Why IMU is a multi multi bagger, page-25381

Hey TB here is another gem, this was published in January and YF and SP are among the 8 authors noted on the original article Published in the
Journal of the American College of Surgeons and you can read what they say below, so I would suggest now it is actually in patients in an FDA supervised trial that they have seen exactly what they saw in this trial, and they are excited and it also explains the interest in Pancreatic cancer types.

Good times coming me thinks, Noosa in Spring is lovely

Background CAR-T cells targeting the B-cell antigen CD19 are standard therapy for relapsed/ refractory B-cell lymphoma and leukemia. CAR-T cell therapy in solid tumors is limited due to an immunosuppressive tumor microenvironment (TME) and a lack of tumor-restricted antigens. We recently engineered an oncolytic virus (CF33) with high solid tumor affinity and specificity to deliver a non-signaling truncated CD19 antigen (CD19t), allowing targeting by CD19-CAR-T cells. Here, we tested this combination against pancreatic cancer. Study Design We engineered CF33 to express a CD19t (CF33-CD19t) target. Flow cytometry and ELISA were performed to quantify CD19t expression, immune activation, and killing by virus and CD19-CAR-T cells against various pancreatic tumor cells. Subcutaneous pancreatic human xenograft tumor models were treated with virus, CAR-T cells, or virus+CAR-T cells. Results In vitro, CF33-CD19t infection of tumor cells resulted in >90% CD19t cell-surface expression. Co-culturing CD19-CAR-T cells with infected cells resulted in IL-2 and IFN-γ secretion, upregulation of T cell activation markers, and synergistic cell killing. Combination therapy of virus+CAR-T cells caused significant tumor regression (Day 13): control (n=16, 485 ± 20 mm ³ ), virus alone (n=20, 254 ± 23 mm ³ , P=0.0001), CAR-T cells alone (n=18, 466 ± 25 mm ³ , P=NS) virus+CAR-T cells (n=16, 128 ± 14 mm ³ , P<0.0001 vs. control; P=0.0003 vs. virus).
Conclusions Engineered CF33-CD19t effectively infects and expresses CD19t in pancreatic tumors, triggering cell killing and increased immunogenic response by CD19-CAR-T cells. Notably, CF33-CD19t can turn cold immunologic tumors hot, enabling solid tumors to be targetable by agents designed against liquid tumor antigens

https://www.researchgate.net/publication/377361646_Using_Oncolytic_Virus_to_Retask_CD19-Chimeric_Antigen_Receptor-T_Cells_for_Treatment_of_Pancreatic_Cancer_Toward_a_Universal_Chimeric_Antigen_Receptor-T_Cell_Strategy_for_Solid_Tumors