Ductectatic‐type Mucinous Cystadenoma and Cystadenocarcinoma of the Human Pancreas: A Novel Clinicopathological Entity

Yanagisawa, Akio; Ohashi, Kazuhiko; Hori, Masaharu; Takagi, Kunio; Kitagawa, Tomoyuki; Sugano, Haruo; Kato, Yukio

doi:10.1111/j.1349-7006.1993.tb00161.x

Cited by 63 publications

(31 citation statements)

References 13 publications

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“…Bcat1 catalyzes the first step of branched-chain amino-acid catabolism and appears to be involved in apoptosis (Eden and Benvenisty, 1999). Somatic mutations of the Kras2 gene play a causal role in lung tumorigenesis (Johnson et al, 2001) and have also been found in chronic inflammation conditions, such as chronic pancreatitis and ulcerative colitis (Yanagisawa et al, 1993;Lang et al, 1999). A transgenic mouse expressing the human c-H-ras gene showed enhanced susceptibility to autoimmune hepatitis (Tsunematsu et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Pulmonary adenoma susceptibility 1 (Pas1) locus affects inflammatory response

et al. 2003

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Two outbred mouse lines, phenotypically selected for differential subcutaneous (s.c.) acute inflammatory response (AIR), were analysed for urethane-induced lung inflammatory response and susceptibility to lung tumorigenesis. AIR min mice, which show a low response to s.c. acute inflammation, developed a persistent subacute lung inflammatory response and a 40-fold higher lung tumor multiplicity than did AIR max mice, which are selected for high response to s.c. acute inflammation and showed a transient lung inflammatory response. A highly significant linkage disequilibrium pattern was observed in AIR max and AIR min mice at marker alleles located within a 452-kb pulmonary adenoma susceptibility 1 (Pas1) locus region, thus defining the location of gene candidacy for inflammatory response and for the biological effects of Pas1 in this region. AIR min and AIR max mice segregated by descent the Pas1 s and Pas1 r alleles, respectively, providing evidence for the involvement of the Pas1 locus in the inflammatory response. The 452-kb region contains Kras2 and four additional genes, including the lymphoidrestricted membrane protein (Lrmp) gene, whose ProLeu nonconservative variation was linked with inflammatory response and Pas1 allelotype. These results provide a model to explore the mechanism underlying inherited predisposition to lung cancer in the context of a link to inflammation.

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Section: Discussionmentioning

confidence: 99%

Pulmonary adenoma susceptibility 1 (Pas1) locus affects inflammatory response

et al. 2003

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“…In the last two decades, intraductal neoplasms that present as cystic masses have received considerable attention in the literature (4,14,15). Two such entities, intraductal papillary mucinous neoplasms (IPMN) and intraductal oncocytic papillary mucinous neoplasms (IOPN), are now well recognized (2)(3)(4)(5)(6).…”

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confidence: 99%

Lymphoepithelial Cysts of the Pancreas: a Report of 12 Cases and a Review of the Literature

et al. 2002

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Lymphoepithelial cyst (LEC) of the pancreas is a rare lesion of undetermined pathogenesis that had been documented almost exclusively in males. The literature on this entity is limited to reports of single or small numbers of cases. Here is presented a clinicopathologic analysis of 12 patients with LEC, 4 of whom were female. The mean age of the patients was 56 years. Four patients presented with abdominal pain and nausea, but in two patients, the cysts were detected incidentally. Only one patient had a history of chronic pancreatitis, and another had a family member with pancreatic cancer. In one patient, a clinical diagnosis of pseudocyst was rendered, and the remaining patients were clinically thought to have cystic neoplasms. None of the patients had any identifiable immunosuppression, HIV positivity, autoimmune disorder (such as Sjogren syndrome) or lymphoma. Seven cysts were located in the head of the pancreas, and 5 were in the tail. The mean size was 4.8 cm (range, 1.2-17 cm). Five LECs were multilocular, three were unilocular; in others, the number of loculi was not recorded. All were "macrocystic" lesions. Two patients had two separate lesions, both in the tail of the pancreas. Histologically, all cases were characterized by cysts, some containing keratin, and lined by mature stratified squamous epithelium surrounded by dense lymphoid tissue, often with prominent follicles. In some areas, the lining epithelium had more cuboidal, flattened, or transitional appearance. Mucinous goblet-like cells were seen in one case. Acute inflammation was not seen. Cystic lesions of the pancreas are relatively rare (1-3), but they constitute an important category with a challenging differential diagnosis at the clinical, radiological, and pathologic levels. In the past decade, wider application of radiographic techniques, coupled with the improvement in the surgical approach to this organ, has brought new attention to the cystic processes in the pancreas. As more cases of pancreatic cysts are being diagnosed and operated on, new clinicopathologic entities are being recognized (4 -6), and the old ones are becoming better characterized (7-10). Pseudocysts are the most common cystic lesions of the pancreas and usually occur as a complication of pancreatitis (11). True cysts, on the other hand, are most often neoplastic (1). The classification and understanding of these neoplastic pancreatic cysts have progressively improved in the last three decades. The serous and mucinous cystic neoplasms (SCN and MCN) described by Compagno and Oer-

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“…At any event, our ®ndings strongly indicate that, in the same pancreas, morphologically indistinguishable candidate precursor lesions harbor cells with distinct K-RAS mutations, and that their clonal expansion might variably contribute to full development of PC. The frequency of K-RAS mutation in PC precursor lesions is known to be higher in histologically advanced papillary lesions than in nonpapillary ductal changes (Yanagisawa et al, 1993;Caldas et al, 1994;Moskaluk et al, 1997). In addition, genetic alterations other than K-RAS mutation can be found in PC precursors (Yamano et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…K-RAS activation has been recognized also in microdissected foci of PanIN, the candidate precursor lesion of PC previously known as ductal cell hyperplasia (Cubilla and Fitzgerald, 1976;Hruban et al, 2000a,b). The frequency of K-RAS mutations was found to be higher in hyperplastic foci associated with pancreatic cancer (65% to 75%), than in those associated with chronic pancreatitis (62%), or detected at necropsy in otherwise normal pancreas (24%) (Caldas et al, 1994;Yanagisawa et al, 1993;Tada et al, 1996). A major role of K-RAS mutation in committing hyperplastic areas to cancer development was then postulated.…”

Section: Introductionmentioning

confidence: 98%

Common occurrence of multiple K-RAS mutations in pancreatic cancers with associated precursor lesions and in biliary cancers

et al. 2002

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Recent studies on small series of pancreatic cancer (PC) with foci of pancreatic intraepithelial neoplasia (PanIN), a putative precursor lesion, have shown that multiple K-RAS mutations may coexist in the same neoplastic pancreas. To see whether mutant-K-RAS polyclonality is a common and speci®c feature of pancreatic carcinogenesis, we investigated a unselected series of periampullary cancers (41 pancreatic, 13 biliary and two ampullary adenocarcinomas). After hemi-nested polymerase chain reaction (PCR), mutations identi®ed with single strand conformation polymorphism (SSCP) were con®rmed by allele-speci®c PCR and sequencing. K-RAS codon 12 was mutated in 34 (83%) pancreatic cancers and in 11 (85%) biliary cancers. Multiple distinct K-RAS mutations were found in 16 PC (39% of all cases, 47% of those with mutated K-RAS) and in eight biliary cancers (62 and 72%, respectively). In PC, multiple K-RAS mutations were more frequent (P50.001) in cancers with (nine of 12, 75%) than in those without detectable PanIN (seven of 29, 24%). Individual precursor lesions of the same neoplastic pancreas were found to harbor distinct mutations. Results show that multiple K-RAS mutations are frequent both in PC with associated PanIN and in biliary cancers, and indicate that clonally distinct precursor lesions of PC might variably contribute to tumor development.

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Ductectatic‐type Mucinous Cystadenoma and Cystadenocarcinoma of the Human Pancreas: A Novel Clinicopathological Entity

Cited by 63 publications

References 13 publications

Pulmonary adenoma susceptibility 1 (Pas1) locus affects inflammatory response

Pulmonary adenoma susceptibility 1 (Pas1) locus affects inflammatory response

Lymphoepithelial Cysts of the Pancreas: a Report of 12 Cases and a Review of the Literature

Common occurrence of multiple K-RAS mutations in pancreatic cancers with associated precursor lesions and in biliary cancers

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