Abstract: The present invention provides a novel method to determine the likelihood of effectiveness of a treatment in an individual affected with or at risk for developing cancer. The method involves detecting the presence or absence of Met amplification in an individual. The presence of Met amplification indicates that a Met targeting treatment is likely to be effective. Preferably, the Met targeting treatment is PHA-665752 or PF-02341066. In addition, the present methods allow for the detection of cancer in an individual, wherein the presence of Met amplification indicates that cancer is present and further that it will be treatable, namely with a Met targeting treatment.

Abstract: Methods for treating cancer, e.g., cancer of epithelial origin, by specifically targeting human satellite II (HSATII) using sequence specific agents such as oligonucleotides.

Abstract: This disclosure relates to new assay methods for analysis of RNA, e.g., from circulating tumor cells (CTCs), tumor-specific exosomes, or tumor-specific cell-free RNA, in a subject's blood sample to determine an expression level of one or more lineage markers in the blood sample, wherein the expression level of a specific one or more lineage markers is predictive of progression-free survival and overall survival for a specific anti-cancer treatment regimen in that subject.

Abstract: Methods for treating cancer, e.g., cancer of epithelial origin, by specifically targeting human satellite II (HSATII) using sequence specific agents such as oligonucleotides. As shown herein, the hetero chromatic HSATII satellite repeat is silenced in normal cells, but massively over expressed in epithelial cancers and in cancer cell lines when grown as xenografts or in 3D culture. Induction of HSATII RNA, either in xenografts or using in vitro reconstitution models, suggests the appearance of complementary DNA intermediates.

Abstract: A method of identifying insights related to the occurrence of an adverse health outcome of interest, comprises extracting electronic clinical data associated with historical healthcare encounters. The method also comprises defining patient groups based upon similar data patterns present in the extracted electronic clinical data wherein the patient groups have varying likelihood for the adverse health outcome. Still further, the method comprises deriving hypothesized etiological explanations for why one or more patient groups have higher likelihood when compared to other patient groups. Optionally, the method comprises identifying clinical interventions that are intended to reduce the likelihood of the adverse outcome for certain patient groups.

Abstract: Verified electronic products are created and distributed by an electronic platform, which includes a client interface, a creator interface, a decider interface, and a backer interface. An unverified product associated with a creator entity is received through the creator interface, where the unverified product comprises an electronic product having a set of clauses. A decider entity and backer entity are associated with the unverified product, which is converted to a verified product. The verified product is then added to a search engine associated with other previously verified products to define a collection of searchable verified products. Client information is obtained through the client interface and is used to identify a verified product from the collection of searchable verified products via the search engine. Based on the identified verified product, and instrument is built and is communicated to the client entity via the client interface for acceptance by the client entity.

Abstract: A method of identifying insights related to the occurrence of an adverse health outcome of interest, comprises extracting electronic clinical data associated with historical healthcare encounters. The method also comprises defining patient groups based upon similar data patterns present in the extracted electronic clinical data wherein the patient groups have varying likelihood for the adverse health outcome. Still further, the method comprises deriving hypothesized etiological explanations for why one or more patient groups have higher likelihood when compared to other patient groups. Optionally, the method comprises identifying clinical interventions that are intended to reduce the likelihood of the adverse outcome for certain patient groups.

Abstract: Methods of isolating, enriching, capturing, identifying, or detecting the presence of, cancerous cells in a sample, e.g., a blood sample from a subject, by detecting the presence of one or more cancer cell surface markers selected from the group consisting of cadherin 1 (CDH1), CDH2, CDH3, CDH4, CDH5, CDH9, CDH11, CDH17, CDH19, protocadherin 9 (PCDH9) and/or PCDH beta 13 (PCDHb13), and optionally an additional cancer cell surface marker, e.g., EpCAM, MUC1, EphB4, EGFR, CEA, and/or HER2.

Abstract: Disclosed herein are methods and reagents for determining the responsiveness of cancer to an epidermal growth factor receptor (EGFR) targeting treatment. The detection of these mutations will allow for the administration of gefitinib, erlotinib and other tyrosine kinase inhibitors to those patients most likely to respond to the drug.

Abstract: Disclosed herein are methods and reagents for determining the responsiveness of cancer to an epidermal growth factor receptor (EGFR) targeting treatment. The detection of these mutations will allow for the administration of gefitinib, erlotinib and other tyrosine kinase inhibitors to those patients most likely to respond to the drug.

Abstract: Ultra-sensitive assays for the detection of mutations, e.g., from blood-based sources of tumor genetic material (circulating tumor cells or plasma), or other settings in which limiting amounts of DNA, e.g., tumor DNA, is available. The assay is exemplified in the estrogen receptor, but is broadly customizable to target mutations in other genes.

Abstract: This disclosure relates to new assay methods for analysis of circulating tumor cells (CTCs) in blood samples for detection, e.g., early detection, and/or monitoring of disease, e.g., cancer. The methods provide ultra-high sensitivity and specificity, and include the use of microfluidic isolation of CTCs and digital detection of RNA derived from the CTCs.

Abstract: Methods for diagnosing cancer based on detecting the presence of increased levels of expression of satellite repeats and/or Line-1.

Abstract: Provided herein are assays and methods related to determining a ratio of expression levels of PSA/PSMA or determining the expression level of PSMA in circulating tumor cells for diagnosis and/or for the purpose of monitoring treatment efficacy for prostate cancers that are likely hormone resistant.

Abstract: Methods for diagnosing cancer and monitoring treatment efficacy based on detecting the presence of increased levels of expression of satellite correlated genes.

Abstract: Provided herein are assays and methods related to determining a ratio of expression levels of PSA/PSMA or determining the expression level of PSMA in circulating tumor cells for diagnosis and/or for the purpose of monitoring treatment efficacy for prostate cancers that are likely hormone resistant.

Abstract: Methods for treating cancer, e.g., cancer of epithelial origin, by specifically targeting human satellite II (HSATII) using sequence specific agents such as oligonucleotides. As shown herein, the hetero chromatic HSATII satellite repeat is silenced in normal cells, but massively over expressed in epithelial cancers and in cancer cell lines when grown as xenografts or in 3D culture. Induction of HSATII RNA, either in xenografts or using in vitro reconstitution models, suggests the appearance of complementary DNA intermediates.

Abstract: Methods of isolating, enriching, capturing, identifying, or detecting the presence of, cancerous cells in a sample, e.g., a blood sample from a subject, by detecting the presence of one or more cancer cell surface markers selected from the group consisting of cadherin 1 (CDH1), CDH2, CDH3, CDH4, CDH5, CDH9, CDH11, CDH17, CDH19, protocadherin 9 (PCDH9) and/or PCDH beta 13 (PCDHb13), and optionally an additional cancer cell surface marker, e.g., EpCAM, MUC1, EphB4, EGFR, CEA, and/or HER2.

Abstract: The present invention is directed to methods for the treatment of gefitinib and/or erlotinib resistant cancer. An individual with cancer is monitored for cancer progression following treatment with gefitinib and/or erlotinib. Progression of the cancer is indicative that the cancer is resistant to gefitinib and/or erlotinib. Once progression of cancer is noted, the subject is administered a pharmaceutical composition comprising an irreversible epidermal growth factor receptor (EGFR) inhibitor. In preferred embodiments, the irreversible EGFR inhibitor is EKB 569, HKI-272 and HKI-357.

Abstract: The technology described herein relates to methods of detecting circulating tumor cells (CTCs), e.g. by detecting changes in the expression of certain CTC marker genes. Aberrant expression of CTC marker genes, e.g. changes in expression indicative of CTCs can also be targeted in order to treat cancer.