Abstract: It has been discovered that the human GT198 gene (gene symbol PSMC3IP) at chromosome 17q21 acts as a tumor suppressor. The mutation of the GT198 gene causes the increased dominant negative splice variant activity and leads to the loss of wild type GT198 function, and in turn, induces breast and ovarian cancers. One embodiment provides compositions and methods for treating or alleviating one or more symptoms associated with cancer due to the GT198 gene mutations. Another embodiment provides methods and compositions for detecting cancer due to the mutation of the GT198 gene. Still another embodiment provides methods for identifying compounds, antibodies and natural product molecules that are useful for treating cancer due to the mutations of the GT198 gene. Preferably the disclosed compositions antagonize or interfere with the biological activity of splice variants of GT198.

Abstract: The present invention generally relates to the fields of cancer therapy and cancer prevention. More particularly, the present invention generally relates to a diagnostic marker for predicting the efficacy of topoisomerase I (topo I) inhibitors in the treatment of cancers. More specifically, the present invention relates to methods, machines, computer systems, computable readable media and kits which can be used to identify and determine the effectiveness of topoisomerase I (topo I) inhibitors in the treatment of cancers, and in some embodiments, the level of sensitivity or resistance of a tumor cell to a topoisomerase I inhibitor, such as camptothecin (CPT), or CPT analogues such as topotecan and irinotecan and derivatives thereof. More specifically, the present invention related to methods, machines, computer systems, computable readable media and kits which can be used to determine a mutation in the BRCA1 gene, e.g.

Abstract: The invention provides methods of dosing for the treatment of cancers, such as B cell proliferative disorders, with anti-cluster of differentiation 20 (CD20)/anti-cluster of differentiation 3 (CD3) bispecific antibodies.

Abstract: Provided is a method for evaluating the progression of glioma in an individual comprising monitoring the levels of circulating exosomes that are positive for survivin and a glial marker (such as glial fibrillary acidic protein). An increase in the level of such exosomes is indicative of poor prognosis. Levels of circulating exosomes that are positive for survivin and glial marker can also be used for evaluating the efficacy of a therapy for glioma in an individual, and modifying the therapy or introducing additional therapy if levels of such exosomes are found to be increasing.

Abstract: The present invention provides KLK3 peptides, FOLH1 peptides, recombinant polypeptides comprising same, recombinant nucleotide molecules encoding same, recombinant Listeria strains comprising same, and immunogenic and therapeutic methods utilizing same.

Abstract: Described herein are methods for diagnosing high-risk cancer in a subject by detecting PolySialic Acid (polySia) in a biological sample obtained from the subject, or by detecting polySia and one or more tissue-specific markers in a biological sample obtained from the subject.

Abstract: Methods of testing tumor samples for mutational burden and/or for expression profiles permit the prediction of responsiveness of an individual to immunotherapy comprising PVSRIPO. Those predicted to respond are treated with PVSRIPO and those predicted not to respond are treated with other agents.

Abstract: Provided herein, in some embodiments, are methods and composition for treating cancer in a subject. The methods may include administering to the subject a nucleic acid encoding MIP3? fused to a cancer antigen, administering to the subject a CpG oligodeoxynucleotide, administering to the subject interferon alpha (IFN?), and administering to the subject 5-aza-2?-deoxycytidine (Aza), in effective amounts to treat the cancer.

Abstract: Provided herein are diagnostic antibodies that bind to glucocorticoid-induced tumor necrosis factor receptor (GITR). Such antibodies are useful for methods of detecting the expression of GITR in biological samples, for example, tumor tissue, and identifying a cancer patient likely to respond to anti-GITR immunotherapy or predicting whether a cancer patient will respond to anti-GITR immunotherapy.

Abstract: The present invention relates to biomarkers of lung cancer, particularly to markers that enable distinguishing between subtypes of non-small cell lung cancer (NSCLC), particularly between adenocarcinoma (AC) and squamous cell carcinoma (SCC). In particular, the present invention relates to means and methods for diagnosing, assessing the level of severity and selecting methods of treating NSCLC.

Abstract: The present invention provides for recombinant monoclonal antibodies that bind to human colorectal and pancreatic carcinoma-associated antigens, along with nucleic acid sequences encoding the antibody chains, and the amino acid sequences corresponding to the nucleic acids, and uses for these antibodies, nucleic acids and amino acids.

Abstract: The present disclosure relates to a method of identifying an individual having non-small cell lung carcinoma as to be treated by chemotherapy based on marker molecules cytokeratin-19 fragments (CYFRA 21-1) and carcinoembryonic antigen (CEA) as well as the use of the marker molecules for the identification of an individual to be treated by chemotherapy.

Abstract: The instant disclosure provides biomarkers and methods for identifying subjects at risk of developing cytokine release syndrome (CRS), neurotoxicity, or both after adoptive immunotherapy to guide preemptive intervention, modified therapy, or the like. For example, adverse event biomarkers may be measured in a subject before pre-conditioning chemotherapy, before immunotherapy (e.g., adoptive immunotherapy infusion comprising a chimeric antigen receptor (CAR) modified T cell), or shortly after pre-conditioning chemotherapy and/or immunotherapy. Exemplary biomarkers include temperature, cytokine levels and endothelial activation biomarkers, such as angiopoietin 2, von Willebrand factor (vWF), ratio of angiopoietin 2 to angiopoietin 1, and ratio of ADAMTS13 to vWF. Also provided are methods of treating subjects identified as at risk of developing cytokine release syndrome (CRS), neurotoxicity, or both to minimize such potential adverse events.

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

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

Abstract: The present invention relates to compositions, methods, uses and kits for treating cancer. The present invention relates to methods for minimising the progression of cancer in a subject, the method comprising administering to the subject therapeutically effective amounts of chymotrypsinogen and trypsinogen, thereby minimising the progression of cancer in the subject. In particular, the methods provide a means for treating cancer by reducing the number of cancer stem cells in the subject.

Abstract: Methods for the treatment of CD30-expressing cancers are provided. The methods comprise administering to a subject in need thereof a weekly dose of from about 0.8 mg/kg to about 1.8 mg/kg of an antibody-drug conjugate compound having formula (I); or a pharmaceutically acceptable salt thereof; wherein: mAb is an anti-CD30 antibody unit, S is a sulfur atom of the antibody, A- is a Stretcher unit, and p is from about 3 to about 5.

Abstract: The present invention relates to compositions and methods for the immunomodulation mediated by the interaction of PD-L2 and RGMb.

Abstract: The present invention is directed to heterodimeric antibodies that bind CD3 and CD38.

Abstract: Herein are described methods of treating a human subject having acute myeloid leukemia (AML) that is refractory to induction therapy, wherein an MDM2 inhibitor is administered before or concurrently with chemotherapy, which may comprise induction therapy. Refractory AML may be predicted based on decreased expression of MTF2 in cells from a hematological sample obtained from the subject. Also provided are methods of predicting and treating AML responsive to MDM2/HDM2 inhibitors, based on MTF2 expression. One set of additional biomarkers useful in the predictions comprise one or more of H3K27me3, CD84, CD92, MDM2, NPM1, PRICKLE1, SET, ABCB6, POLQ, POLK, POLH, ARTIMIS, MCM6, CD327, CD90 and PARP1. Another set of additional biomarkers useful in the predictions include at least one of H3K27me3, MDM2, NPM1, SET, CD84 and PRICKLE1. Methods of selecting a patient for treatment with an MDM2 inhibitor before or concurrently with chemotherapy are also provided, along with kits and uses.