Colloid carcinoma or mucinous noncystic carcinoma arising from an IPMN. (a) Large mucin “lakes” representing invasive adenocarcinoma replacing normal pancreatic parenchyma (residual parenchyma in the left edge of the picture). Clusters of tumor epithelial cells are seen “floated” in the mucin, as seen in higher magnification in panel (b).

Colloid carcinoma or mucinous noncystic carcinoma arising from an IPMN. (a) Large mucin “lakes” representing invasive adenocarcinoma replacing normal pancreatic parenchyma (residual parenchyma in the left edge of the picture). Clusters of tumor epithelial cells are seen “floated” in the mucin, as seen in higher magnification in panel (b).

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Intraductal papillary mucinous neoplasm (IPMN) is a cystic tumor of the pancreas. The etiology is unknown, but increasing evidence suggests the involvement of several tumorigenesis pathways, including an association with hereditary syndromes. IPMN occurs more commonly in men, with the mean age at diagnosis between 64 and 67 years old. At the time o...

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... Gasztrikus metaplázia körülbelül 98%-ban mellékduktusz-érintettségű IPMN-nél fordul elő (57), morfológiájára a magas hengerhámsejtek jellemzőek, apikális elhelyezke-désű mucinnal, bazális orientációjú sejtmagokkal (58). Immunhisztokémiai vizsgálattal MUC5AC-és fokális MUC6-pozitivitás a típusos (59). ...
... A hám általában low grade diszpláziát mutat, a malignizálódási rizikó alacsony, míg az invazív eseteket a rendkívül rossz prognózisú tubuláris adenokarcinóma alkotja (59). A duktuszrendszer foveoláris metapláziája gyakran társul duodenális peptikus fekéllyel, valamint szűkületeket, krónikus fekélyeket és sipolyokat okozó Crohn-betegséggel (58). ...
... Az intesztinális fenotípus inkább MD-típusú IPMN mellett fordul elő (73%) (57). Szövettanilag villózus papillákat alkotó magas hengerhám jellemzi, kehelysejtekkel és fokozott mucintermeléssel (58). Immunhisztokémiai reakciókat végezve MUC2-és CDX2-pozitivitás dominál, genotipizálással GNASés SMAD1/5/8 mutációk gyakran azonosíthatóak (60). ...
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... Gasztrikus metaplázia körülbelül 98%-ban mellékduktusz-érintettségű IPMN-nél fordul elő (57), morfológiájára a magas hengerhámsejtek jellemzőek, apikális elhelyezke-désű mucinnal, bazális orientációjú sejtmagokkal (58). Immunhisztokémiai vizsgálattal MUC5AC-és fokális MUC6-pozitivitás a típusos (59). ...
... A hám általában low grade diszpláziát mutat, a malignizálódási rizikó alacsony, míg az invazív eseteket a rendkívül rossz prognózisú tubuláris adenokarcinóma alkotja (59). A duktuszrendszer foveoláris metapláziája gyakran társul duodenális peptikus fekéllyel, valamint szűkületeket, krónikus fekélyeket és sipolyokat okozó Crohn-betegséggel (58). ...
... Az intesztinális fenotípus inkább MD-típusú IPMN mellett fordul elő (73%) (57). Szövettanilag villózus papillákat alkotó magas hengerhám jellemzi, kehelysejtekkel és fokozott mucintermeléssel (58). Immunhisztokémiai reakciókat végezve MUC2-és CDX2-pozitivitás dominál, genotipizálással GNASés SMAD1/5/8 mutációk gyakran azonosíthatóak (60). ...
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... Preoperative imaging using CT or MRI is unable to differentiate ICPN from Carcinoma of gall bladder. The features described in view of ICPN are: [1] intramucosal, [2] preinvasive neoplastic (dyspla-stic), [3] mass forming: exophytic (papillary or polypoid), [4] size more than 1.0 cm, [5] compact, and [6] distinct from the neighboring mucosa. However, ICPN is a novel concept, and the diagnostic features remain uncertain [27] . ...
... Preoperative imaging using CT or MRI is unable to differentiate ICPN from Carcinoma of gall bladder. The features described in view of ICPN are: [1] intramucosal, [2] preinvasive neoplastic (dyspla-stic), [3] mass forming: exophytic (papillary or polypoid), [4] size more than 1.0 cm, [5] compact, and [6] distinct from the neighboring mucosa. However, ICPN is a novel concept, and the diagnostic features remain uncertain [27] . ...
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We present a case report of a 57year old lady who presented with complaints of right sided upper abdominal pain. The patient was initially diagnosed with carcinoma gall bladder(CAGB) by CECT Abdomen and PET CT imaging studies. Intra cholecystic papillary tubular neoplasm of the gall bladder(ICPN) was diagnosed after histopathological examination of the radical cholecystectomy specimen. ICPN can be managed with a cholecystectomy if the diagnosis is known pre operatively as the prognosis for ICPN is much better as compared with that for gallbladder adenocarcinoma.
... IPMNs are benign, premalignant, mucin-producing neoplasms within the pancreatic duct (main or branch ducts). The lining epithelium is tall columnar, with or without papillary projections, and can show gastric, intestinal, oncocytic or pancreaticobiliary differentiation [6]. IPMNs on histology do not have the distinctive sub-epithelial ovarian-type stroma, which differentiates them from mucinous cystic neoplasms of the pancreas [7]. ...
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... Currently, there are no well-established risk factors for IPMN development (2) but some have been linked it to genetic syndromes like familial adenomatous polyposis, Peutz-Jeghers and even Lynch syndrome (5,6). ...
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Intraductal papillary mucinous neoplasm (IPMN) of the pancreas are pre neoplastic lesions defined by the World Health Organization as a grossly visible intraductal epithelial neoplasm that arises in the pancreatic ductal system, composed of mucin producing cells. The predisposing factor for their development as well as genetics are still largely unknown. Pathologists have a pivotal role in IPMN management since features like IPMN subtype, degree of atypia, margins status and presence or absence of an invasive component imply different patient management. In this article, we perform a review of the pathological features and molecular markers of IPMNs.
... These are the most common cystic lesions of the pancreas and result from in situ neoplastic cells that hypersecrete mucin, causing focal or diffuse cystic dilation of the main duct or side branches. Main duct intraductal papillary mucinous neoplasms (IPMNs) have higher risk of malignancy (with invasive carcinoma in up to 37%) compared to side-branch IPMNs (with various dysplasia or carcinoma in situ in up to 15%) [13]. They are T2 hyperintense and are best identified on MRCP (Fig. 16). ...
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... Main duct IPMNs have the highest risk of malignancy, with mean risk around 65% to 70%. Branch duct IPMNs (BD-IPMNs) have mean risk of malignancy around 25% (3), The presence of pancreatitis-like symptoms or mural nodule in BD-IPMN is associated with higher and faster malignant risk (7,8). ...
Article
Mucinous cystic neoplasms (MCNs) and intraductal papillary mucinous neoplasms (IPMNs) are two well recognized entities of precursor cystic lesions of pancreatic duct adenocarcinoma. The characteristic features of MCNs are the lined mucinous epithelium with underlying ovarian-type stroma, but without communication with the ducts, while that for IPMNs are the communication with the ducts but without the underlying ovarian-type stroma. Here we report a case of MCN communicating with the main pancreatic duct in a 68-year-old woman. The initial radiographic diagnosis was pancreatic IPMN with main pancreatic involvement and this was also confirmed during gross examination. Histologically, the pancreatic cystic neoplasm was lined with mucinous epithelium with underlying ovarian-type of stroma. Immunohistochemical stains confirmed that the stroma cells were positive for ER, PR, alpha-inhibin and focally positive for CD10. The final pathologic diagnosis was pancreatic mucinous cystic neoplasm communicating with the main pancreatic duct. To the best of our knowledge, this is the second pathology confirmed case of MCN communicating with the main pancreatic duct. A careful gross examination and bivalvation of the main duct communicating with the cystic neoplasm helps render the correct diagnosis. If more cases are reported in the future, the MCN communicating with duct could become a new entity of pancreatic mucinous neoplasm.
... IPMN of the pancreas is an epithelial neoplasm of mucin producing cells arising in the main or branch ducts [31]. Based on cytoarchitectural atypia, IPMN is classified into low-and high-grade dysplasia [32]. ...
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Annexins are a multigene family of calcium and phospholipid-binding proteins that play important roles in calcium signaling, cell motility, differentiation and proliferation. Our previous mass spectrometry-based proteomics study revealed that annexin A10 (ANXA10) was uniquely overexpressed in pancreatic CD24⁺ adenocarcinoma cells that were dissected from clinical PDAC tissues but was absent in CD24⁻ adjacent normal cells. The correlation between ANXA10 expression and the progression of pancreatic cancer remains unknown. In this study, we performed an immunostaining assay to evaluate ANXA10 expression in 155 primary human tissue specimens, including normal pancreas, chronic pancreatitis (CP), pancreatic adenocarcinoma (PDAC), pancreatic intraepithelial neoplasia (PanIN, the most important precursor of PDAC), and intraductal papillary mucinous neoplasm (IPMN). The immunostaining result showed that ANXA10 was significantly overexpressed in PanINs, IPMNs, and PDACs but negative in normal pancreas and the majority of chronic pancreatitis tissues. Statistical analysis revealed that ANXA10 expression was significantly associated with PDAC and its precursor lesions (p<0.0001). Abundant ANXA10 expression was predominantly present in pancreatic ductal epithelial cells of PanINs, IPMNs, and tumor cells of PDACs. Since PDAC develops through a series of PanINs which in turn arise from pancreatic ducts, the consistent overexpression of ANXA10 in ductal epithelial cells in PanINs and PDACs but negative in normal pancreatic ducts suggests that ANXA10 could serve as a potential marker indicating the presence of PDAC at its earliest precancerous stages. Double immunostaining of ANXA10 and CD24 showed that there was a large overlap between these two markers in PDAC and high-grade neoplasia lesions. The statistical analysis showed that the coexpression of ANXA10 and CD24 was significantly correlated with the progression of pancreatic precursor lesions towards PDACs.