Provided herein are uses of fibroblast growth factor receptor 2 (FGFR2) inhibitors in cancer treatment, in some cases in combination with immune stimulating agents, such as inhibitors of PD-1 or PD-L1. In some embodiments, FGFR2 inhibitors may comprise FGFR2 antibodies or FGFR2 extracellular domain (ECD) polypeptides, or FGFR2 ECD fusion molecules comprising an FGFR2 ECD and a fusion partner. In some embodiments, PD-1/PD-L1 inhibitors may comprise anti-PD-1 antibodies such as antibodies that bind to PD-1 or to PD-L1 and inhibit interactions between these proteins, as well as PD-1 fusion proteins or polypeptides.

Sarcomas are rare malignant tumors arising from the mesenchymal tissues at all body sites. The inventors show that in a mouse model of p16/p19 deficiency prone to tumor development, the absence of the mouse pantetheinase Vnn1 enhances the frequency of aggressive fibrosarcomas. They also show that reintroduction of a catalytically active form of the Vnn1 pantetheinase limits tumor growth in vivo. Interestingly, VNN1 expression in human sarcomas is associated with reduced aggressiveness and lower risk of metastatic relapse in patients. In conclusion, Vnn1 represents a novel marker of sarcoma and may modulate tumor aggressiveness by sustaining myofibroblast cell differentiation, thereby limiting evolution towards undifferentiated tumors. The present invention relates to the use of Vnn1 as a biomarker and a therapeutic target in sarcomas.

Methods for diagnosing a subject as a candidate for removal of a solid tumor without preoperative chemoradiation therapy, and methods for treating patients having solid tumors, who have one or more of genomic instability, elevated double stranded DNA breaks, elevated gamma-H2AX foci, or elevated replication stress and/or double stranded break-signalling (DSB-signalling) biomarkers in peripheral blood lymphocytes (PBLs) are provided herein.

A novel human bladder cancer marker AG-CD71 and a monoclonal antibody ABC71 for preventing AG-CD71 are provided. The human bladder cancer marker AG-CD71 is an abnormal glycosylated transferrin receptor TFRC; the abnormal glycosylated transferrin receptor TFRC refers to the TFRC carrying a saccharide structure Fucal-4(GlcNAcbl-3)[6OSO3]GlcNAc as an epitope. Also provided is an antibody for the human bladder cancer marker AG-CD71; the antibody is the monoclonal antibody ABC71 specific for the human bladder cancer AG-CD71; the monoclonal antibody is secreted from the hybridoma cell strain the preservation number of which is CGMCC No. 14312.

The present invention relates to a companion diagnosis biomarker composition and a companion diagnosis kit containing the same and, particularly, to a companion diagnosis biomarker composition for predicting a therapeutic response to at least one immune checkpoint inhibitor from among a PD-1 immune checkpoint inhibitor and a PD-L1 immune checkpoint inhibitor, and a companion diagnosis kit containing the same. According to the present invention, there is an effect that it is possible to predict a therapeutic response to at least one immune checkpoint inhibitor from among a PD-1 immune checkpoint inhibitor and a PD-L1 immune checkpoint inhibitor not only through a companion diagnosis through cancer patient tissues, but also through proteomic analysis of cancer patient blood.

Disclosed are methods of detecting and treating suspected B-cell lymphoma.

The present invention is directed to a method of detecting a DEK protein in a human urine sample using an ELISA assay. Methods and compositions for detection of DEK using mAb 260-6F9F6 (as detection antibody) and mAb 16-2C9C3 (as capture antibody) in human urine are provided herein. Specifically, the ELISA assay utilizes a capture mAb and a detection mAb to yield a high sensitivity of <50 ng/mL. The presence of DEK in urine is useful in predicting or diagnosing the occurrence of bladder cancer in humans.

The present invention related to a method for detecting a history of exposure to a chemical(s) comprising measuring the concentration of thrombomodulin in a sample isolated from a subject, and determining whether the concentration of thrombomodulin is altered compared to control reference levels.

The present invention relates to peptides, proteins, nucleic acids and cells for use in immunotherapeutic methods. In particular, the present invention relates to the immunotherapy of cancer. The present invention furthermore relates to tumor-associated T-cell peptide epitopes, alone or in combination with other tumor-associated peptides that can for example serve as active pharmaceutical ingredients of vaccine compositions that stimulate anti-tumor immune responses, or to stimulate T cells ex vivo and transfer into patients. Peptides bound to molecules of the major histocompatibility complex (MHC), or peptides as such, can also be targets of antibodies, soluble T-cell receptors, and other binding molecules.

A method of qualifying whether a cell population is a suitable therapeutic for treating an eye condition is disclosed. The method comprises analyzing co-expression of premelanosome protein (PMEL17) and at least one polypeptide selected from the group consisting of cellular retinaldehyde binding protein (CRALBP), lecithin retinol acyltransferase (LRAT) and sex determining region Y-box 9 (SOX 9) in the population of cells.