The present invention provides an antigen binding protein specifically binding to a CT45 antigenic peptide that is in a complex with a major histocompatibility complex (MHC) protein, wherein the CT45 antigenic peptide comprises or consists of the amino acid sequence of SEQ ID NO: 138 (KIFEMLEGV) and wherein the antigen binding protein comprises a first polypeptide comprising a variable domain V.sub.A comprising complementarity determining regions CDRa1, CDRa2 and CDRa3 and a second polypeptide comprising a variable domain V.sub.B comprising CDRb1, CDRb2 and CDRb3. Also provided are nucleic acids encoding the antigen binding proteins, vectors comprising the nucleic acids, recombinant cells expressing the antigen binding proteins and pharmaceutical compositions comprising the antigen binding proteins. The invention further provides the antigen binding proteins for use in medicine and a method of producing the antigen binding protein.

The present invention relates to the discovery that inhibition of Dickkopf2 (DKK2) increases CD8.sup.+ cytotoxic T lymphocyte (CTL) activity, attenuates tumor angiogenesis, and hence suppresses tumor formation. Thus, in various embodiments described herein, the methods of the invention relate to methods of treating cancer by administering to a patient an effective amount of DKK2 gene depleting agent, methods for providing anti-tumor immunity and anti-tumor angiogenesis in a subject, methods of stimulating a T cell mediated immune response to a cell population or a tissue and suppressing tumor angiogenesis in a subject. Additionally, the current invention includes methods of diagnosing a cancer or a predisposition of developing a cancer or a metastasis and methods for determining the use of immunotherapy treatment or cancer vaccine for treating cancer. Furthermore, the invention encompasses a pharmaceutical composition for treating cancer as well as a kit for carrying out the aforementioned methods.

The present invention relates to the field of cancer. More specifically, the present invention provides compositions and methods useful for detecting and treating esophageal cancer. In a specific embodiment, a method for identifying a subject having esophageal adenocarcinoma (EAC) comprises (a) extracting genomic DNA from a sample obtained from the subject; (b) performing a conversion reaction on the genomic DNA in vitro to convert unmethylated cytosine to uracil by deamination; and (c) detecting nucleic acid methylation of one or more genes in the converted genomic DNA, wherein detecting nucleic acid methylation identifies the subject as having EAC. The one or more genes can comprise ABCB1, BMP3, COL23A1, FBN1, FADS1 and PRDM2. In a more specific embodiment, the one or more genes comprise at least three of ABCB1, BMP3, COL23A1, FBN1, FADS1 and PRDM2.

A cancer test device (1) is provided with: an application unit (40) for applying a staining agent (45), which can selectively stain a product of a cancer-relating gene in a living cell a chromatic color, onto a group of living cells; an imaging unit (10) for imaging the group of living cells having the staining agent (45) applied thereto; and a determination unit (52) for determining the level of malignancy of cancerization of the group of living cells on the basis of the state of the stained expression pattern of the cancer-relating gene in the group of living cells in an image obtained by the aforementioned imaging.

The disclosure relates to methods for treating cancers (e.g., cancers having a BRCA1 and/or BRCA2 mutation(s)) by administering to the subject an effective amount of a ubiquitin-specific protease 1 (USP1) inhibitor.

The present disclosure is directed to the use of inhibitors of glutamate metabolism to treat cancers that have mutations in ARID1A. Thus, in accordance with the present disclosure, there is provided a method of treating a subject determined to have an ARIDIA-mutated cancer, pre-cancer or benign tumor comprising administering to said subject at least one inhibitor of glutamate metabolism.

The present application provides pyrazolyl bicyclic amines of Formula (I):

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and their pharmaceutically acceptable salts thereof, that are inhibitors of cyclin-dependent kinase 2 (CDK2), as well as pharmaceutical compositions thereof, and methods of treating cancer using the same.

Provided herein are methods of treating a patient having a cancer that exhibits (i) a hemizygous loss of the TP53 gene; (ii) a hemizygous loss of the POLR2A gene; and/or (iii) a decreased level of expression of a POLR2A gene product relative to a reference (i.e., control) expression level. The methods comprise administering a therapeutically effective amount of a POLR2A inhibitor (e.g., a nucleic acid that inhibits the expression of a POLR2A protein, an amatoxin, alpha-amanitin, or alpha-amanitin conjugated to a cell targeting moiety, such as an EpCAM antibody) to a patient having or determined to have (i) a hemizygous loss of the TP53 gene; (ii) a hemizygous loss of the POLR2A gene; and/or (iii) a decreased level of expression of a POLR2A gene product relative to a reference (i.e., control) level.

An RNA fluorescent probe for rapidly distinguishing cancer tissue from normal tissue based on nucleolar morphological changes, the probe being (E)-1-(3-aminopropyl)-4-(2-(9-ethyl-9H-carbazol-3-yl)vinyl)pyridine-1-ium dibromide, abbreviated as CAPY-AP. The probe can target RNA in culture cells and normal tissue as well as cancer tissue and then display nucleolar morphology. The judging criteria of distinguishing the cancer tissue from the normal tissue based on the nucleolar morphological changes is only single and unconspicuous nucleolus in most cells of normal tissue, while the enlarged nucleoli and/or multiple nucleoli exist in many cells of cancer tissue. Compared with other existing RNA probes, the probe has super-high RNA affinity and super-high permeability, and can rapidly image the RNA and nucleoli in tissue sections. Additionally, the probe has characteristics of good membrane permeability, strong fluorescence and good photostability, and is expected to be applied in preparation of intraoperative pathological diagnostic reagents for tumors.

The present invention relates to methods of determining cancer cell sensitivity to treatment by using antibodies to detect the presence of heterodimers in the cell, as well as to determine the relationship between the antibody binding to the heterodimer in the cancer cell and the sensitivity of the cell to cancer treatment. The invention also provides a method of predicting therapeutic efficacy in a cancer patient.