Analysis of the tumour suppressor genes, FHIT and WT-1, and the tumour rejection genes, BAGE, GAGE-1/2, HAGE, MAGE-1, and MAGE-3, in benign and malignant neoplasms of the salivary glands.
(9/113)
AIMS: Molecular genetic changes involved in tumorigenesis and malignant transformation of human tumours are novel targets of cancer diagnosis and treatment. This study aimed to analyse the expression of putative tumour suppressor genes, FHIT and WT-1, and tumour rejection genes, BAGE, GAGE-1/2, MAGE-1, MAGE-3, and HAGE (which are reported to be important in human cancers), in salivary gland neoplasms. METHODS: Gene expression was analysed by reverse transcription polymerase chain reaction (RT-PCR) in normal salivary gland tissue and 44 benign and malignant salivary gland tumours. RESULTS: Aberrant FHIT transcripts were found in one of 38 normal salivary glands, three of 28 adenomas, and two of 16 carcinomas. WT-1 mRNA was detectable in two adenomas and five carcinomas. Immunoblotting showed that WT-1 mRNA expression was associated with raised WT-1 protein concentrations. RT-PCR for detection of BAGE, GAGE, and MAGE gene expression was positive in two adenomas and nine carcinomas, but negative in normal salivary gland tissue. HAGE mRNA was found in two normal salivary glands, 11 benign, and eight malignant tumours. CONCLUSIONS: FHIT mRNA splicing does not appear to be involved in the genesis of salivary gland neoplasms. The upregulation of WT-1 mRNA in tumours of epithelial/myoepithelial phenotype may imply a potential role of WT-1 in the genesis and/or cellular differentiation of these salivary gland tumours. The tumour rejection genes were more frequently, but not exclusively, expressed in malignant salivary gland tumours than in benign neoplasms, although none was suitable as a diagnostic marker of malignancy in salivary gland neoplasms. (+info)
The c-myc and PyMT oncogenes induce different tumor types in a somatic mouse model for pancreatic cancer.
(10/113)
We have generated a mouse model for pancreatic cancer through the somatic delivery of oncogene-bearing avian retroviruses to mice that express TVA, the receptor for avian leukosis sarcoma virus subgroup A (ALSV-A), under the control of the elastase promoter. Delivery of ALSV-A-based RCAS vectors encoding either mouse polyoma virus middle T antigen (PyMT) or c-Myc to elastase-tv-a transgenic, Ink4a/Arf null mice induced the formation of pancreatic tumors. RCAS-PyMT induced pancreatic tumors with the histologic features of acinar or ductal carcinomas. The induced pancreatic lesions express Pdx1, a marker for pancreas progenitor cells, and many tumors express markers for both exocrine and endocrine cell lineages, suggesting that the tumors may be derived from progenitor cells. In contrast, RCAS-c-myc induced endocrine tumors exclusively, as determined by histology and detection of differentiation markers. Thus, specific oncogenes can induce the formation of different pancreatic tumor types in a single transgenic line, most likely from one or more types of multipotential progenitor cells. Our model appears to be useful for elucidating the genetic alterations, target cells, and signaling pathways that are important in the genesis of different types of pancreatic cancer. (+info)
ADAM9 expression in pancreatic cancer is associated with tumour type and is a prognostic factor in ductal adenocarcinoma.
(11/113)
Gene expression profiling revealed ADAM9 to be distinctly overexpressed in pancreatic ductal adenocarcinoma (PDAC). We examined the relevance of ADAM9 expression in PDAC diagnosis and prognosis. A total of 59 infiltrating PDACs, 32 specimens from patients with chronic pancreatitis, 11 endocrine tumours and 24 acinar cell carcinomas were immunohistochemically analysed for ADAM9 expression. Staining for ADAM9 was detected in 58 out of 59 (98.3%) PDACs and in two out of 24 (8.3%) acinar cell carcinomas, but not in endocrine tumours. In the non-neoplastic pancreas, whether normal or chronically inflamed, ADAM9 was expressed in centroacinar and intralobular duct cells, but not in interlobular duct cells and their hyperplastic lesions. Pancreatic ductal adenocarcinomas showing cytoplasmic ADAM9 expression correlated with poor tumour differentiation and also with shorter overall survival than in cases showing only an apical membranous staining pattern (P=0.001). Multivariate analysis identified cytoplasmic ADAM9 expression as an independent marker of shortened survival in a set of 42 curatively (R0) resected PDAC (P<0.05, hazard ratio 2.85, 95% confidence interval: 1.21-6.71). The results show that ADAM9 expression distinguishes PDACs from other solid pancreatic tumours. In addition, cytoplasmic ADAM9 overexpression is associated with poor differentiation and shortened survival. Therefore, ADAM9 overexpression might contribute to the aggressiveness of PDACs. (+info)
Recurrent pancreatitis due to a cystic pancreatic tumor: a rare presentation of acinar cell carcinoma.
(12/113)
CONTEXT: Acinar cell carcinoma is an uncommon malignancy of the pancreas. It has characteristic histomorphology, immunohistochemistry profile, and clinicopathological behavior. CASE REPORT: We report a rare case of recurrent pancreatitis secondary to acinar cell carcinoma of the pancreas. We describe the endoscopic ultrasound characteristic, treatment and the surgical outcome. CONCLUSIONS: Acinar cell carcinoma should be considered in the differential diagnosis of cystic pancreatic tumors presenting with recurrent pancreatitis. (+info)
Endoscopic ultrasound-guided fine-needle aspiration cytology diagnosis of solid-pseudopapillary tumor of the pancreas: a rare neoplasm of elusive origin but characteristic cytomorphologic features.
(13/113)
Clinical histories, endoscopic ultrasound (EUS)-guided fine-needle aspiration (FNA) material, and immunohistochemical stains performed on cell block samples of 6 solid-pseudopapillary tumors of the pancreas (SPTPs) were reviewed in the cases of 5 females (13-58 years) and 1 man (57 years); all had abdominal pain. Preliminary cytologic diagnoses at endoscopy included 1 SPTP 2 low-grade neoplasms, and 3 pancreatic endocrine tumors. Variable numbers of branching fragments with central capillaries and myxoid stroma were seen in the smears of 5 of 6 cases but were more apparent in the cell block material of all cases. The cells had bland nuclear features and rare grooves. Extensive necrosis was noted in 1 case and rare mitotic figures in 1. SPTPs showed strong cellular immunoreactivity for vimentin and focal weak keratin reactivity. Neuron-specific enolase, alpha1-antitrypsin, and alpha1-antichymotrypsin stains performed in 2 cases were strongly positive. Subsequent surgical resection confirmed all diagnoses. EUS-guided FNA diagnosis of SPTP is accurate. The characteristic branching papillae with myxoid stroma are best seen in cell block slides. Clinical setting, cytomorphologic features, and immunostains of the cell block help distinguish SPTP from pancreatic endocrine tumors, acinar cell carcinoma, and papillary mucinous carcinoma. (+info)
Tissue plasminogen activator in murine exocrine pancreas cancer: selective expression in ductal tumors and contribution to cancer progression.
(14/113)
Tissue plasminogen activator (tPA) is absent from normal human pancreas and is expressed in 95% of human pancreatic adenocarcinomas. We have analyzed the expression of components of the tPA system in murine pancreatic tumors and the role of tPA in neoplastic progression. Transgenic mice expressing T antigen and c-myc under the control of the elastase promoter (Ela1-TAg and Ela1-myc, respectively) were used. tPA was undetectable in normal pancreas, acinar dysplasia, ductal complexes, and in all acinar tumors. By contrast, it was consistently detected in Ela1-myc tumors showing ductal differentiation. Crossing transgenic Ela1-myc with tPA-/- mice had no effect on the proportion of ductal tumors, indicating that tPA is not involved in the acinar-to-ductal transition. Ela1-myc:tPA-/- mice showed an increased survival in comparison to control mice. All ductal tumors, and none of the acinar tumors, overexpressed the tPA receptor annexin A2, suggesting its participation in the effects mediated by tPA. Our findings indicate that murine and human pancreatic ductal tumors share molecular alterations in the tPA system that may play a role in tumor progression. (+info)
Significance of preserving the posterior branch of the great auricular nerve in parotidectomy.
(15/113)
OBJECTIVE: Sensory disturbance due to excision of the great auricular nerve in patients who have undergone parotidectomy sometimes causes discomfort to the patients. In order to reduce the postoperative discomfort of the pinna, we tried to preserve the posterior branch of the great auricular nerve. METHODS: Forty patients with parotid tumor were included in this study. Twenty-one of these patients had pleomorphic adenoma, 16 had adenolymphoma and 3 had a low grade malignant tumor. Sensations of the pinna and the quality of life (QOL) after parotidectomy were evaluated using a 0-100 Visual Analogue Scale (VAS) assessed at 2 weeks, 1 month, 2 months, 3 months and 6 months after parotidectomy. RESULTS: The posterior branch of the great auricular nerve was preserved in 26 out of 40 patients (65%). No difference was observed in the incidence of complications except sensory disturbance of the pinna with this surgical procedure as compared to the surgical technique where the great auricular nerve was excised. The VAS score for the sensation was significantly higher in the group of patients whose great auricular nerve was preserved at 2 months (35.0+/-20.8 vs. 18.5+/-9.2), 3 months (64.4+/-18.3 vs. 26.4+/-13.8) and 6 months (66.9+/-16.2 vs. 26.6+/-11.4) after parotidectomy. The VAS score for the QOL was also significantly higher in the group of patients whose great auricular nerve was preserved at 2 months (50.3+/-21.8 vs. 35.1+/-14.5), 3 months (69.5+/-27.5 vs. 45.9+/-22.6) as well as 6 months (71.9+/-24.1 vs. 45.7+/-19.1) after parotidectomy. CONCLUSION: Preservation of the posterior branch of the great auricular nerve during parotidectomy is valuable in order to reduce the postoperative sensory disturbance of the pinna that follows conventional surgery. It further helps to improve the QOL of these patients after parotidectomy. (+info)
Acinic cell carcinoma found by recurrence of a mucous cyst in the sublingual gland.
(16/113)
This case report describes an acinic cell carcinoma found by a recurrence of a ranula in the sublingual gland. A 42-year-old male was admitted to the hospital of the Tokyo Dental College with a swelling in his right oral floor but without pain. The lesion was treated by windowing the same day under the diagnosis of a ranula, but the swelling appeared again at the same area eight months after the first operation. A resection was performed, and the specimen was sent to the clinical laboratory for pathological diagnosis. Proliferating serous cells were seen in part of the wall of an exudative mucous cyst. PAS staining was partially positive, and immunohistochemical staining for S-100 protein, lactoferrin, and amylase were also positive in cytoplasmic granules. This report concludes that the pathological diagnosis is beneficial in clarifying the reasons for the recurrence of a benign lesion. (+info)