The present invention relates to expanded NK cells. The NK cells have been expanded ex vivo, are activated and have a cytotoxic phenotype. The cytotoxicity against malignant cells is markedly increased compared to non-expanded NK cells. The invention also relates to a method of treatment.

The invention provides a chimeric receptor comprising NKG2D, DAP10 and CD3 zeta. Also disclosed is a composition comprising this chimeric receptor and methods for making and using it to enhance the cytotoxicity and antitumor capacity of NK cells. The invention also encompansses methods for use of NKG2D-DAP10-CD3 zeta polypeptides, vectors and cells in methods for treating cancer and other proliferative disorders, as well as infectious diseases.

Disclosed herein are methods and compositions dock and lock (DNL) complexes comprising an AD moiety selected from an AKAP protein and a DDD moiety selected from a protein kinase A regulatory subunit. Also disclosed are fusion proteins comprising an AD moiety or DDD moiety attached to an effector moiety. The DDD moieties form dimers that bind to the AD moiety to form the DNL complexes. The effector moieties may be selected from a wide range of known effector moieties that produce one or more physiological effects, including but not limited to cell death. The DNL complexes may further comprise one or more diagnostic and/or therapeutic agents. The DNL complexes are of use for treating and/or diagnosing a variety of diseases or conditions.

The present invention relates to expanded NK cells. The NK cells have been expanded ex vivo, are activated and have a cytotoxic phenotype. The cytotoxicity against malignant cells is markedly increased compared to non-expanded NK cells. The invention also relates to a method of treatment.

Provided herein are uses of anti-B cell maturation antigen (BCMA) chimeric antigen receptors (CARs) for treating B-cell related conditions, such as BCMA-expressing cancers.

Provided herein are anti-CD24 antibodies that selectively bind human CD24 expressed in cancer cells, but not human CD24 expressed in non-cancerous cells, and the use of such antibodies in cancer therapy.

The present invention relates to activated lymphocytes comprising cytokine-induced killer cells in which CD8.sup.+CD56.sup.+NKG2D.sup.+ cells are present at a proportion of 20% or more, and a preparation method therefor, and more particularly, to activated lymphocytes comprising cytokine-induced killing cells which have high tumor cell killing abilities and growth rates and are almost free of side effects because they do not require the combined administration of interleukin-2, and a preparation method therefor.

Provided herein are antibodies and antigen-binding portions thereof that bind to tumor endothelial marker 1 (TEM1), as well as methods of using the disclosed antibodies and antigen-binding portions thereof, including methods of treating cancer, reducing tumor growth, reducing tumor metastasis, and/or reducing tumor-associated fibrosis in a subject in need thereof.

The present invention is directed to a humanized BCMA single-chain variable fragment (scFv), comprising V.sub.H having the amino acid sequence of SEQ ID NO: 3 and V.sub.L having the amino acid sequence of SEQ ID NO: 5. The present invention is also directed to a BCMA chimeric antigen receptor fusion protein comprising from N-terminus to C-terminus: (i) a single-chain variable fragment (scFv) of the present invention, (ii) a transmembrane domain, (iii) at least one co-stimulatory domains, and (iv) an activating domain. This humanized BCMA-CAR-T cells have specific killing activity against BCMA-positive tumor cells.

Provided is a cell, comprising and/or expressing a chimeric antigen receptor targeting claudin 18.2 (CLDN18.2), and a chimeric antigen receptor targeting mesothelin (MSLN) protein. Also provided is an expression vector, comprising a nucleic acid sequence which encodes the chimeric antigen receptor targeting CLDN18.2 and a nucleic acid sequence which encodes the chimeric antigen receptor targeting MSLN. Also provided are a preparation method for and a use of the cell and/or the expression vector.