In cancers such as prostate cancer, the combination of PTEN loss and activation of Myc activates an adaptive stress response that enables tumor cells to escape the stress of massively upregulated protein synthesis. This pro-survival response is mediated by the PERK-phosphorylated eIF2α axis of the UPR adaptive response. Agents that disrupt PERK-eIF2α pathways disrupt the adaptive response and lead to cancer cell death from uncontrolled growth. For example, ISRIB and derivatives may be employed as therapeutic agents to disrupt PERK-mediated adaptive mechanisms. Additionally PTEN loss and activation of Myc provides a diagnostic marker that enables better prognosis and the selection of amenable treatments.

Compositions and methods for determining post-transfusion survival or toxicity of red blood cells and the suitability of red blood cell units for transfusion by measuring the levels of one or more markers in a red blood cell sample are provided.

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.

Provided herein are compositions, methods and uses involving antibodies that bind to ErbB, a receptor tyrosine kinase, and modulate the activity of ErbB. Also provided are uses and methods for treating disorders, such as cancer, by administering to subject an antibody that binds to ErbB.

The identification of Her2-specific monoclonal antibody m860 is described. The m860 antibody was identified from a human naïve phage display Fab library by panning against the extracellular domain of human Her2. M860 binds to cell surface-associated Her2 with an affinity comparable to that of trastuzumab (Herceptin®), but binds to a different epitope. Using site-specific glycan engineering, m860 was conjugated to the small molecule drug auristatin F. The antibody-drug conjugate was stable, bound cell-surface expressed Her2 and exhibited potent cell killing of Her2-positive cancer cells, including trastuzumab-resistant breast cancer cells.

The data provided herewith show that, biomarkers found within the cells of a tumor or cancer may also be present at adequate levels within the patient's urine to enable detection. Method of diagnosis, patient selection and treatment are provided, along with kits and devices.

The invention relates to a method for quantifying bispecific antibodies, in particular bispecific antibody therapeutics, in biological samples by quantifying a unique signature peptide of said antibody by mass spectrometry. The invention relates also to a kit comprising the unique signature peptide.

An objective of the present invention is to provide antigen-binding molecules that specifically bind to HER2 mutant. The present invention provides antigen-binding molecules that specifically bind to HER2 mutant, and are capable of modulating and/or activating an immune response; compositions comprising the antigen-binding molecule; and methods of using the same.

This invention provides biomarkers (e.g., methylation of R198 or R200 of EGFR or the presence of an arginine at position 497 of EGFR) for the prediction of resistance to cetuximab therapy. This invention also provides methods for the selection of patients for combination therapy with cetuximab and PRMT inhibitors.

The present invention relates to a method for the diagnosis or the prognosis of metastasis in prostate cancer which comprises determining if the c-MAF gene is amplified in a primary tumor sample. Likewise, the invention also relates to a method for the diagnosis or the prognosis of metastasis in prostate cancer, as well as to a method for determining the tendency to develop bone metastasis with respect to metastasis in other organs, which, comprise determining the c-MAF expression level. Finally, the invention relates to the use of a c-MAF inhibitor as therapeutic target for treating the prostate cancer.