The present invention is based on the identification of novel biomarkers predictive of responsiveness to anti-immune checkpoint therapies.

Provided are a polypeptide and nucleic acid for encoding the polypeptide, a nucleic-acid construct, an expression vector, and a host cell containing the nucleic acid, an antigen-presenting cell presenting the polypeptide on the surface of the cell, and immune effector cell thereof, a pharmaceutical composition containing the polypeptide, a vaccine containing the nucleic acid, the nucleic acid construct, the expression vector, the host cell, the antigen-presenting cell, and the immune effector cell, and an antibody recognizing the polypeptide. Also provided is a therapeutic method using the polypeptide, the nucleic acid, the pharmaceutical composition, the vaccine, and the antibody. Also provided are a diagnosis method and diagnosis apparatus for detecting the described polypeptide. Also provided is an application of the polypeptide in preparing a vaccine, a tumor diagnosis kit, or a pharmaceutical composition, and an application of the polypeptide or the nucleic acid as a test target in tumor diagnosis.

The present invention relates generally to methods of accurately quantifying HER2 and/or p95 expression in subjects with a HER2 positive cancer and indicating the risk of brain relapse in such patients.

The purpose of the present invention is to provide a novel tumor treatment agent. In GREB1-positive tumors that do not exhibit sex hormone sensitivity, GREB1 is a downstream target gene of the Wnt/β-catenin signal. Through the use as an active ingredient of a substance that can inhibit GREB1 expression, the growth of GREB1-positive tumor cells that do not exhibit sex hormone sensitivity can be effectively inhibited and such a tumor can be treated.

The current disclosure provides for methods of identifying and treating small cell neuroendocrine (SCN) tumors and small-round-blue cell tumor (SRBCT). Aspects of the disclosure relate to a method comprising measuring the level of expression of one or more biomarkers from Tables 1-3 in a biological sample from a cancer patient. Further aspects relate to a method for treating small cell neuroendocrine (SCN) cancer or small-round-blue cell tumor (SRBCT) in a patient comprising administering a cancer treatment to the patient, wherein the cancer treatment is a treatment selected from Table 4A, 4B, or combinations of treatments from Table 4A and/or 4B.

Provided are a method, an apparatus, and a kit for detecting a neuroblastoma in a subject and/or for monitoring a therapeutic effect on the neuroblastoma, by measuring a urinary tumor marker(s) in a sample from the subject.

The present invention relates to an antibody specifically binding to a WRS (tryptophanyl-tRNA synthetase) protein, and a use thereof. More specifically, the present invention pertains to an antibody specifically binding to a polypeptide of an amino acid sequence represented by SEQ ID NO:2 in the WRS (tryptophanyl-tRNA synthetase) protein, or a fragment of the antibody, a polynucleotide encoding the antibody, a vector comprising the polynucleotide, a cell transformed using the vector, and a use of the cell.

Provided herein, are methods of identifying neoantigens for treating and preventing cancer. Also disclosed are methods and compositions for administering identified neoantigens for the treatment and prevention of cancer.

Provided herein is technology for screening multiple types of cancer from a biological sample, and particularly, but not exclusively, to methods, compositions, and related uses for simultaneously detecting the presence of multiple types of cancer (e.g., liver cancer, esophageal cancer, lung cancer, ovarian cancer, pancreatic cancer, gastric cancer, bladder cancer, breast cancer, cervical cancer, colorectal cancer, prostate cancer, renal cancer, and uterine cancer) from a biological sample (e.g., stool sample, tissue sample, organ secretion sample, CSF sample, saliva sample, blood sample, plasma sample or urine sample).

Heritable pathogenic variants in the mismatch repair (MMR) pathway, also known as Lynch Syndrome (LS), can lead to the development of colon cancer and other cancers. Following mismatch, a complex of proteins consisting of MLH1, MSH2, MSH6 and PMS2 translocate into the nucleus to signal recruitment of repair mechanisms. Flow cytometry-based, functional variant assays (FVAs), were developed to determine whether variants in these MMR repair genes and/or other related genes would augment the nuclear translocation of MLH1 and MSH2 and downstream nuclear phosphorylation of ATM and ATR in response to DNA mismatches. Each assay distinguished pathogenic variants in MMR repair genes (MLH1, MSH2, PMS2 and MSH6) from benign controls. The combination of multiple assays provided robust separation between heterozygous pathogenic variant carriers and benign controls. The ability to produce distinct molecular phenotypes by these assays suggest FVA assays of MMR pathways could be used to identify LS and associated risk of colon and other cancers and could act as an adjunct to MMR gene sequencing panels in categorizing variants.