The present invention relates to immune cells expressing chimeric antigen receptors against p95HER2 and bispecific antibodies for HER2 and CD3 and uses thereof in the treatment of cancer, in particular cancers which overexpress p95HER2.

This disclosure relates to modified receptors comprising a MyD88 domain, as well as cells comprising the same and methods of use thereof.

The present invention belongs to the technical fields of immunology and oncologic therapies. Provided are a tumor microenvironment-regulated CAR-monocyte/macrophage, and a preparation method therefor and the use thereof. When the CAR-monocyte/macrophage forms a chimeric antigen receptor composite structure, GM-CSF can be expressed intracellularly and autocrine to extracellular to promote the differentiation of the CAR-monocyte/macrophage to form an M1 type macrophage, so that the tumor microenvironment can be further regulated while the property of resisting M2 type macrophage reversal in the tumor microenvironment is maintained, thereby sensitizing the anti-tumor effect of the CAR-monocyte/macrophage. On the basis of GM-CSF, a tumor microenvironment-regulated CAR macrophage technology platform is constructed, which can maintain the M1-type characteristics of CAR-M and can also produce a TME reversal effect, thereby achieving the efficient anti-tumor effect of a CAR-monocyte/macrophage.

In certain embodiments, this disclosure provides methods to generate DNA, RNA and/or DNA-peptide nanostructures based chimeric antigen receptor (CAR) T cell (engineered T cell) for cancer immunotherapy, and compositions made by these methods.

The present disclosure provides reagents and methods for treating disease using modified immune cells (e.g., T cell comprising CAR or TCR) in combination with an agent associated with induction of immunogenic cell death (ICD) and optionally further in combination with an agent that specifically binds to and/or inhibits an immune suppression component and/or an agonist of an immune stimulatory molecule.

Compositions and methods for immunization against human breast cancer are disclosed. A breast cancer vaccine comprises an immunogenic polypeptide comprising human -lactalbumin.

Provided are receptor tyrosine kinase-like orphan receptor 1 (ROR1)-binding molecules, in particular, to human antibodies specific for ROR1, including antibody fragments. The present disclosure further relates to recombinant receptors, including chimeric antigen receptors (CARs) that contain such antibodies or fragments, and polynucleotides that encode the antibodies, antigen-binding fragments or receptors specific for ROR1. The disclosure further relates to genetically engineered cells, containing such ROR1-binding proteins and receptors, and related methods and uses thereof in adoptive cell therapy.

The presently disclosed subject matter provides for methods and compositions for treating cancer (e.g., breast cancer). It relates to mutant phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA)-targeted T cell receptors (TCRs) that specifically target a mutant PIK3CA peptide (e.g., a human mutant PIK3CA peptide), and immunoresponsive cells comprising such TCRs. The presently disclosed mutant PIK3CA peptide-specific TCRs have enhanced immune-activating properties, including anti-tumor activity.

Provided are chimeric antigen receptors (CAR) specific to a selected tumor antigen. Also provided are structure designs and function profiles of provided CAR candidates.

Disclosed herein is a method of reprogramming highly motile cells found in tumors, such as these highly motile GSC and/or MDSC clones, into auto-destructive cell missiles (referred to herein as therapeutic stealth cells) that can seek and destroy new foci of recurrence within the body, such as the brain. Cells with enhanced motility can be sorted out from heterogeneous populations and then be rendered auto-destructive by deterministic delivery of an anti-cancer agent, such as an oncolytic virus plasmid cocktail.