Mucinous Cystic Neoplasia
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Pancreatic Intraepithelial Neoplasia
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Pancreatic intraepithelial neoplasms (PanINs) and intraductal papillary mucinous neoplasms (IPMNs) are common pancreatic adenocarcinoma precursor lesions. However, data regarding their respective associations with survival rate and prognosis are lacking. We retrospectively evaluated 72 pancreatic adenocarcinoma tumor resection patients at the University of Kansas Hospital between August 2009 and March 2019. Patients were divided into one of two groups, PanIN or IPMN, based on the results of the surgical pathology report. We compared baseline characteristics, overall survival (OS), and progression free survival (PFS) between the two groups, as well as OS and PFS based on local or distant tumor recurrence for both groups combined. 52 patients had PanINs and 20 patients had IPMNs. Patients who had an IPMN precursor lesion had better median PFS and OS when compared to patients with PanIN precursor lesions. However, the location of tumor recurrence (local or distant) did not show a statistically significant difference in OS.
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Pancreatic ductal adenocarcinoma (PDA) is characterized by an extremely poor prognosis, since it is usually diagnosed at advanced stages. In order to employ tools for early detection, a better understanding of the early stages of PDA development from its main precursors, pancreatic intraepithelial neoplasia (PanIN), and intraductal papillary mucinous neoplasm (IPMN) is needed. Recent studies on murine PDA models have identified a different exocrine origin for PanINs and IPMNs. In both processes, developmental pathways direct the initiation of PDA precursors from their cellular ancestors. In this review, the current understanding of early PDA development is summarized.
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Abstract: Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease, with a 5-year survival rate of less than 5%. To better understand PDAC and to improve its dismal prognosis, we must understand its origins. PDAC has three distinct noninvasive precursor lesions including intraductal papillary mucinous neoplasm, mucinous cystic neoplasm, and pancreatic intraepithelial neoplasia. Each of these precursor lesions has its own unique compendium of clinical findings, morphological features, and genetic aberrations. This review focuses on the clinical significance of precursor lesions of pancreatic cancer and how better understanding of these lesions can aid in early detection and treatment. Keywords: pancreatic ductal adenocarcinoma, precursor lesions, intraductal papillary mucinous neoplasm, mucinous cystic neoplasm, pancreatic intraepithelial neoplasia, PanIN
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To better understand pancreatic ductal adenocarcinoma (PDAC) and improve its dismal prognosis it is essential to understand its origins. This chapter describes the pathology of the four well-established pancreatic cancer precursor lesions: pancreatic intraepithelial neoplasia (PanIN), intraductal papillary mucinous neoplasm (IPMN), intraductal tubulopapillary neoplasm (ITPN), and mucinous cystic neoplasm (MCN). Each of these precursor lesions have their own unique compendium of clinical findings, gross and microscopic features, and molecular aberrations. PanINs are microscopic lesions, whereas IPMNs are grossly visible lesions. ITPNs are rare, nodular tumors, often in the pancreatic head, and composed of densely packed tubular glands. MCNs are cystic lesions but, in contrast to IPMN and ITPN, do not communicate with the pancreatic-duct system and are characterized by surrounding ovarian-type stroma. PanINs, IPMNs, and MCNs are graded by a two-tiered system into low- and high-grade dysplastic lesions.
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Pancreatic Intraepithelial Neoplasia
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Pancreatic ductal adenocarcinoma (PDA), one of the most lethal cancers worldwide, is associated with two main types of morphologically distinct precursors-pancreatic intraepithelial neoplasia (PanIN) and intraductal papillary mucinous neoplasm (IPMN). Although the progression of PanIN into invasive cancer has been well characterized, there remains an urgent need to understand the biology of IPMNs, which are larger radiographically detectable cystic tumors. IPMNs comprise a number of subtypes with heterogeneous histopathologic and clinical features. Although frequently remaining benign, a significant proportion exhibits malignant progression. Unfortunately, there are presently no accurate prognosticators for assessing cancer risk in individuals with IPMN. Moreover, the fundamental mechanisms differentiating PanIN and IPMN remain largely obscure, as do those that distinguish IPMN subtypes. Recent studies, however, have identified distinct genetic profiles between PanIN and IPMN, providing a framework to better understand the diversity of the precursors for PDA. Here, we review the clinical, biological, and genetic properties of IPMN and discuss various models for progression of these tumors to invasive PDA.
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To better understand pancreatic ductal adenocarcinoma (PDAC) and improve its dismal prognosis, it is essential to understand its origins. This chapter describes the characteristics of the five well-established pancreatic cancer precursor lesions: pancreatic intraepithelial neoplasia (PanIN), intraductal papillary mucinous neoplasm (IPMN), intraductal oncocytic papillary neoplasm (IOPN), intraductal tubulopapillary neoplasm (ITPN), and mucinous cystic neoplasm (MCN). Each of these precursor lesions has its own unique compendium of clinical findings, gross and microscopic features, and molecular aberrations. PanINs are microscopic lesions, whereas IPMNs are grossly visible cystic lesions. IOPNs and ITPNs are rare tumors, which resemble IPMNs, but have been recognized as separate entities due to their unique histologic appearance and distinctive molecular features. MCNs are cystic lesions that do not communicate with the pancreatic duct system and are defined by their surrounding ovarian-type stroma. These precursor lesions enable valuable insights into the molecular mechanisms of pancreatic tumorigenesis. In addition, detection and surgical resection of these precursor lesions provide an opportunity to prevent their progression to PDAC or early detection of PDAC, substantially improving prognosis.
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