View clinical trials related to Resectable Pancreatic Cancer.
Filter by:At present there is no validated prognostic tool for patients with resectable pancreatic cancer (RPC) to determine how best to tailor individual therapy. This study is to see if tumor features in blood and imaging prior to surgery correspond with tumor heterogeneity in the specimen after surgery.
This is a phase II multi-center study of nab-paclitaxel, gemcitabine and cisplatin (NGC triple regimen) as preoperative therapy in potentially resectable pancreatic cancer patients. DISEASE STATE - Potentially operable or borderline resectable pancreatic adenocarcinoma as assessed by standard CT criteria and histologically confirmed. - Staging by pancreatic protocol, helical abdominal computed tomography (with contrast) or MRI (with contrast) required (endoscopic ultrasound is not required). - No evidence of metastatic disease. Lymphadenopathy (defined as nodes measuring >1 cm in short axis) outside the surgical basin (i.e., para-aortic, peri-caval, celiac axis, or distant nodes) is considered M1 (unless nodes are biopsied and are negative, then enrollment can be considered after review with the study PI). Potentially Resectable Pancreatic Cancer - No involvement of the celiac artery, common hepatic artery, and superior mesenteric artery (SMA) and, if present, replaced right hepatic artery. - No involvement or <180° interface between tumor and vessel wall of the portal vein and/or superior mesenteric vein (SMV-PV) and patent portal vein/splenic vein confluence. - For tumors of the body and tail of the pancreas, involvement of the splenic artery and vein of any degree is considered resectable disease. Borderline Resectable Pancreatic Cancer - Tumor-vessel interface ≥180° of vessel wall circumference, and/or reconstructible occlusion of the SMV-PV. - Tumor-vessel interface <180° of the circumference of the SMA. - Tumor-vessel interface <180° of the circumference of the celiac artery. - Reconstructible short-segment interface of any degree between tumor and hepatic artery.
We hypothesize that administration of LDE-225 in humans with pancreatic cancer will result in inhibition of paracrine HH signaling in the pancreatic tumor stroma while having no effect on autocrine signaling in the tumor cell compartment. Furthermore we hypothesize that treatment with LDE-225 will result in changes in the tumor stroma (decreased desmoplasia, increased vascularity) that will result in improved tumor blood flow. The purpose of this study is to determine if, where and how LDE-225 works in pancreatic cancer. A cancer cell's growth can depend on the cells and tissue around it. The cells and tissue make chemical signals to influence the cancer's growth. This research study is evaluating LDE-225 designed to interfere with one of the growth signals causing pancreatic cancer growth.