Relation of adenoma to carcinoma in the gallbladder

Kozuka, Satoshi; Tsubone, Mikio; Yasui, Akihiro; Hachisuka, Kitao

doi:10.1002/1097-0142(19821115)50:10<2226::aid-cncr2820501043>3.0.co;2-3

Cited by 267 publications

(128 citation statements)

References 12 publications

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“…On the other hand, adenomyomatosis of the gallbladder is generally considered to carry no risk of malignant transformation, although a few cases have been reported where adenocarcinoma was associated with adenomyomatosis (Katoh et al, 1988;Ootani et al, 1992). Adenoma has been characterized as a precursor of GBC (Kozuka et al, 1982). We immunostained sections of pre-cancerous lesions together with sections from positive control specimens affixed to the same glass slides to minimize the chance of a false-negative result.…”

Section: Discussionmentioning

confidence: 99%

RCAS1 as a tumour progression marker: an independent negative prognostic factor in gallbladder cancer

et al. 2001

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Receptor-binding cancer antigen expressed on SiSo cells (RCAS1) induces apoptosis in immune cells bearing the RCAS1 receptor. We sought to determine RCAS1 involvement in the origin and progression of gallbladder cancer, and also implications of RCAS1 for patient survival. RCAS1 expression was examined immunohistochemically in 110 surgically resected gallbladder specimens. The gallbladders represented 20 cases of cholecystitis with no associated pancreaticobiliary maljunction; 23 cases of cholecystitis with pancreaticobiliary maljunction; 14 cases of adenomyomatosis; 7 adenomas; and 46 cancers. High expression of RCAS1 (immunoreactivity in over 25% of cells) was observed in 32 of the 46 cancers (70%), but not in other diseases, including pre-cancerous conditions. RCAS1 immunoreactivity was associated with depth of tumour invasion ( P = 0.0180), lymph node metastasis ( P = 0.0033), lymphatic involvement ( P = 0.0104), venous involvement ( P = 0.0224), perineural involvement ( P = 0.0351) and stage by the tumour, nodes and metastases (TNM) classification ( P = 0.0026). Thus, RCAS1 expression may be a relatively late event in gallbladder carcinogenesis possibly promoting tumour progression. Cox regression multivariate analysis demonstrated RCAS1 positivity to be an independent negative predictor for survival ( P = 0.0337; risk ratio, 12.690; 95% confidence interval, 1.216–132.423). High expression of RCAS1 significantly correlated with tumour progression and predicted poor outcome in gallbladder cancer. © 2001 Cancer Research Campaign http://www.bjcancer.com

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Section: Discussionmentioning

confidence: 99%

RCAS1 as a tumour progression marker: an independent negative prognostic factor in gallbladder cancer

et al. 2001

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“…3) [1,3,33,34]. The sequence of hyperplasia-dysplasia-carcinoma, regarded as the prevailing mechanism underlying the development of biliary tract cancer in PBM, is thought to differ from both the adenoma-carcinoma sequence and de novo carcinogenesis associated with biliary tract cancer in the population without PBM [35][36][37].…”

Section: Mechanism Of Biliary Carcinogenesismentioning

confidence: 99%

Pancreaticobiliary maljunction and biliary cancer

et al. 2014

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Pancreaticobiliary maljunction (PBM) is a congenital malformation in which the pancreatic and bile ducts join anatomically outside the duodenal wall. Japanese clinical practice guidelines on how to deal with PBM were made in 2012, representing a world first. According to the 2013 revision to the diagnostic criteria for PBM, in addition to direct cholangiography, diagnosis can be made by magnetic resonance cholangiopancreatography (MRCP), 3-dimensional drip infusion cholangiography computed tomography, endoscopic ultrasonography (US), or multiplanar reconstruction images by multidetector row computed tomography. In PBM, the common channel is so long that sphincter action does not affect the pancreaticobiliary junction, and pancreatic juice frequently refluxes into the biliary tract. Persistence of refluxed pancreatic juice injures epithelium of the biliary tract and promotes cancer development, resulting in higher rates of carcinogenesis in the biliary tract. In a nationwide survey, biliary cancer was detected in 21.6 % of adult patients with congenital biliary dilatation (bile duct cancer, 32.1 % vs. gallbladder cancer, 62.3 %) and in 42.4 % of PBM patients without biliary dilatation (bile duct cancer, 7.3 % vs. gallbladder cancer, 88.1 %). Pathophysiological conditions due to pancreatobiliary reflux occur in patients with high confluence of pancreaticobiliary ducts, a common channel C6 mm long, and occlusion of communication during contraction of the sphincter. Once the diagnosis of PBM is established, immediate prophylactic surgery is recommended. However, the surgical strategy for PBM without biliary dilatation remains controversial. To detect PBM without biliary dilatation early, MRCP is recommended for patients showing gallbladder wall thickening on screening US under suspicion of PBM.

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“…Subsequently, the atypical epithelium undergoes increased stratification leading to the high-grade premalignant lesion called carcinoma in situ (27,28). Besides this most frequent evolution, a small number of gallbladder carcinomas seems to evolve from preexisting adenomas (29).…”

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confidence: 99%

Estrogen-dependent gallbladder carcinogenesis in LXRβ ^−/− female mice

Gabbi

Kim

Barros

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Gallbladder cancer is a highly aggressive disease with poor prognosis that is two to six times more frequent in women than men. The development of gallbladder cancer occurs over a long time (more than 15 y) and evolves from chronic inflammation to dysplasia/metaplasia, carcinoma in situ, and invasive carcinoma. In the present study we found that, in female mice in which the oxysterol receptor liver X receptor-β (LXRβ) has been inactivated, preneoplastic lesions of the gallbladder developed and evolved to cancer in old animals. LXRβ is a nuclear receptor involved in the control of lipid homeostasis, glucose metabolism, inflammation, proliferation, and CNS development. LXRβ −/− female gallbladders were severely inflamed, with regions of dysplasia and high cell density, hyperchromasia, metaplasia, and adenomas. No abnormalities were evident in male mice, nor in LXRα −/− or LXRαanimals of either sex. Interestingly, the elimination of estrogens with ovariectomy prevented development of preneoplastic lesions in LXRβ −/− mice. The etiopathological mechanism seems to involve TGF-β signaling, as the precancerous lesions were characterized by strong nuclear reactivity of phospho-SMAD-2 and SMAD-4 and loss of E-cadherin expression. Upon ovariectomy, E-cadherin was reexpressed on the cell membranes and immunoreactivity of pSMAD-2 in the nuclei was reduced. These findings suggest that LXRβ in a complex interplay with estrogens and TGF-β could play a crucial role in the malignant transformation of the gallbladder epithelium.cancer | hormone | oxysterols | SMAD | E-cadherin

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Relation of adenoma to carcinoma in the gallbladder

Cited by 267 publications

References 12 publications

RCAS1 as a tumour progression marker: an independent negative prognostic factor in gallbladder cancer

RCAS1 as a tumour progression marker: an independent negative prognostic factor in gallbladder cancer

Pancreaticobiliary maljunction and biliary cancer

Estrogen-dependent gallbladder carcinogenesis in LXRβ ^−/− female mice

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Relation of adenoma to carcinoma in the gallbladder

Cited by 267 publications

References 12 publications

RCAS1 as a tumour progression marker: an independent negative prognostic factor in gallbladder cancer

RCAS1 as a tumour progression marker: an independent negative prognostic factor in gallbladder cancer

Pancreaticobiliary maljunction and biliary cancer

Estrogen-dependent gallbladder carcinogenesis in LXRβ −/− female mice

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Product

Resources

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Estrogen-dependent gallbladder carcinogenesis in LXRβ ^−/− female mice