A bivalent, anti-MICA human monoclonal antibody formed by two or more heavy and light chains with a variable immunoglobulin domain neutralises the MICA protein in its soluble state and opsonises tumour cells expressing the antigen, stimulating adaptive immunity in the treatment of gastric cancer or other types of cancer in which the tumour cells express MICA in the soluble form or abundantly on their surface.

A nucleic acid molecule comprising a nucleotide sequence encoding an inhibitory chimeric antigen receptor (iCAR) capable of preventing or attenuating undesired activation of an effector immune cell, wherein the iCAR comprises an extracellular domain that specifically binds to a single allelic variant of a polymorphic cell surface epitope absent from mammalian tumor cells due to loss of heterozygosity (LOH) but present at least on all cells of related mammalian normal tissue; and an intracellular domain comprising at least one signal transduction element that inhibits an effector immune cell is provided. Vectors and transduced effector immune cells comprising the nucleic acid molecule and methods for treatment of cancer comprising administering the transduced effector immune cells are further provided.

Provided herein is a recombinant antibody or an epitope binding fragment thereof that specifically binds to a lectin-like oxidized low-density lipoprotein (LDL) receptor-1 (LOX-1) epitope, as well as compositions and methods using these antibodies and fragments for therapeutic and diagnostic protocols.

Polypeptides and proteins that specifically bind to and immunologically recognize CD276 are disclosed. Chimeric antigen receptors (CARs), anti-CD276 binding moieties, nucleic acids, recombinant expression vectors, host cells, populations of cells, and pharmaceutical compositions relating to the polypeptides and proteins are also disclosed. Methods of detecting the presence of cancer in a mammal and methods of treating or preventing cancer in a mammal are also disclosed.

Provided herein are anti-FGL2 monoclonal antibodies. Further provided herein are methods to reverse suppressive immune mechanisms, such as for the treatment of cancer or infectious diseases.

According to an embodiment of the present invention, there is provided a method of screening a prostate cancer patient by optical image analysis of a circulating tumor cell marker and a prostate-specific membrane antigen.

A method for separation and detection of exosomes may include: bringing a biological sample into contact with a capture molecule, the capture molecule including a specific binding substance for an antigen expressed on a cancer cell surface, to form a complex of an exosome and the capture molecule; and a bringing the complex into contact with a detector molecule, the detector molecule including a specific binding substance for an antigen expressed on a cancer cell surface and a labeling substance, to detect the complex by using the detector molecule, in which the antigen expressed on a cancer cell surface for at least one of the capture molecule and the detector molecule is cell-surface vimentin.

The present disclosure provides methods and kits for determining whether a cancer in a subject is susceptible to a treatment with a combination therapy comprising a bispecific anti-epidermal growth factor receptor (EGFR)/hepatocyte growth factor receptor (c-Met) antibody and an EGFR tyrosine kinase inhibitor (TKI). The present disclosure also provides methods for treating a cancer in a subject based on the susceptibility of the cancer to the treatment with a combination therapy comprising a bispecific EGFR/c-Met antibody and an EGFR TKI.

Materials and methods for treating potentially chemoresistant tumors (e.g., using DNA-PKcs inhibitors and anti-B7-H1 antibodies) are provided herein.

The present invention relates to the field of the production, identification and selection of biological binding molecules such as antibodies or fragments thereof, as well as to their use in the therapy and prophylaxis of cancer diseases, such as, in particular, malignant B-cell neoplasia. The binding molecules are able to selectively bind to autonomously active or autonomously activated B-cell receptors, the autonomously active or autonomously activated B-cell receptors being characterized by the presence of structural domains to which the binding molecule selectively binds and which are responsible for the autonomously active or autonomously activated state of the B-cell receptors.