			Home About us Contact

Epithelial Malignancies (epithelial + malignancy)

Distribution by Scientific Domains

Medical Sciences	87%

Selected Abstracts

Analysis of Aurora-A and hMPS1 mitotic kinases in mantle cell lymphoma

INTERNATIONAL JOURNAL OF CANCER, Issue 2 2006
Emma Camacho
Abstract Aurora-A and hMPS1 are kinases involved in spindle checkpoint and centrosome duplication regulation and whose alterations have been associated with cell transformation and chromosome instability in different tumor models. In this study, we have examined the possible alterations of these genes in 58 mantle cell lymphomas (MCLs) and 4 MCL-related cell lines. Aurora-A was also examined in 46 diffuse large B-cell lymphomas (DLBCLs). Aurora-A and hMPS1 mRNA expression levels were related to tumor proliferative activity. Interestingly, a MCL case with the highest number or chromosomal imbalances also showed an extremely high value of Aurora-A mRNA expression. No Aurora-A gene amplifications were detected in any tumor or cell line, whereas hemizygous hMPS1 gene deletions were observed in 23% of MCLs and 3 of the 4 cell lines. However, no expression alterations or gene mutations were detected in these cases. The Aurora-A proposed cancer susceptibility polymorphic variant (P31I) was observed with a similar frequency in MCL, DLBCL, chronic lymphocytic leukemia and in the 431 healthy controls. However, the 3 MCLs and 4 DLBCLs with the homozygous variant of this polymorphism had particular clinical characteristics with an unusual early-age presentation and second epithelial malignancies in MCL and extranodal origin in DLBCL. These findings indicate that Aurora-A and hMPS1 aberrations are uncommon in aggressive lymphomas but Aurora-A overexpression may contribute to numerical chromosomal alterations in occasional MCL. Although the Aurora-A P31I polymorphic variant is not directly involved in a genetic predisposition to these lymphomas, it may modulate the clinical presentation of these tumors. © 2005 Wiley-Liss, Inc. [source]

Stromelysin-3 suppresses tumor cell apoptosis in a murine model,

JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 4 2001
Erxi Wu
Abstract Stromelysin-3 (STR-3) is a matrix metalloproteinase with a unique pattern of expression and substrate specificity. During embryogenesis and remodeling of normal adult tissues, STR-3 is produced by stromal cells in direct contact with epithelial cells undergoing regional apoptosis and selective cell survival. STR-3 is also overexpressed by interdigitating stromal cells in primary epithelial malignancies. Although STR-3 does not degrade classic extracellular matrix components, the enzyme promotes the establishment of local tumors in nude mice by as yet undefined mechanisms. STR-3 is induced when malignant epithelial cells come into contact with surrounding stromal elements; the active stromal cell-derived 45 kDa enzyme is subsequently processed to a 35 kDa protein without enzymatic activity. We have generated MCF-7 transfectants expressing wild type or catalytically inactive 45 kDa STR-3 (STR-3wt and STR-3cat- ) or secreted 35 kDa STR-3 (35 kDa STR-3sec) and evaluated their implantation and survival in nude mice. Tumors developed significantly more rapidly in animals receiving STR-3wt, rather than vector-only, STR-3cat- or 35 kDa STR-3sec transfectants. Most importantly, STR-3wt tumors had a significantly lower percentage of apoptotic cells than tumors derived from vector-only, STR-3cat- or 35 kDa STR-3sec transfectants. Taken together, these studies suggest that the active STR-3 enzyme may increase tumor take by suppressing tumor cell apoptosis and that 45 kDa to 35 kDa STR-3 processing limits STR-3 activity at the tumor/stromal interface. Because STR-3 is secreted as an active enzyme rather than a proform, subsequent 45 kDa to 35 kDa STR-3 processing may represent a novel mechanism for regulating enzymatic activity. J. Cell. Biochem. 82: 549,555, 2001. © 2001 Wiley-Liss, Inc. [source]

Management and Outcome of Patients With Mucoepidermoid Carcinoma of Major Salivary Gland Origin: A Single Institution's 30-Year Experience,

THE LARYNGOSCOPE, Issue 2 2008
Katri Aro MD
Abstract Background: Mucoepidermoid carcinoma (MEC) is one of the most frequent epithelial malignancies of the salivary glands. Prediction of clinical outcome of MEC is challenging. Material and Methods: We retrospectively reviewed 52 cases of MEC of major salivary gland origin diagnosed at the Department of Otolaryngology,Head and Neck Surgery, Helsinki University Central Hospital, Helsinki, Finland, during a 30-year period of 1976 to 2005. Criteria used for diagnosis were those of World Health Organization classifications valid at each time point, and criteria for grading were those recommended by Armed Forces Institute of Pathology fascicle (1996). Since 1993, the degree of cell proliferation was used at our institution as an adjunct tool when grading MEC. The majority of cases occurred in the parotid gland (n = 47, 90%) followed by the submandibular gland (n = 5, 10%). Results: We had 39% high-grade (HG), 14% intermediate-grade (IMG), and 44% low-grade (LG) MECs. T categories were T1, n = 18; T2, n = 16; T3, n = 9; T4, n = 9. Forty-nine (94%) patients were treated with curative intent. These patients underwent surgery, and 24 (49%) patients received postoperative radiotherapy. Follow-up time varied from 6 months to 9 years. Forty-five percent of HG-MEC patients and 67% of IMG-MEC patients developed locoregional failures or distant metastases during a 3-year follow-up as opposed to none of the LG-MEC patients. Of MEC patients with N0 neck, two HG-MEC patients and one IMG-MEC (8%) patient developed regional recurrence during follow-up. Conclusions: Patient outcome in the different grades of MEC suggests a need for overview of the treatment protocol, especially with regard to LG-MEC and IMG-MEC. The apparently unusual occurrence of locoregional failures and metastases in LG-MEC suggests a restrictive approach in surgical management. However, the frequent occurrence of such failures in IMG-MEC warrants an aggressive approach with these tumors. [source]

Cyclooxygenase-2 expression and connection with tumor recurrence and histopathologic parameters in gastrointestinal stromal tumors

APMIS, Issue 11 2009
HÜSEYIN KEMAL TÜRKÖZ
Tissue cyclooxygenase-2 (COX-2) is a rate-limiting enzyme in prostaglandin synthesis and has been shown to have roles in carcinogenesis and tumor progression. Evaluation of COX-2 overexpression in malignancies has been performed mostly on tumors of epithelial origin, and little is known about its presence in mesenchymal tumors, especially gastrointestinal stromal tumors (GIST). COX-2 has been reported to be widely expressed in GIST and has been suggested as a potential diagnostic marker. We evaluated the overexpression and roles of COX-2 in tumorigenesis in GIST with regard to its relation to prognostic parameters and tumor recurrence. We studied the presence of COX-2 expression immunohistochemically and its relation to clinicopathologic prognostic variables in 41 cases of GIST. COX-2 was overexpressed in 21 (51%) of 41 tumors. The extent of overexpression was greater in tumors that recurred after surgical resection. COX-2 overexpression was also higher in tumors with coagulative necrosis, high mitotic index and an infiltrative pattern of growth. The observation of greater COX-2 expression levels in GIST with unfavorable histopathologic variables is contrary to previous reports and consistent with the reported roles of COX-2 in carcinogenesis of epithelial malignancies. [source]

Right hemicolectomy does not confer a survival advantage in patients with mucinous carcinoma of the appendix and peritoneal seeding

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 3 2004
S. González-Moreno
Background: Traditionally epithelial malignancies of the appendix with or without carcinomatosis have been treated by right hemicolectomy. Recent accumulation of a large number of patients with this disease has enabled a re-evaluation of this surgical judgement. Methods: Clinical data on 501 patients with epithelial malignancy of the appendix were collected prospectively. All patients had peritoneal seeding at the time of referral and were treated by cytoreductive surgery and perioperative intraperitoneal chemotherapy. The main independent variable for statistical analysis was the surgical procedure used to resect the primary cancer (appendicectomy alone versus right hemicolectomy). Nineteen other clinical and pathological variables were considered as control variables. The endpoint for all analyses was survival. Results: Median follow-up after the initial diagnosis was 4 years. The rate of regional lymph node positivity was 5·0 per cent. When the incidence of lymph node metastasis was determined by histological type, it was statistically significantly higher in intestinal (66·7 per cent) than in mucinous (4·2 per cent) tumours (P < 0·001). The presence of lymph node metastases had no influence on prognosis (P = 0·155). The surgical procedure (appendicectomy alone versus right hemicolectomy) had an influence on patient survival by univariate analysis (P < 0·001), but not by multivariate analysis (P = 0·258). Conclusion: Right hemicolectomy does not confer a survival advantage in patients with mucinous appendiceal tumours with peritoneal seeding. These data suggest that right hemicolectomy should be avoided unless metastatic involvement of the appendiceal or distal ileocolic lymph nodes is documented by biopsy, or the resection margin is inadequate. Copyright © 2004 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source]

Squamous cell carcinoma arising from a congenital duplication cyst of the esophagus in a young adult

DISEASES OF THE ESOPHAGUS, Issue 3-4 2001
S. Singh
Squamous cell carcinomas arising from the congenital anomalies in the esophagus are rare. One such case of an 18-year-old man, with an associated history of ventricular septal defect, who developed an epithelial malignancy within the duplication cyst extending to involve the lower third of esophagus is presented here. He responded well to radical treatment using concurrent chemo-irradiation, and continues to be free of disease after a follow-up of 14 months. [source]

DNA copy number changes in carcinoma in pleomorphic adenoma of the salivary gland: A comparative genomic hybridization study

PATHOLOGY INTERNATIONAL, Issue 8 2002
Takashi Morio
Pleomorphic adenoma is the most common benign tumor of the salivary glands and is rarely associated with concurrent epithelial malignancy, which is designated as carcinoma in pleomorphic adenoma (CPA). Genetic abnormalities potentially related to the development of CPA have not been fully investigated. We analyzed DNA copy number changes in each of the adenomatous and carcinomatous components of seven CPA by comparative genomic hybridization using DNA extracted from microdissected tissues of formalin-fixed, paraffin-embedded tumor samples. Carcinomatous components of CPA showed multiple DNA copy number changes at 1,18 different genomic sites (mean 13 sites). Adenomatous components displayed less frequent DNA copy number changes (0,13 sites; mean, 5). In both components, the majority of the changes were gains. The most common recurrent gains in carcinomatous components were seen at 6q (four cases in each), whereas gains at 13q1,2 and 15q1 were most frequently detected in adenomatous components (three cases in each). In five CPA, the same chromosomal regions were involved in the DNA copy number changes detected in both components. Our data suggest that an accumulated or increased number of chromosomal changes including 6q abnormalities may be associated with the development of carcinomatous components in a subset of CPA. [source]