Abstract: Biosensors and methods for localized surface plasmon resonance biosensing are disclosed. The biosensor can include a substrate having a substrate surface to which a plurality of localized surface plasmon resonance (LSPR) antennae are affixed. The LSPR antennae can be affixed via an affixation surface of the LSPR antenna. The LSPR antennae can have a functional surface opposite the affixation surface. Each functional surface can be functionalized by a plurality of single-stranded DNA.

Abstract: Biosensors and methods for localized surface plasmon resonance biosensing are disclosed. The biosensor can include a substrate having a substrate surface to which a plurality of localized surface plasmon resonance (LSPR) antennae are affixed. The LSPR antennae can be affixed via an affixation surface of the LSPR antenna. The LSPR antennae can have a functional surface opposite the affixation surface. Each functional surface can be functionalized by a plurality of single-stranded DNA.

Abstract: The differential expression of select miRNA in plasma and bile among patients with PDAC, chronic pancreatitis (CP), and controls were measured. Patients (n=215) with treatment-naïve PDAC (n=77), CP with bile or pancreatic duct pathology (n=67), and controls (n=71) that had been prospectively enrolled in a Pancreatobiliary Disease Biorepository at the time of endoscopic retrograde cholangiopancreatography (ERCP) or endoscopic ultrasound (EUS) were identified. Controls were patients with choledocholithiasis but normal pancreata. The sample was separated into training (n=95) and validation (n=120) cohorts to establish and then test the performance of PDAC Signature Panels in diagnosing PDAC. The training cohort (n=95) included age-matched patients with CP and controls. Panels were derived from the differential expression of 10-candidate miRNA in plasma or bile.

Abstract: The differential expression of select miRNA in plasma and bile among patients with PDAC, chronic pancreatitis (CP), and controls were measured. Patients (n=215) with treatment-naïve PDAC (n=77), CP with bile or pancreatic duct pathology (n=67), and controls (n=71) that had been prospectively enrolled in a Pancreatobiliary Disease Biorepository at the time of endoscopic retrograde cholangiopancreatography (ERCP) or endoscopic ultrasound (EUS) were identified. Controls were patients with choledocholithiasis but normal pancreata. The sample was separated into training (n=95) and validation (n=120) cohorts to establish and then test the performance of PDAC Signature Panels in diagnosing PDAC. The training cohort (n=95) included age-matched patients with CP and controls. Panels were derived from the differential expression of 10-candidate miRNA in plasma or bile.

Abstract: The present invention is directed to systems and methods of conducting a purchase transaction of eligible goods or services using a stored value associated with an indicia.

Abstract: The present invention provides a method of treating pancreatic cancer by inhibiting the activity cyclin D1 activity in tumor cells. The invention is based on the finding that cyclin D1 shRNA molecules are capable of attenuating tumor growth and interfering with tumor angiogenesis.

Abstract: The present invention provides methods for determining response to neoadjuvant therapy and metastasis-free survival in pancreatic ductal adenocarcinoma based upon the level of microRNA expression and optionally the presence of a protein cancer cell marker in biological samples such as formalin-fixed paraffin-embedded specimens using in situ hybridization and optionally an immunohistochemical assay.

Abstract: The present invention includes methods for screening for drug resistance in cancer tissue ex vivo which comprises a novel 3-dimensional cell culture system that mimics the tumor microenvironment.

Abstract: The present invention provides a method of treating pancreatic cancer by inhibiting the activity cyclin D1 activity in tumor cells. The invention is based on the finding that cyclin D1 shRNA molecules are capable of attenuating tumor growth and interfering with tumor angiogenesis.

Abstract: The present invention provides a method of treating pancreatic cancer by inhibiting the activity cyclin D1 activity in tumor cells. The invention is based on the finding that cyclin D1 shRNA molecules are capable of attenuating tumor growth and interfering with tumor angiogenesis.

Abstract: The present invention provides methods for determining response to neoadjuvant therapy and metastasis-free survival in pancreatic ductal adenocarcinoma based upon the level of microRNA expression and optionally the presence of a protein cancer cell marker in biological samples such as formalin-fixed paraffin-embedded specimens using in situ hybridization and optionally an immunohistochemical assay.

Abstract: The present invention includes compositions and methods for diagnosing and treating pancreatic cancer. These compositions and methods are based on the finding that 14-3-3? protein is secreted from pancreatic cancer cells and is therefore a specific biomarker protein.

Abstract: The present invention provides a method of treating pancreatic cancer by inhibiting the activity cyclin D1 activity in tumor cells. The invention is based on the finding that cyclin D1 shRNA molecules are capable of attenuating tumor growth and interfering with tumor angiogenesis.

Abstract: Glycosylphosphatidylinositol-(GPI-) anchored HSPG glypican-1 is strongly expressed in human breast and pancreatic cancer—both by the cancer cells and in the case of pancreatic cancer the adjacent fibroblasts—whereas expression of glypican-1 is low in the normal pancreas and in chronic pancreatitis. Treatment of two pancreatic cancer cell lines, which express glypican-1, with the enzyme phosphoinositide-specific phospholipase-C (PI-PLC) abrogated their mitogenic responses to two heparin-binding growth factors: fibroblast growth factor-2 (FGF2) and heparin-binding EGF-like growth factor (HB-EGF). Treatment of MDA-MB-231 and MDA-MB-468 breast cancer cells with PI-PLC abrogates the mitogenic response to two heparin-binding growth factors, heparin-binding epidermal growth factor-like growth factor (HB-EGF) and fibroblast growth factor-2 (FGF-2). Syndecan-1 is also expressed at high levels in breast cancer tissues as well as breast cancer cells by comparison with breast normal tissues.

Abstract: Glycosylphosphatidylinositol-(GPI-) anchored HSPG glypican-1 is strongly expressed in human breast and pancreatic cancer—both by the cancer cells and in the case of pancreatic cancer the adjacent fibroblasts—whereas expression of glypican-1 is low in the normal pancreas and in chronic pancreatitis. Treatment of two pancreatic cancer cell lines, which express glypican-1, with the enzyme phosphoinositide-specific phospholipase-C (PI-PLC) abrogated their mitogenic responses to two heparin-binding growth factors: fibroblast growth factor-2 (FGF2) and heparin-binding EGF-like growth factor (HB-EGF). Treatment of MDA-MB-231 and MDA-MB-468 breast cancer cells with PI-PLC abrogates the mitogenic response to two heparin-binding growth factors, heparin-binding epidermal growth factor-like growth factor (HB-EGF) and fibroblast growth factor-2 (FGF-2). Syndecan-1 is also expressed at high levels in breast cancer tissues as well as breast cancer cells by comparison with breast normal tissues.

Abstract: Glycosylphosphatidylinositol-(GPI-) anchored HSPG glypican-1 is strongly expressed in human breast and pancreatic cancer—both by the cancer cells and in the case of pancreatic cancer the adjacent fibroblasts—whereas expression of glypican-1 is low in the normal pancreas and in chronic pancreatitis. Treatment of two pancreatic cancer cell lines, which express glypican-1, with the enzyme phosphoinositide-specific phospholipase-C (PI-PLC) abrogated their mitogenic responses to two heparin-binding growth factors: fibroblast growth factor-2 (FGF2) and heparin-binding EGF-like growth factor (HB-EGF). Treatment of MDA-MB-231 and MDA-MB-468 breast cancer cells with PI-PLC abrogates the mitogenic response to two heparin-binding growth factors, heparin-binding epidermal growth factor-like growth factor (HB-EGF) and fibroblast growth factor-2 (FGF-2). Syndecan-1 is also expressed at high levels in breast cancer tissues as well as breast cancer cells by comparison with breast normal tissues.