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That is old fried rice from Catherine Wu bio bought with uncle sam welfare handout
ICE that does ADCP has value. AFM 13 mono had >75% response on AITL/PTCL. No HPD as in NIVO.
Too many high paid spoiled PhDs. Too much CART competition. Bios can no longer print money. Many already died. Many will
CAR NK looks like CART. What is the point? NK should behave like a termite. It is for the war of attrition.
NK is a slow cooker looking at MDACC data. It takes a lot of convincing before it starts killing, unlike CART. None has died on auto and allo NK as many claimed.
CSO left. Worse significant antigen expression decrease after CAR T-cell therapy
https://onlinelibrary.wiley.com/doi/epdf/10.1111/his.14910
CD123 is found in CSCs, which are not effectively eliminated by chemotherapy, have the capacity to self-renew, and are capable recapitulating disease. Thus, approaches to target are highly sought and have been tested in preclinical and clinical settings.
CD123 is found in CSCs, which are not effectively eliminated by chemotherapy, have the capacity to self-renew, and are capable recapitulating disease. Thus, approaches to target are highly sought and have been tested in preclinical and clinical settings.
It will be delayed in May. CART is too toxic for CART relapsed pts.
Have you seen any tumor biopsy studies comparing T cell counts baseline and post atezolizumab IV or other PD1 mAbs?
Have you seen this in gene modified NK cells study?
From AFM13 study, Shedding actually allowed NK cells performing three or more kills in sequence, including cells expressing low levels of CD30
19A, B kept alive so many PhDs can draw a paycheck. 4/4 CR for CART relapsed pts. in AFM13 MDACC trial. No CRS, death....NK is the future IMO
The update will be under the rug.
This CART is great, targeting is still a big issue. GD2 for NB?
local secretion of the CD47 inhibitor bypasses the CD47 sink found on all cells in the body and should prevent systemic toxicities. This combination of CAR T cell therapy, local CD47 blockade, and orthogonal antibody may be a strategy to overcome the limitations of tumor antigen loss and heterogeneity and immunosuppression of the CAR T cell.
https://pipelinereview.com/index.php/2023020382612/DNA-RNA-and-Cells/CoImmune-Announces-Novel-Engineered-CAR-T-Cells-Improve-Anti-Tumor-Activity-and-Reverse-Immunosuppression-in-Preclinical-Models.html
CART, NK need partners that target the hypoxic TME. Low dose VEGF + eganelisib for a few weeks will make the TME livable before administrating the edited cells. I prefer CBNK +ICE +PD1 and no LD.
I think all NK cells need a ICE like AFM-24.
Since the BCMA, CD19 space are too crowded, most ACT bios will fail unless they can figure out how to get pass the TAM in solid cancers TME. Higher and higher CART counts will be more and more toxic as the target is far from perfect.
Turning TAM into a trojan horse is way better than any CART.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9589917/
oc631, since China is refusing free mRNA shots from the west, we will know if CCP is smarter than FDA. Many fact checkers have brushed off the Africa experience, it will be hard to ignore 1 billion pts study.
FYI cardiac symptoms is only one issue. The British cardiologist who used to back vaccine changed his mind because his dad died from cancer hyperprogression after getting vaxxed. Is it caused by T cell exhaustion? who knows? It is another risk/reward balancing act for everyone.
You are fair and balanced. The problem is the strategy needs to change. The limitless covid variants created by these antibodies in people are unpredictable. In northern china, the circulating variant is a lot more virulent than omicron. USA needs antivirals to stop the transmission and the rampant creation of new variants now.
That is funny. Both virus and the mRNA create spike proteins in the infected. Every vax or natural infection add more harmful proteins that increase blood clots and risk of cardiac arrest. Why everyone is so eager to have spike proteins circulating in their blood is beyond me.
763 (17.1%) had at least one cardiac symptom after the second vaccine dose.
After the first dose, 209 (5.7%) had at least one cardiac symptom
Bios like ENTA should be paid with tax $ to come up with antivirals. Anyway no need to get excited over a few questions posted for DD. Everyone is entitled to have a different take on how well FDA/CDC, mRNA have performed.
Conspiracy always buckle. Hard data won't. FDA reputation will be shredded to pieces by the damages done to the kids around the world.
763 students (17.1%) had at least one cardiac symptom after the second vaccine dose, mostly chest pain and palpitations.
https://pubmed.ncbi.nlm.nih.gov/36602621/
Just look at all the healthy mice treated by Pfizer bivalent.
No. Don't get me wrong. I respect ENTA prowess to develop antivirals. I just don't trust this FDA anymore. Look at the way they treated NVAX, they probably will put up a few road blocks for ENTA. I am sure the former FDA commissioner will want to protect Pfizer's sales with all the strings he can pull.
What is ENTA strategy? Get EDP-235 approved for the unvaxxed 65 yr. old who are in pretty good shape? EDP-235 will be Paxlovid - ritonavir.
I wish ENTA would run another P2 to recruit any non-hospitalized adult with mild or moderate COVID-19 and symptom onset within 5 days who have been vaccinated > 3 months. The current P2 will leave many questions unanswered.
I pray E-235 will stop transmission. Why ENTA is recruiting unvaxxed who might have developed natural immunity in the P2 only? Looks like they are picking pts who are in pretty good shape.
Non-hospitalized adults with mild or moderate COVID-19 and symptom onset within 5 days, who are not at increased risk for developing severe disease and have not been vaccinated or infected with SARS-CoV-2 less than 90 days of enrollment
Albumin carrying 2 small molecules turning M2 in TME into M1 is coming. mAbs have trouble getting thru. the stroma and the immuno suppressive cloud. None have worked so far after billions spent. T cells also face the same issues no matter how many gene edits and source IPSC.
Looks like changing M2 to M1 with a high dose small molecule + anti-PD1 will be enough. Unleashing trojan horses inside the fortress is the best strategy.
Our finding that glioblastoma cells leveraged cellular constituents in their microenvironment to protect themselves from the deleterious effects of cancer therapeutics is reminiscent of
findings reported in breast and ovarian cancer, where the percentage of stromal cells in the clinical specimen prognosticated survival after systemic therapy
https://www.pnas.org/doi/pdf/10.1073/pnas.2009290118
No TAM flipper or TME drug will show single agent activity in late stage pts. Too few naive T cells or NK cells to stop the run away train.
Targeting SIRPa was targeted when CD47 mAbs were shown to decrease RBC count years ago. I can't find any ongoing trial in https://clinicaltrials.gov/
What is your opinion on AFM24 + PD1 + 4B cbNK + TAM flipper combo to treat solid cancers?
Off target editing will be a headache for genetically modified cells.
Strange the most striking ASH data is from AFM13+NK cells with no edits. NK cells from Cord blood is as good as any including IPSC
Unless one is a fact checker who claims natural immunity is inferior to a man made vaccine.
Cell Therapies need eganelisib for TME and durability.