reconstruction. Their patents cover long-acting, controlled-release, and depot strategies that support sustained restoration — not short-lived inflation. That is why CYT107 is used in federally run immune-reconstitution programs: it behaves in humans as a stable, physiologic rebuilding signal. On durability: the only setting where IL-7 looks transient is in aged primates with nonfunctional thymus tissue, a model where nothing can regenerate. Humans — even older adults — retain measurable thymic output. And in modern IL-7 trials, CD4 and CD8 levels remain elevated for months to years because IL-7 expands both circulating populations and the progenitor pools that maintain them. Now compare that to IL-15. IL-15 produces a sharp, temporary burst of NK and CD8 activation and then falls off as those cells become less responsive to the signal. That exhaustion pattern appears with ALT-803, recombinant IL-15, and every IL-15 superagonist tested. IL-15 is stimulation, not reconstruction. It does not rebuild immune compartments. It does not support memory. It does not restore the architecture needed for long-term tumor control. And this matters when you talk about pairing a cytokine with DCVax. DCVax depends on a T-cell ecosystem that can form long-term, tumor-specific memory and tissue residency. That requires actual rebuilding, not a momentary surge. IL-7 is the cytokine that accomplishes that. IL-15 isn’t. That is why CYT107 is being tested in exactly the settings where durable immunity needs to be restored, not temporarily inflated. If IL-15 ever plays a role as a minor adjunct, DCVax’s combination patents already cover IL-15 in any form — recombinant, generic, or branded — but the biology rarely justifies using it because properly primed dendritic cells naturally provide localized IL-15 trans-presentation at the immune synapse. So here are the facts: IL-7 rebuilds the immune foundation. IL-15 produces a spike and fades. CYT107 is engineered for long-term reconstruction. DCVax requires durable, tumor-specific memory. IL-7 enables that. IL-15 doesn’t. This isn’t speculation. This is what human data show over and over again. And this is why DCVax stands alone — not as another stimulant, but as the platform that actually fixes recognition, rebuilding the only architecture that matters for long-term control of solid tumors.10:46 AM · Nov 30, 2025·Views183
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Thanks
@andrewcaravello
for another great post!
IL-7 as the master regulator of immune system is absolutely amazing. We have seen the stunning efficacy from a trial on using DC vaccine in combination with IL-7 to treat rare pediatric sarcomas. Did Martin Cheever mention in the paper published the beginning of this year that IL-7 can significantly increase the number of stem cell-like memory T (Tscm) cells vital for long-term immune memory?
aacrjournals.org/clincancerres/…
aacrjournals.org/clincancerres/…
It's exciting to see researchers at Moffitt Cancer Center is including IL-7 in a trial. They even gave the trial a great name: NATASHA.
clinicaltrials.gov/study/NCT05378…
The preliminary results from the trial are absolutely phenomenal. I am really surprised no media was covering it. Seven out of 11 patients had pathologic complete response. We are talking about stage IV cancer patients here.
DCs were pulsed with the antigen HER2 and the vaccine was injected intratumorally into tumor. Here is the amazing part. All HER2 negative patients had pathologic complete response! The $NWBO longs should open a champagne for this trial.
Short answer: No other dendritic cell therapy has shown better results than DCVax-L for glioblastoma (GBM), but that is because none has been proven to work. DCVax-L’s own evidence is also less settled than the posts you pasted suggest.
How DCVax-L compares with other dendritic cell vaccines for GBM
DCVax-L: The Phase III trial enrolled 331 patients and was published in JAMA Oncology in 2022. Northwest Biotherapeutics has submitted a marketing application to the UK’s MHRA, which is still under review. It has no approval anywhere yet. I could not confirm a decision as of the latest sources I found. nwbio
AV-GBM-1 (AIVITA): This is the closest competitor. A Phase II study reported a median progression-free survival of 10 months, compared with 6.9 months in the landmark trial that set the standard of care. That comparison is against historical data, not a control group. A randomized, double-blind Phase III trial has been registered but was listed as not yet enrolling, so it has not produced any results. healioveeva
Other dendritic cell vaccines have been tested mostly in small or early trials. None has produced a randomized result that clearly beats DCVax-L.
Why “as effective” is hard to answer
The DCVax-L trial’s headline survival comparison used an external control group built from other trials, because patients in the trial could cross over to the vaccine after progression. Many oncologists have criticized that design. It is not the same as a clean randomized win.
The 5-year survival figures quoted in the posts (13% vs 5.7%) come from that comparison. They are suggestive but not definitive.
Regulators have not yet ruled on whether the data are enough, which is why approval is still pending.
About Braelyn’s case
I’m glad she has had four clear MRIs. But one patient’s course cannot show that a treatment prevented recurrence. GBM is almost always treated with surgery, radiation and chemotherapy, and some patients do well for a period regardless. The claims that the vaccine “wiped out the remaining 10% of the tumor” and that “the risk of recurrence can drop dramatically” are the poster’s interpretation, not established fact. “It cannot be toxic” is also too strong. DCVax-L has had a good safety profile in trials, but no cancer treatment can be called incapable of toxicity.
A note on the documents you shared
The posts are written by NWBO investors. They contain real science (αDC1 biology, the SITC abstract, the IL-7 trials), but they mix preclinical results, small early trials and company plans, and they state things as settled that are not. Examples are “the only platform that addresses the full biology of solid tumors,” “IL-15 spikes and fades,” and “DCVax stands alone.” The Moffitt NATASHA trial (7 of 11 pathologic complete responses) is a small early trial in breast cancer, not GBM, and does not tell us how DCVax-L performs. These are not medical or investment conclusions.
If you or someone you know is considering treatment, I’d suggest asking a neuro-oncologist about clinical trials, including the AIVITA trial and any DCVax-L access options. I’m not a doctor, and this is not medical advice. Would you like me to go through the DCVax-L Phase III design and its criticisms in more detail?
❤️🙏 ANOTHER MRI. ANOTHER ANSWERED PRAYER!View quoted post on X
NO EVIDENCE OF DISEASE!!! 🎉❤️
Today, Braelyn had another brain MRI, and I am absolutely OVERJOYED to share that it once again showed NO EVIDENCE OF DISEASE!
NO CHANGE from her August MRI!
And just FOUR DAYS AGO, on Friday, November 6, Braelyn received her 5th DCVax-L treatment in London! 🇬🇧
I cannot begin to describe the emotions.
After more than three years of fighting this devastating brain cancer, three major brain tumor surgeries, radiation, countless treatments, and more fear than I ever imagined a mother could endure, we are now celebrating another MRI showing NO EVIDENCE OF DISEASE!
I wish I could tell you that the scanxiety gets easier. But it doesn’t. At least not for me.
Every MRI brings back the memories of devastating scans, heartbreaking news, and the terrifying uncertainty of what might come next.
I still find myself holding my breath, praying desperately for those words.
And today, we heard them again.
NO EVIDENCE OF DISEASE. ❤️🙏
My heart is overflowing with gratitude.
To every single person who has prayed for Braelyn, supported our family, donated to help make her treatments possible, shared her story, or simply sent us words of encouragement—THANK YOU!
You have helped carry us through the darkest days of our lives, and you are now helping us celebrate some of the brightest.
And to Northwest Biotherapeutics ($NWBO), the brilliant Dr. Linda Liau at UCLA, and the extraordinary Professor Keyoumars Ashkan at King’s College Hospital—there are simply no words adequate to express our gratitude.
Thank you for your dedication, your compassion, and your determination to bring new hope to patients facing this devastating disease.
Braelyn is 19 years old. She’s attending college. She’s dreaming about her future.
And today, once again, her MRI shows NO EVIDENCE OF DISEASE!
GOD IS GOOD! ❤️🙏
#DCVax #BrainCancer #BraelynsFight #NoEvidenceOfDisease
#DCvaxForBraelyn
$nwbo @alphavestcapView quoted post on X
@andrewcaravello
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$nwbo @alphavestcap, in a regimen built entirely around the immune response with no chemotherapy or radiation in it at all. Its interim survival curve shows the shape the biology predicts. In the arm given the vaccine and Keytruda together after surgery, the curve does not fall away but flattens into a plateau, with roughly 65% of patients still alive well past the point where recurrent glioblastoma kills nearly everyone. That plateau is the signature of a response that took hold and lasted, the type 1 attack forming durable immune memory so that once the disease is controlled it stays controlled. That is where this points, and where it is already arriving, a treatment that works through the response itself, one that could in time lean less on the harsh radiation and chemotherapy that have defined glioblastoma care and barely moved its survival. These are interim results, from Prins, Cloughesy, and Liau at UCLA. PART TWO: IS IT REAL? The trial was randomized, an independent experiment shows the outside comparison is trustworthy, and every separate check points the same way. The objection, and why it misses the mark So much for what happened; the harder question is whether to believe it. The trial has the feature critics attacked: it could not keep a normal placebo group, because patients assigned to placebo were allowed, by design and by medical ethics, to switch to the vaccine once their cancer returned, and almost all did. That erased the internal comparison, so survival was measured against closely matched patients from other completed trials, an approach called an external control, which critics argued could tilt toward the vaccine. What the objection misses is where the randomization went. This was a randomized, blinded trial. The patients who got the vaccine were assigned to it at random, not hand-picked, so the treated group is an ordinary slice of the trial population, not a favorable one. The crossover removed the placebo group but never touched how patients were assigned. That leaves exactly one place for bias to enter, the outside comparison group, which is precisely what the next checks test. The check that makes it trustworthy Before trusting a scale to weigh something unknown, you confirm it reads zero with nothing on it. That is what the calibration does, and it is the strongest part of the case. A separate, independent randomized trial called INSIGhT was run through the very same external-control method, and it gave two answers. First, three experimental drugs that had already failed were run through it, and it correctly found nothing (hazard ratios of 1.00, 0.93, and 0.88): the method does not manufacture a benefit where none exists. Second, INSIGhT's external controls were set head to head against its own randomized internal controls, and they were statistically indistinguishable. In this disease, an external control reproduces the answer a real randomized control would have given, and because that trial belonged to a different group, no one can say a sponsor graded its own work. The one place bias could enter, the control side, is the one place an independent randomized experiment certified as clean. There is a deeper fit worth naming, and it is what makes the two halves of this case one. The same instrument that reported those three failures as failures reads the vaccine as a success, and the biology says why: those drugs could not hold a tumor this varied, and the vaccine builds the broad, lasting response that finally does. One method, opposite readings, and one mechanism behind both. The statistics and the biology are not two arguments. They are the same argument seen twice. Was the comparison stacked in the vaccine's factor? A natural worry is that the outside comparison was arranged after the fact to flatter the vaccine. The trial was built to prevent that. The patients to compare against, and the rules for matching them, were fixed in writing before anyone saw results, and an independent firm, not the company, chose the comparison trials against those rules. The trial also switched its main measure partway through, from delaying tumor growth to overall survival, but that was not a maneuver: immune treatments cause a harmless swelling that mimics tumor growth on scans and made the growth measure unreliable, and the switch was made while everyone was still blinded. Three further checks point the same way. Survival in this disease has not improved over the years the comparison spans, so same-era controls are sound. When the borrowed controls were tested directly, the comparison came out conservative rather than flattering. And the controls were counted from the same point in the disease as the vaccine patients, so neither side got a head start. Where the comparison can err, it errs against the drug. The more careful analysis made the benefit bigger, not smaller The first comparison used whole groups. A sharper one became possible once patient-level records from three other trials could be obtained, pairing each vaccine patient with controls matched on the traits that drive survival in glioblastoma, above all MGMT methylation status, matched exactly, plus age, sex, extent of surgery, residual disease, and performance status. When the comparison got sharper, the benefit grew in every one of these analyses. The original cohort-level estimate was 2.8 months. Patient-level matching across the three trials put the gain between 3.4 and 6.3 months, and a method that weights patients rather than pairing them put it between 3.4 and 4.3, with several of the matched comparisons roughly doubling the original figure. The hazard ratio moved the same way, from 0.80 to between 0.69 and 0.77. The direction matters. A real effect blurred by crude matching gets clearer when the matching improves, while a biased one tends to shrink. It got stronger. How much hidden bias would it take to explain this away A fair question is how much hidden bias it would take to erase the result. Statisticians measure that with the E-value, and here a hidden factor would have to be about as strong as age is on survival, would also have to drive who received the vaccine, and would have to have escaped the decades of research that mapped every known risk factor in this disease. A second, independent check, Rosenbaum's Gamma, comes at it from the other side, asking how large an unseen imbalance between matched patients it would take to break the result, and it reaches the same verdict. Every factor strong enough to matter was already matched. A hidden one that clears that bar is not plausible. Why the result is hard to fake The strongest point is not any single result. It is that a hidden bias big enough to explain the effect away would have to produce the same answer in every independent test at once: • The independent randomized calibration trial. • Three separate comparison trials, drawn from different studies. • Two different statistical methods that handle the data in different ways. • A separate pooled analysis of other dendritic-cell vaccine trials. • The internal math of the survival curve, which points to the same result (about 0.71 at five years) that the patient matching found. And it would have to fall in the exact direction the biology predicted before any data existed: a slow, widening benefit concentrated in long-term survivors. A single hidden factor that could forge all of that at once is not a hidden factor. It is a coincidence that does not happen. PART THREE: WHAT IT MEANS The drug is nearly free of harm, the evidence fits an established and approved regulatory path, and what remains unrun changes nothing about the case. The safety Two things decide whether a real effect reaches patients: whether the drug is safe enough to use, and whether regulators will accept the evidence. The first is settled. Across 2,151 doses, only five serious side effects were even possibly related to the vaccine, with no autoimmunity and no cytokine storm. It is made once, in about eight days, then stored and given as a simple injection. When a treatment barely harms, the benefit needed to justify it falls, and the benefit here clears that lower bar easily. Why the stronger data appeared only now A reasonable person asks why the sharper analysis appeared in 2026 and not in 2023. The answer is access, not choice. The patient-level analysis was written into the trial's plan from the start, to run if and when the data could be obtained. The company tried and could not get it in 2023, because the trials that held it had not released it; it became available later through a data-sharing repository, on the data owners' timeline, not the company's. The stronger analysis was always the plan. It was waiting on data that other parties control. Patients whose cancer returned also benefited The vaccine helped not only newly diagnosed patients but also those whose tumor had already come back, and there the effect was the largest seen anywhere in the trial. In that group, median survival ran 13.2 months from recurrence against 7.8 for the controls. The separation opened immediately, with 90.6% of vaccine patients alive at six months against 64.0% of controls, and the lead held to the later marks, where survival more than doubled: 20.7% against 9.6% at two years, 11.1% against 5.1% at two and a half. These are the original cohort-level results, already published. The high-resolution patient-level matching that was applied to the newly diagnosed group has not yet been done here, for a practical reason: it needs patient records from other recurrent-cancer trials, held by a European research organization that shares them through its own formal request. Obtaining them is a routine next step, not an obstacle, and the newly diagnosed experience suggests the sharper analysis would only make the recurrent result stronger. The approval case rests on the newly diagnosed evidence, so nothing important depends on this step; it would simply sharpen a result that is already the strongest in the trial. What this means for approval Regulators do not treat an external control as a first choice, but the MHRA's guideline allows it in exactly this situation: a severe disease where a placebo trial is not ethical or feasible, and an effect large enough to interpret despite the design. The guideline even gives its own worked example of an acceptable external control, and it reads almost like a description of this trial: a rare disease, no ethical placebo, same-era standard-of-care controls, an objective survival endpoint, and an effect too large to blame on bias. DCVax-L fits on every count, and it was the first medicine ever to receive the MHRA's Promising Innovative Medicine designation, which asks essentially the same questions. The newly diagnosed case carries the decision on its own evidence, and regulators weigh that evidence against the disease it treats: in a cancer this lethal, with nothing better on offer, the question is whether the benefit is large, clear, and consistent enough to act on, and a benefit of this size, pointing the same way from every direction, is. This has been done before, and approved External controls are not a novelty invented for this drug. Over the past two decades they have factored into roughly forty-five drug approvals by the United States regulator, each granted under the conditions that apply here: a serious or rare disease, a placebo that would be unethical, and high unmet need. Regulators do not grant this lightly. They grant it when the disease is serious, its course is predictable and objectively measured, and the effect is large. Glioblastoma meets all three. The named cases cover every part of this disease's profile. Defibrotide, for a life-threatening transplant complication, was approved on a propensity-score comparison to a historical control, the same kind of method used here. Blinatumomab, for an aggressive relapsed leukemia, is the precedent for a fast-killing cancer, cleared by both the United States and European regulators. Cerliponase alfa is the precedent for a fatal brain disease, cleared by both agencies on treated patients versus a matched natural-history group. Glioblastoma is both at once, a fast-killing cancer of the brain, read by the same method, so no part of its profile lacks a close approved precedent. And on the one axis that governs how far an external-control result can be trusted, DCVax-L goes beyond all three. Each of those drugs was tested in a single-arm trial, with no randomization at all. DCVax-L began as a randomized trial and became an external-control comparison only when ethics consumed its placebo group. It sits in that tradition, and at the top of it. The bottom line This began as a randomized trial. Medical ethics forced it into an external-control comparison. Every independent way of checking it, on different data and different math, points the same direction, and the biology predicted that direction in advance. The first analysis did not overstate the vaccine's effect. Read with the right tools, it understated it. 2)flipper44 Re: DocLee post# 832491 Saturday, July 04, 2026 7:21:40 PM Post# of 832528 I think MHRA worked through this data quite some time ago. I tell people to refer back to the ASM, but here, let me show you the quote again, and remember during this time, both before and after, I had been stating NWBO may in fact be trying to accumulate/review patient level data. December 29, 2025. (When this weekend’s propensity data would have been in the thick of review, regarding three different scientific models.) Linda Powers. The first thing I can say, and it’s quite important, is that we are really, really gratified by how much work and how much resources the agency is devoting to our case. They’re doing an enormous amount of work on our case, inspections and analyses and so forth. And our advisors have commented on this too, and have expressed to us that they are impressed with the amount of resources being devoted.GoodGuyBill $nwbo@alphavestcap, July 04, 2026 9:24 1)Here's a post by Andrew Caravello, DO (@andrewcaravello) that explains Bosch's PSM analysis better than anyone else. $NWBO DCVax-L: The evidence in Plain Terms A short, plain-language reading of the survival evidence for DCVax-L in #glioblastoma, and what it means under the@MHRAgovukguideline on external control arms. PART ONE: WHAT THE TRIAL FOUND AND WHY IT MATTERS DCVax-L more than doubled five-year survival, and the benefit is durability: a subset gets lasting disease control and simply stays alive. What the drug is DCVax-L is a personalized cancer vaccine for glioblastoma, the deadliest form of brain cancer and a designated orphan disease. It is a living drug: its active ingredient is the patient's own immune cells, primed with proteins from that patient's surgically removed tumor, so the immune system learns to attack the cancer. Unlike a chemical drug that is metabolized and cleared, it switches on a living immune response that keeps working long after the injection. Glioblastoma comes back in almost everyone: even with the full standard of surgery, radiation, and temozolomide chemotherapy, most patients live under two years, and only about one in twenty reaches five. DCVax-L is given on top of that standard care, not in place of it: every patient in the trial received surgery, radiation, and temozolomide, and the vaccine was added to it, so the comparison measures what the vaccine adds. For two decades, nearly every new drug tried in this disease has failed. That is the backdrop against which any positive result must be judged. What the trial found In a Phase 3 trial of 331 patients, those who received DCVax-L lived longer. At the median the gain looks modest, about three months (19.3 versus 16.5). The number that matters sits at the far end of the survival curve: more than twice as many vaccine patients were alive at five years, 13.0% versus 5.7%, and a few reached ten years in a disease that usually kills within three. In patients whose tumor had already returned, the effect was larger still, cutting the risk of death by about 42%. Every group benefited, even the hardest to treat The benefit was not confined to the easy cases. Of the six prespecified subgroups the trial examined, every single one favored DCVax-L, and there was no group in which it did worse than standard care. The largest gains came in patients whose tumors carry MGMT methylation, who reached a median survival of 30.2 months from randomization against 21.3 for the controls. But even the hardest-to-treat patients, whose tumors lack that methylation, resist standard chemotherapy, and carry the worst prognosis in this disease, still came out ahead with the vaccine, at a hazard ratio of 0.93. A treatment that helps across the whole population, and helps most where the biology is most favorable, is acting like a real drug. Why the median hides the real story That five-year number is the whole story, and the median buries it. Almost every treatment that ever helped in glioblastoma did the same modest thing: it slid the survival curve a few months to the right, then let it fall back. Doubling five-year survival is different in kind. A three-month gain at the median cannot, by itself, double the fraction alive at five years. The only shape that produces both numbers is a split: most patients get the small delay the median measures, while a subset gets durable disease control that lasts for years, well past where glioblastoma should have ended them. That subset is the long tail of the curve, and it is where the benefit lives. A median ignores extremes, the way a town's median income tells you nothing about its millionaires. The real story is not a longer delay; it is that a meaningful share of patients simply stay alive. Why the biology predicts this shape The tail is not luck. It is what this biology is built to produce. The vaccine carries proteins from the patient's own tumor, so it aims the immune system at whatever that tumor is made of, not a fixed short list of targets. And it amplifies: one trained immune cell drives many others that multiply into cancer-killers. Andres Salazar, the neurologist who developed poly-ICLC into the clinical adjuvant given with the vaccine, puts it in a line: you start the fire, and you keep it burning. A response like that does not produce a one-time bump. It builds and widens over time. What matters is not just that a response forms, but what kind. Dendritic cells are the immune system's master switch for that, the cells that set what kind of attack the body mounts, and this vaccine is built from them. It drives what immunologists call a type 1 polarized response: an interferon-driven, cytotoxic program aimed squarely at the tumor. That direction comes from the vaccine itself; the poly-ICLC adjuvant given with it drives the same interferon program and sustains it. That is the active ingredient, and it has been measured. In UCLA studies of this approach, the patients whose immune systems mounted the strongest interferon response lived the longest. The response also spreads. In a different cancer, a vaccine carried on this same poly-ICLC adjuvant drove more than 70% of a patient's cancer-killing T cells to target proteins that were never in the vaccine: the immune system outgrew its original targets and went after the rest of the tumor on its own. This is called epitope spreading, and it is not particular to one tumor; it is what this kind of response does, and it is the kind of response DCVax-L builds. That breadth is the likeliest thing separating the long-term survivors from everyone else, a response that breaks past its targets and clears the disease rather than one that stays caged and stops. There is even a tell in who benefits most: the effect is largest in tumors whose biology builds up more mutations under chemotherapy, and more mutations mean more targets for a whole-tumor vaccine to find. The same logic explains what the vaccine is not, and what it does not need. Checkpoint inhibitors, the drugs that release the immune system's brakes, have failed on their own in glioblastoma because there was no active response to release; the vaccine supplies that response first. That makes the vaccine the natural foundation for combination therapy. Combining it with its poly-ICLC adjuvant, made by Oncovir, has already shown meaningful survival gains in a published analysis. In the pivotal trial, the vaccine's proven benefit came added on top of standard chemotherapy and radiation; the newer question is how much the immune response can carry on its own. A UCLA trial is now testing that in patients whose tumors have returned, adding #Keytruda (pembrolizumab), the checkpoint antibody from$MRK ViewsLast edited10:49 PM · Jul 4, 2026·2,351
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@andrewcaravelloView quoted post on X
@alphavestcap. .
When you look at how modern immunotherapy actually works, $NWBO #DCVax is the only platform that addresses the full biology of solid tumors. Other approaches focus on one slice of the problem — stimulating NK cells, removing a checkpoint, inflaming a tissue, or adding a cytokine. DCVax is the only one that fixes the upstream failure that makes cancer invisible in the first place: the collapse of antigen recognition. And once you understand that, the IL-7 versus IL-15 question becomes central, because you cannot build durable tumor-specific immunity unless the underlying T-cell architecture is healthy. IL-7 does not behave the way you described, especially not in humans and especially not with RevImmune’s clinical-grade IL-7 (CYT107). The idea that IL-7 “expands everything” or behaves erratically mostly comes from engineered mouse models that do not reflect human immunology. In human trials — HIV, post-sepsis, post-chemotherapy, radiation injury, and bone-marrow failure — IL-7 reliably expands exactly the compartments the immune system needs to rebuild: naïve CD4, naïve CD8, central memory populations, and NK precursors. It improves T-cell receptor diversity, reduces exhaustion markers, preserves stem-like T cells, and repairs the immune architecture that chronic disease and cytotoxic therapy damage. And the safety signal is extremely consistent: IL-7 does all of this without autoimmune flares. If IL-7 were really expanding harmful clones, the NIH and NIAID trials would have shown it. They didn’t. RevImmune’s IL-7 (CYT107) is designed specifically for durable immune reconstruction. Their patents cover long-acting, controlled-release, and depot strategies that support sustained restoration — not short-lived inflation. That is why CYT107 is used in federally run immune-reconstitution programs: it behaves in humans as a stable, physiologic rebuilding signal. On durability: the only setting where IL-7 looks transient is in aged primates with nonfunctional thymus tissue, a model where nothing can regenerate. Humans — even older adults — retain measurable thymic output. And in modern IL-7 trials, CD4 and CD8 levels remain elevated for months to years because IL-7 expands both circulating populations and the progenitor pools that maintain them. Now compare that to IL-15. IL-15 produces a sharp, temporary burst of NK and CD8 activation and then falls off as those cells become less responsive to the signal. That exhaustion pattern appears with ALT-803, recombinant IL-15, and every IL-15 superagonist tested. IL-15 is stimulation, not reconstruction. It does not rebuild immune compartments. It does not support memory. It does not restore the architecture needed for long-term tumor control. And this matters when you talk about pairing a cytokine with DCVax. DCVax depends on a T-cell ecosystem that can form long-term, tumor-specific memory and tissue residency. That requires actual rebuilding, not a momentary surge. IL-7 is the cytokine that accomplishes that. IL-15 isn’t. That is why CYT107 is being tested in exactly the settings where durable immunity needs to be restored, not temporarily inflated. If IL-15 ever plays a role as a minor adjunct, DCVax’s combination patents already cover IL-15 in any form — recombinant, generic, or branded — but the biology rarely justifies using it because properly primed dendritic cells naturally provide localized IL-15 trans-presentation at the immune synapse. So here are the facts: IL-7 rebuilds the immune foundation. IL-15 produces a spike and fades. CYT107 is engineered for long-term reconstruction. DCVax requires durable, tumor-specific memory. IL-7 enables that. IL-15 doesn’t. This isn’t speculation. This is what human data show over and over again. And this is why DCVax stands alone — not as another stimulant, but as the platform that actually fixes recognition, rebuilding the only architecture that matters for long-term control of solid tumors.10:46 AM · Nov 30, 2025·Views183