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Pancreatic cystic lesions are commonly encountered today with the routine use of cross-sectional imaging modalities such as computed tomography (CT) and magnetic resonance imaging (MRI). The majority of patients discovered to have a pancreatic cyst are completely asymptomatic; yet the presence of such a finding instills fear in the minds of both patient and physician, as the concern for malignant transformation to pancreatic cancer is great despite the relatively low overall likelihood of cyst progression. Not all cysts in the pancreas represent pancreatic cystic neoplasms (PCNs), and not all PCNs have significant malignant potential. Mucinous PCNs are the most concerning, as these lesions have the greatest potential for cancerous transformation to adenocarcinoma. Within the group of mucinous PCNs, intraductal papillary mucinous neoplasms (IPMNs) involving the main pancreatic duct are the most worrisome, and surgical resection should be pursued if the patient has appropriate operative risks. IPMN lesions involving the branch ducts, and mucinous cystadenomas, have a lower likelihood for malignancy, and they may be closely followed for the development of any worrisome or high-risk features. Surveillance of known PCNs is performed with a combination of CT, MRI and endoscopic ultrasound (EUS). EUS-guided fine-needle aspiration (EUS-FNA) may be used to assess cyst fluid cytology, and also to detect cyst fluid amylase level, carcinoembryonic antigen level, and DNA molecular analysis in certain cases. The presence or absence of specific cyst morphological features, as well as the cyst fluid analysis, is what enables the physician to guide the patient towards continued surveillance, versus the pursuit of surgical resection.

Sodium taurocholate-cotransporting polypeptide (ntcp) is considered to be a major determinant of bile acid uptake into hepatocytes. However, the regulation of ntcp and the degree that it participates in the accumulation of specific substrates are not well understood. We utilized fluorescent bile acid derivatives and direct quantitation of fluorescent microscopy images to examine the regulation of ntcp and its role in the cell-to-cell variability of fluorescent bile acid accumulation. Primary-cultured rat hepatocytes rapidly accumulated the fluorescent bile acids, chenodeoxycholylglycylamidofluorescein (CDCGamF), 7-β- nitrobenzoxadiazole 3-α hydroxy 5-β cholan-24-oic acid (NBD-CA), and cholyl-glycylamido-fluorescein (CGamF). However, in stably transfected HeLa cells, ntcp preferred CDCGamF, whereas the organic anion transporter, organic anion transporting polypeptide 1 (oatp1a1), preferred NBD-CA, and neither ntcp nor oatp1a1 showed strong accumulation of CGamF by these methods. Ntcp-mediated transport of CDCGamF was inhibited by taurocholate, cyclosporin, actin depolymerization, and an inhibitor of atypical PKC-ζ. The latter two agents altered the cellular distribution of ntcp as visualized in ntcp-green fluorescent protein-transfected cells. Although fluorescent bile acid accumulation was reproducible by the imaging assays, individual cells showed variable accumulation that was not attributable to changes in membrane permeability or cell viability. In HeLa cells, this was accounted for by variable levels of ntcp, whereas, in hepatocytes, ntcp expression was uniform, and low accumulation was seen in a large portion of cells despite the presence of ntcp. These studies indicate that single-cell imaging can provide insight into previously unrecognized details of anion transport in the complex environment of polarized hepatocytes.