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.

The technology described herein is directed to methods of treating and diagnosing bronchial premalignant lesions, e.g. by determining the lesion subtype using one or more biomarkers described herein.

The technology described herein is directed to methods of treating and diagnosing bronchial premalignant lesions, e.g. by determining the lesion subtype using one or more biomarkers described herein.

The present invention relates to antigen-binding compounds that inhibit the enzymatic activity of soluble human CD39. The invention also relates to cells producing such compounds; methods of making such compounds, and antibodies, fragments, variants, and derivatives thereof; pharmaceutical compositions comprising the same; methods of using the compounds to diagnose, treat or prevent diseases, e.g., cancer.

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.

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.

Provided are methods of selecting a patient with cancer and/or treating a patient with cancer that comprises a deleterious alteration in FBXW7 and/or an amplification of CCNL1 for CDK11 inhibitor and/or ATR inhibitor treatment. For example, the method of selecting a patient afflicted with a cancer likely to benefit from a CDK11 inhibitor and/or ATR inhibitor treatment, the method comprising: obtaining a biological sample; testing the sample for i) loss of function FBXW7, optionally for a deleterious mutation in F box WD-repeat containing protein (FBXW7) substrate binding domain and/or ii) upregulated CCNL1, optionally a gain or amplification of CCNL1; and selecting the patient having i) loss of function FBXW7, optionally a deleterious mutation in the FBWX7 substrate-binding domain or ii) upregulated CCNL1, optionally a gain or amplification of CCNL1, as likely to benefit and/or for treatment with the CDK11 inhibitor and/or ATR inhibitor.

The present invention provides a method for quantifying a monoclonal (M-) protein in a sample of a subject, the method comprising the steps of:—subjecting a serum sample of a subject to serum protein electrophoresis (SPE) in a gel, preferably serum protein electrophoresis in an agarose gel, to separate serum proteins into different serum protein fractions, optionally followed by immunofixation electrophoresis (IFE) and further optionally involving immunostaining of the gel;—excising from said gel a gel part comprising, or suspected of comprising, a M-protein;—performing an enzymatic digestion of proteins present in said gel part in order to provide a peptide digest comprising at least one M-protein peptide;—subjecting said peptide digest comprising said at least one M-protein peptide to liquid chromatography-mass spectrometry (LC-MS) to determine a quantity of said at least one M-protein peptide, thereby quantifying said M-protein in said sample.

The present application contemplates methods of screening therapeutic agents for treating cancer comprising co-culturing immune cells and tumor cells isolated from a subject under conditions that allow the immune cells and the tumor cells to form a cancer spheroid. The cancer spheroid may then be exposed to at least one therapeutic agent, and the responsiveness of the tumor cells the spheroid to the therapeutic agent may be measured.

The present application contemplates methods of screening therapeutic agents for treating cancer comprising co-culturing immune cells and tumor cells isolated from a subject under conditions that allow the immune cells and the tumor cells to form a cancer spheroid. The cancer spheroid may then be exposed to at least one therapeutic agent, and the responsiveness of the tumor cells the spheroid to the therapeutic agent may be measured.