Methods of expanding tumor infiltrating lymphocytes (TILs) using a potassium channel agonist, such as a K.sub.Ca3.1 (IK channel) agonist, and uses of such expanded TILs in the treatment of diseases such as cancer are disclosed herein.

The present disclosure concerns combination therapy for cancer that utilizes (i) an oncolytic virus; (ii) a virus comprising nucleic acid encoding an immunomodulatory factor, and (iii) at least one cell comprising a chimeric antigen receptor (CAR) specific for a cancer cell antigen. In particular embodiments, the virus comprises nucleic acid encoding an immunomodulatory factor comprises nucleic acid encoding IL-12 and/or antagonist anti-PD-L1 antibody.

Methods and compositions for treating cancer, particularly improved CAR-T methods, are disclosed.

Provided herein are chimeric antigen receptors (CARs) for cancer therapy, and more particularly, CARs containing a scFv from an anti-MUC16 monoclonal antibody. Provided are immune effector cells containing such CARs, and methods of treating proliferative disorders.

This invention is in the area of compositions and methods for regulating chimeric antigen receptor immune effector cell, for example T-cell (CAR-T), therapy to modulate associated adverse inflammatory responses, for example, cytokine release syndrome and tumor lysis syndrome, using targeted protein degradation.

The present invention relates to chimeric antigen receptors (CAR) comprising an inert and modifiable spacer that evades the off-target binding by Fc receptor (FcR) expressing cells in CAR T cell therapy. The spacer is based on Ig-like C1 domain of signal-regulatory protein alpha.

The present invention provides methods for inducing and expanding anti-tumor immunity leading to enhanced clinical and immunotherapeutic responses. The invention also provides novel compositions and methods for the treatment of cancer.

Memory-like cytokine enhanced NK (M-CENK) cells have superior cytotoxicity and can be generated/expanded from a single batch of mononuclear cells to in sufficient quantities to so form a cell-based therapeutic suitable for infusion. Advantageously, the M-CENK cells can be cryopreserved and thawed without compromising viability and cytotoxicity.

This disclosure describes, generally, a modified form of CD 16, genetically-modified cells that express the modified CD 16, and methods that involve the genetically-modified cells. The modified form of CD 16 can exhibit increased anti-tumor and/or anti- viral activity due, at least in part, to reduced susceptibility to ADAM17-mediated shedding upon NK cell stimulation.

A patient having cancer can be treated using coordinated treatment regimens based on at least two omics data sets obtained from a solid tumor and a liquid biopsy that may indicates a plurality of tumor status in the patient's body. The treatment regimens can use various compounds and compositions that drive a tumor from the escape phase of cancer immunoediting to the elimination and equilibrium phase of cancer immunoediting.