The investigators believe DCAMKL-1 is a stem cell tumor marker and is elevated in patients with pancreatic cancer. The investigators would like to analyze its expression pre and post treatment, to gauge the correlation between current pancreatic cancer therapies and the expression of DCAMKL-1

Pancreatic adenocarcinoma has the worst prognosis of any major malignancy with a 3% 5 year survival. Major obstacles in treating pancreatic cancer include extensive local invasion and early metastasis. The incidence of pancreatic adenocarcinoma (PAC) has been increasing steadily. Epithelial-mesenchymal transition (EMT) plays a key role in cancer invasion and metastasis. Recently, a direct link between EMT and the gain of epithelial stem cell properties has been described. We have recently determined that DCAMKL-1, a microtubule-associated kinase expressed in post mitotic neurons, is a putative intestinal stem cell marker. We have also demonstrated that DCAMKL-1, a protein expressed in both normal stem cells and in cancer, likely promotes tumorigenesis through the regulation of pri-let-7a microRNA and c-Myc. We have recently demonstrated evidence that DCAMKL-1 is a marker for pancreatic cancer stem cells in surgical specimens. This study will investigate expression of DCAMKL-1 in pancreatic tissue obtained through EUS-FNA. Furthermore expression of DCAMKL-1 will also be investigated in serum obtained simultaneously.

Inclusion Criteria:

• pancreatic cancer

Exclusion Criteria:

• age < 18, history of other types of cancer

Human patients with pancreatic cancer undergo various treatments for pancreatic cancer. We will examine the expression of Dcamkl-1 pre and post therapy (including, chemotherapy only, surgery only, neoadjuvant and adjuvant therapies) to correlate treatment with a change in DCAMKl-1 expression.