The present invention provides a tumor blood marker and a use thereof. Specifically, the present invention provides a use of a reagent, which is used to detect GAPDH in a blood sample, in a preparation of a detecting composition for tumor screening, risk evaluation of tumor development in subjects, distinction of tumor progression stages, identification of therapeutic efficacy of tumor and/or risk analysis of tumor progression. The present invention also provides a kit and a method for detecting GAPDH concentrations in blood samples.

This invention concerns various methods of using labeled HSP90 inhibitors to improve treatment of cancer patients with HSP90 inhibitors, including ex vivo and in vivo methods for determining whether a tumor will likely respond to therapy with an HSP90 inhibitor.

Disclosed are diagnosis/detection methods that enable early diagnosis and treatment of patients with Glioblastoma brain tumor (GB) and/or advanced stage glioma brain tumor by using patient sera. The methods provide GB diagnosis with high sensitivity and specificity by the anti-SLC (especially anti-SLC3a2) autoantibody found in GB patient sera and the interaction of the mutant, isomer or modified SLC autoantigen with which this antibody interacts.

The disclosure provides novel personalized therapies, kits, transmittable forms of information and methods for use in treating patients having cancer, wherein the cancer is amenable to therapeutic treatment with an inhibitor, e.g., an inhibitor of any of the targets disclosed herein. Kits, methods of screening for candidate inhibitors, and associated methods of treatment are also provided.

From gene expression analysis with a long-term recurrence-free group and a recurrence metastasis group of stomach cancer, CHRNB2 and NPTXR were identified as drug discovery targets. Tumor growth was successfully inhibited by an antibody medicine or a nucleic acid medicine targeting CHRNB2 or NPTXR. Furthermore, a polyclonal antibody and a monoclonal antibody linking to CHRNB2 or NPTXR are provided. Since these receptor molecules are novel molecular targets, treatment of cases which the existing therapeutic drugs have no effect on is made possible.

Methods of detecting and treating an epithelial carcinoma, such as pancreatic ductal adenocarcinoma cancer or bladder cancer, expressing antithrombin-binding heparan sulfate (HS.sup.AT) in a subject, comprising combining a biological sample of the subject containing HS.sup.AT with antithrombin and detecting binding of HS.sup.AT and the antithrombin, optionally determining that the antithrombin inhibits factor Xa.

A method of detecting or diagnosing squamous cancers in a sample from a subject, including isolating extracellular vesicles from the sample, wherein the extracellular vesicles are cancer specific.

Disclosed is an isolated or purified T cell receptor (TCR) having antigenic specificity for mutated Kirsten rat sarcoma viral oncogene homolog (KRAS) presented in the context of an HLA-Cw*0802 molecule. Related polypeptides and proteins, as well as related nucleic acids, recombinant expression vectors, host cells, populations of cells, and pharmaceutical compositions are also provided. Also disclosed are methods of detecting the presence of cancer in a mammal and methods of treating or preventing cancer in a mammal.

The present invention describes an integrated apparatus that enables identification of invasive tumor cells directly from a specimen. The methods using the apparatus can be used to prognose or predict the survivability of the cancer in a subject and the risk of recurrence of the cancer in the subject after treatment. The methods disclosed herein can be used to determine which chemotherapeutic or other therapies most strongly inhibit the tumor cells invasiveness as a form of personalized therapy.

The present disclosure relates to compounds that are capable penetrating to the blood brain barrier to modulate the activity of EGFR tyrosine kinase. The disclosure further relates to methods of treating glioblastoma and other EGFR mediated cancers. The disclosure further relates to methods of treating glioblastoma and other EGFR mediated cancers that have been determined to have altered glucose metabolism in the presence of inhibitors. The present disclosure also provides methods of administering to a subject a glucose metabolism inhibitor and a cytoplasmic p53 stabilizer.