Targeting metastasis stem cells through a fatty acid receptor. The disclosure provides the use of blockers or inhibitors of CD36 activity or expression for the treatment of oral squamous cell cancer (OSCC), particularly for the treatment of generated metastases and for diminish is generation from primary tumours. Apart from shRNAs, anti-CD36 antibodies are provided as blockers or inhibitors, especially those that block the binding of CD36 to oxidized LDL and fatty acids and their incorporation into cells, because the promotion of their transport is indicated as the mechanism by which CD36 promote metastases dissemination and growth. Also provided is a method for identifying candidates to anticancer agents, particularly for OSCC metastasis, among those that promote in CD36+ cells, in vivo or in vitro, effects associated to CD36 depletion or blocking such as decrease of growth accumulation of lipid droplets and decrease of size in the case of metastases.

The present disclosure provides gene expression profiles that are associated with cancer, including certain gene expression profiles that differentiate between cancer that is at a high risk of recurrence. The gene expression profiles can be measured at the nucleic acid or protein level. The gene expression profiles can also be used to identify a subject for cancer treatment. Also provided are kits for use in predicting cancer recurrence and/or prognosing cancer and an array comprising probes for detecting the unique gene expression profiles associated with cancer.

Disclosed is a method of treating cancer, involving the administration of a therapeutically effective amount of an inhibitor of the epidermal growth factor receptor (EGFR) pathway and the integrin/focal adhesion kinase (FAK) pathway to a patient in need of such treatment, where the inhibitor comprises at least the first 94 amino acids of a Tinagl1 protein, any fragments with conservative substitution showing 90% or greater homology to amino acids 22-94 of a Tinagl1 protein, or a signaling peptide fused or attached to a fragment with conservative substitution showing 90% or greater homology to amino acids 22-94 of a Tinagl1 protein.

This disclosure provides methods for treating a subject having small cell lung cancer by determining expression levels of biomarkers highly correlated with a subtype of small cell lung cancer that are sensitive to treatment with pentamidine or a pharmaceutically acceptable salt thereof. The methods are drawn to determining a predictive gene expression profile of a subtype of small cell lung cancer and treating the subject with an effective amount of pentamidine or a pharmaceutically acceptable salt of pentamidine as a chemotherapy agent. The methods generally involve treatment of a subtype of small cell lung cancer predicted to be a responder to pentamidine or a pharmaceutically acceptable salt of pentamidine.

Novel gene deletions and translocations involving chromosome 2 resulting in fusion proteins combining part of Anaplastic Lymphoma Kinase (ALK) kinase with part of a secondary protein have been identified herein in human solid tumors, e.g. non-small cell lung carcinoma (NSCLC). Secondary proteins include Echinoderm Microtubule-Associated Protein-Like 4 (EML-4) and TRK-Fusion Gene (TFG). The EML4-ALK fusion protein, which retains ALK tyrosine kinase activity, was confirmed to drive the proliferation and survival of NSCLC characterized by this mutation. The invention therefore provides, in part, isolated polynucleotides and vectors encoding the disclosed mutant ALK kinase polypeptides, probes for detecting it, isolated mutant polypeptides, recombinant polypeptides, and reagents for detecting the fusion and truncated polypeptides. The disclosed identification of this new fusion protein enables methods for screening for compounds that inhibit the proteins, and methods for inhibiting the progression of a cancer characterized by the mutant polynucleotides or polypeptides.

The present invention provides a method of treating cancer in a subject, the method comprising administering to the subject at least one nicotinamide phosphoribosyltransferase (NAMPT) inhibitor, thereby treating the cancer, wherein protein phosphatase Mg.sup.2+/Mn.sup.2+ dependent 1D (PPM1D) is elevated in the cancer.

The present disclosure features methods for identifying pateints having a hyperproliferative disease, disorder, or condition responsive to phosphodiesterase 3 (PDE3) and schlafen family member 12 (SLFN12) complex formation. The hyperproliferative disease, disorder, or condition may be cancer in a patient including glioblastoma, melanoma, ovarian cancer, cervical cancer, sarcoma, or hematopoietic cancers, such as acute myeloid leukemia. Those responsive diseases, disorders, or conditions may be identified using the biomarker AIP and/or TRRAP in combination with those biomarkers pertinent to phosphodieseterase 3 and schlafen family member 12 complexes which may be formed by PDE3 modulation with certain active compounds. Expression of combinations of these biomarkers have been shown to correlate with active compound (e.g., PDE3 modulator, PDE3A modulator, PDE3B modulator) sensitivity.

The present invention provides a method for diagnosing or determining a pancreatic cancer-associated disease state comprising or consisting of the steps of: (a) providing a sample from an individual to be tested; and (b) determining a biomarker signature of the test sample by measuring the presence and/or amount in the test sample of one or more biomarker selected from the group defined in Table A; wherein the presence and/or amount in the test sample of the one or more biomarker selected from the group defined in Table A is indicative of the pancreatic cancer-associated disease in the individual; uses and methods of determining a pancreatic cancer-associated disease state, and methods of treating pancreatic cancer, together with arrays and kits for use in the same.

The present invention relates to biomarkers which comprise one or more genomic sequence(s) comprising epigenetic modification and their use in a method for predicting resistance to cancer treatment, in particular for patient stratification.

A method for selecting an individual to be a candidate for administration of an immune checkpoint inhibitor in treatment of a tumor, comprising: (1) a step of collecting a tumor tissue from the individual, (2) a step of determining the extent of B7-H3 expression in the tumor tissue collected in step (1), and (3) a step of selecting the individual as an individual to be a candidate for administration of the immune checkpoint inhibitor if the B7-H3 expression level is considered to be negative, is provided.