Cystic precursors to invasive pancreatic cancer

The Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, The Johns Hopkins University School of Medicine, 1550 Orleans Street, Baltimore, MD 21231, USA.
Nature Reviews Gastroenterology &#38 Hepatology (Impact Factor: 10.81). 03/2011; 8(3):141-50. DOI: 10.1038/nrgastro.2011.2
Source: PubMed

ABSTRACT Improvements in the sensitivity and quality of cross-sectional imaging have led to increasing numbers of patients being diagnosed with cystic lesions of the pancreas. In parallel, clinical, radiological, pathological and molecular studies have improved the systems for classifying these cysts. Patients with asymptomatic serous cystic neoplasms can be managed conservatively with regular monitoring; however, the clinical management of patients with intraductal papillary mucinous neoplasms and mucinous cystic neoplasms is far more challenging, as it is difficult to determine whether these lesions will progress to malignancy. Fortunately, prospective studies have helped to establish that proposed clinical and radiological criteria (the Sendai guidelines) can be used to guide the care of patients with cystic lesions of the pancreas. Despite this progress in imaging and clinical guidelines, sensitive and specific tests have not yet been developed that can reliably predict the histology and biological properties of a cystic lesion. Such biomarkers are urgently needed, as noninvasive precursors of pancreatic cancer are curable, while the vast majority of invasive pancreatic adenocarcinomas are not.

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Available from: Hanno Matthaei, Apr 03, 2014
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    • "In the past, pancreatic cystic lesions (PCL) were rarely identified. In recent years its natural history has been better understood, as they have been increasingly identified by imaging methods [5]. As a result many cases of asymptomatic and non-invasive mucinous cystic neoplasms (MCN) are accidentally discovered [6]. "
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    ABSTRACT: The dramatic increase in the number of patients diagnosed with incidental pancreatic cysts through imaging methods provides a unique opportunity to detect and treat these precursor lesions of ductal adenocarcinoma before their manifestation. However, without any reliable biomarkers, the cost-effectiveness and the limited accuracy of high-resolution imaging techniques for diagnose and staging seems troublesome. Small pancreatic cysts can be easily detected, but many are clinically irrelevant and are not harmful to the patient. Furthermore, patients with clinically benign lesions are at high risk of overtreatment and morbidity and mortality from unnecessary surgical intervention. It is believed that cyst fluid analysis may provide important information for a possible diagnosis, allowing stratification and treatment of these patients. Anyway, only the logical reasoning based on all available information (medical history, imaging, and laboratory analysis of the aspirated cyst fluid) can adequately stratify patients. It has been considered that there are three precursor lesions of the pancreatic cancer (PC): mucinous cystadenoma (MCA), intraductal papillary mucinous tumor (IPMT) and pancreatic intraepithelial neoplasia (PanIN). MCA and IPMT can be diagnosed by imaging methods, but PanIN are difficult to be identified. They must be detected and treated as soon as possible, as this is the only way to increase survival and reduce mortality of pancreatic ductal adenocarcinoma. The aim of this work is to establish diagnosis, staging, and the pathological findings and to compare the effectiveness and accuracy of the other imaging methods versus endoscopic ultrasound guided fine-needle aspiration (EUS-FNA) for diagnosis of malignancy in the precursor lesions of pancreatic cancer.
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    ABSTRACT: Pancreatic cancer, once invasive, is almost uniformly fatal. In order to alleviate the dismal prognosis associated with this disease, it is imperative that pancreatic cancer be recognized and treated prior to invasion. Understanding the morphology and biology of precursor lesions of invasive pancreatic cancer has therefore become an issue of paramount importance. In the last decade, significant progress has been in the recognition and appropriate classification of these precursor lesions, and the current review will focus on our state-of-the-art knowledge on this topic. Mucinous cystic neoplasms (MCNs), intraductal papillary mucinous neoplasms (IPMNs), and pancreatic intraepithelial neoplasia (PanIN) encompass the three known morphologically distinct precursors to invasive pancreatic cancer. In addition to discussion of the "classic" precursor entities, this review will also address some of the recent diagnostic controversies for these lesions, in particular features that distinguish IPMNs from PanIN lesions. Finally, the potential clinical impact of recognizing these precursor lesions in the context of early detection of pancreatic cancer will be discussed.
    Advances in Anatomic Pathology 04/2005; 12(2):81-91. DOI:10.1097/01.pap.0000155055.14238.25 · 3.10 Impact Factor
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    ABSTRACT: Pancreatic intraductal papillary mucinous neoplasms (IPMNs) are mucin-producing neoplasms with a frequent papillary architecture that arise within the pancreatic ducts and are increasingly being recognised. Because they exhibit a spectrum of dysplasia ranging from low grade to high grade and may also have associated invasive carcinoma, and because they are clinically detectable, they are now intensively studied. There is marked overlap between IPMNs and pancreatic intraepithelial neoplasia (PanIN), such that the distinction between these two lesions is nearly impossible in certain cases. In addition, IPMNs sometimes can be confused with other primary cystic lesions of the pancreas. As a result, the correct diagnosis of IPMN can be challenging. This review addresses the clinical and pathological features of IPMNs, emphasising their diagnostic criteria, differential diagnosis and biological behaviour. Problematic issues in the pathological evaluation of IPMNs are discussed.
    Journal of clinical pathology 09/2008; 61(12):1303-13. DOI:10.1136/jcp.2007.049361 · 2.55 Impact Factor
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