Mucin-Secreting Tumors of the Pancreas

Lichtenstein, David R.; Carr‐Locke, David L.

doi:10.1016/s1052-5157(18)30469-0

Cited by 40 publications

(14 citation statements)

References 36 publications

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“…[80][81][82][83] IPMN should be distinguished from the more widely recognised mucinous cystic neoplasms (see below). [84][85][86] Similar to PanINs, IPMNs are regarded as a form of preinvasive neoplasia, acting as a precursor and maybe as even a marker of invasive carcinoma. [87][88][89] Both PanINs and IPMNs are intraductal lesions with papilla forming mucinous cells; however, in the case of IPMNs, the proliferation progresses to form large (clinically and grossly detectable) cystic or papillary masses, whereas PanINs are noted only as incidental findings.…”

Section: Muc1 and Muc2 Expression In Normal Adult Pancreasmentioning

confidence: 99%

MUC1 and MUC2 in pancreatic neoplasia: Figure 1

Levi

2004

J Clin Pathol

109

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MUCs are glycoproteins with various roles in homeostasis and carcinogenesis. Among other actions, MUC1 may inhibit cell–cell and cell–stroma interactions and function as a signal transducer, participating in cancer progression. In contrast, MUC2 is normally found only in goblet cells, where it contributes to the protective barrier function of these cells. Recently, a tumour suppressor role has been demonstrated for MUC2, and both MUC1 and MUC2 appear to have important roles in pancreatic neoplasia. MUC1 appears to be a marker of aggressive phenotype and may facilitate the vascular spread of carcinoma cells. In contrast, MUC2 is rarely detectable in aggressive pancreatic tumours, but is commonly expressed in intraductal papillary mucinous neoplasms (IPMNs), which are rare, indolent tumours, in intestinal IPMNs, and in indolent colloid carcinomas. MUC2 appears to be not only a marker of this indolent pathway, but also partly responsible for its less aggressive nature. Thus, in pancreatic neoplasia, MUC1 and MUC2 have potential diagnostic and prognostic value as markers of aggressive and indolent phenotypes, respectively, and have potential as therapeutic targets.

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Section: Muc1 and Muc2 Expression In Normal Adult Pancreasmentioning

confidence: 99%

MUC1 and MUC2 in pancreatic neoplasia: Figure 1

Levi

2004

J Clin Pathol

109

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“…Mucinous tumors, another type of exocrine pancreatic cancer, is the second most common histologic type of pancreatic cancer, accounting for <10% of all tumors. Mucinous tumors are usually less invasive at diagnosis than other types of exocrine pancreatic cancer (11). These tumors form sac-like structures, secrete mucin, and typically arise from the pancreatic ductal epithelium (11).…”

Section: Introductionmentioning

confidence: 99%

“…Mucinous tumors are usually less invasive at diagnosis than other types of exocrine pancreatic cancer (11). These tumors form sac-like structures, secrete mucin, and typically arise from the pancreatic ductal epithelium (11). Cancers of the endocrine pancreas are less common, occurring at a rate of about five per million person-years, and accounting for <5% of all pancreatic cancers (12).…”

Section: Introductionmentioning

confidence: 99%

Differences in Survival by Histologic Type of Pancreatic Cancer

Fesinmeyer

Austin

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

249

162

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Objective: Although pancreatic cancer has an extremely high case fatality rate, little is known about differences in mortality by histologic types. We examined median survival and risk of mortality for endocrine pancreatic tumors and two types of exocrine tumors, adenocarcinomas, and mucinous tumors. Method: This analysis included 35,276 pancreatic cancer cases reported to the nine population-based cancer registries participating in the Surveillance, Epidemiology, and End Results program from 1973 to 2000. Survival among cases with pancreatic adenocarcinomas, mucinous tumors, and endocrine tumors were compared using Kaplan-Meier plots. Comparative risks of mortality were evaluated using multivariate adjusted Cox regression models. Results: Endocrine pancreatic cancer cases had a median survival of 27 months compared with a median survival of 4 months for adenocarcinoma and mucinous tumor cases. Compared with adenocarcinoma cases, endocrine tumor cases had a 0.28-fold lower risk of mortality [95% confidence interval (95% CI), 0.26-0.30], and mucinous tumor cases had a 0.88-fold lower risk (95% CI, 0.84-0.91). These results were similar for men and women. Within histologic types, advanced tumor stage, older diagnosis age, surgery, and Black race were associated with increased risks of mortality, whereas female sex and more recent year of diagnosis were associated with decreased risks. Conclusion: This study confirms the clinical observation that patients with endocrine pancreatic cancer survive longer than patients with exocrine tumors. A better understanding of these differences could contribute to identifying the underlying causes of pancreatic cancer and to improving survival rates across all histologic types. (Cancer Epidemiol Biomarkers Prev 2005;14(7):1766 -73)

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“…Pancreas cancer is one of the most deadly cancers in the world with a very low (5%) survival rate at 5 years (Huguier and Mason, 1999), and mucinous carcinomas of the pancreas are correlated with poor prognosis (Lichtenstein and Carr-Locke, 1995). Moreover, inability to detect cancer at an early stage and the lack of effective therapeutic treatment are largely responsible for the low survival of the patients (Hruban, 2001).…”

Section: Introductionmentioning

confidence: 99%

A role for human MUC4 mucin gene, the ErbB2 ligand, as a target of TGF-β in pancreatic carcinogenesis

et al. 2004

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MUC4 encodes a large transmembrane mucin that is overexpressed in pancreatic adenocarcinomas. The molecular mechanisms responsible for that altered pattern of expression are unknown. TGF-b, a pleiotropic cytokine, regulates numerous genes involved in pancreatic carcinogenesis via activation of the Smads proteins and MUC4 promoter is rich in Smad-binding elements. Our aim was to study whether the regulation of MUC4 expression by TGF-b in pancreatic cancer cells was strictly dependent on Smad4 activity. Three pancreatic cancer cell lines, CAPAN-1 (MUC4 þ /Smad4À), CAPAN-2 (MUC4 þ / Smad4 þ ) and PANC-1 (MUC4À/Smad4 þ ), were used. By RT-PCR, transfection assays and immunohistochemistry, we show that (i) both MUC4 mRNA and apomucin expression are upregulated by TGF-b, (ii) Smad2 positively cooperates with Smad4 to activate the promoter, (iii) activation of Smad4 by exogenous TGF-b induces Smad4 binding to the promoter, (iv) Smad7 and c-ski both inhibit activation by Smad4. When Smad4 is mutated and inactive, TGF-b activates MUC4 expression via MAPK, PI3K and PKA signaling pathways. Absence of expression in PANC-1 cells is due to histone deacetylation. Altogether, these results indicate that upregulation of MUC4 by TGF-b is restricted to well-differentiated pancreatic cancer cells, and point out a novel mechanism for TGF-b as a key molecule in targeting MUC4 overexpression in pancreatic adenocarcinomas.

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Mucin-Secreting Tumors of the Pancreas

Cited by 40 publications

References 36 publications

MUC1 and MUC2 in pancreatic neoplasia: Figure 1

MUC1 and MUC2 in pancreatic neoplasia: Figure 1

Differences in Survival by Histologic Type of Pancreatic Cancer

A role for human MUC4 mucin gene, the ErbB2 ligand, as a target of TGF-β in pancreatic carcinogenesis

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