Expression of a metalloproteinase family of ADAMTS in human vulnerable carotid lesions.

Aims: ADAMTS family of metalloproteases (a disintegrin and metalloprotease with thrombospondin motifs) possesses high proteolytic activity especially regarding proteoglycans. Their expression pattern in carotid plaques is as-yet unknown. The aim of the study was therefore the analysis of expression of ADAMTS1, 4, 5, and 13 and their inhibitors TIMP-1 and TIMP-3 in stable and unstable carotid plaques.

Loss of 4q21.23-22.1 is a prognostic marker for disease free and overall survival in non-small cell lung cancer.

This study was performed to assess the prognostic relevance of genomic aberrations at chromosome 4q in NSCLC patients. We have previously identified copy number changes at 4q12-q32 to be significantly associated with the early hematogenous dissemination of non-small cell lung cancer (NSCLC), and now aim to narrow down potential hot-spots within this 107 Mb spanning region. Using eight microsatellite markers at position 4q12-35, allelic imbalance (AI) analyses were performed on a preliminary study cohort (n = 86).

Expression and cellular localization of metalloproteases ADAMs in high graded carotid artery lesions.

Metalloproteases with a disintegrin domain (ADAM) has already been implicated in various cellular processes such as cytokine and growth factor shedding, proliferation, migration, and degradation of extracellular matrix. Their role in the development and progression of atherosclerosis in carotid lesions is however unknown. The aim of the study was to analyze expression of proteolytic ADAMs (8, 9, 10, 12, 15, 17) and their inhibitors TIMP-1, -3 in patients with high-graded carotid artery stenosis.

Opposite roles of FOXA1 and NKX2-1 in lung cancer progression.

Gene copy number profiles of primary lung tumors were screened for high-level amplifications. We detected 22 high-level amplifications in various loci, including 14q13. This locus is known to harbor the adenocarcinoma (AC) lineage-specific target gene NKX2-1, which is not expressed in squamous cell carcinoma (SCC).

Heme oxygenase-1 germ line GTn promoter polymorphism is an independent prognosticator of tumor recurrence and survival in pancreatic cancer.

Background: Heme oxygenase-1 (HO-1) correlates with aggressive tumor behavior and chemotherapy resistance in pancreatic cancer (PC). We evaluated the prognostic value of the basal transcription controlling germ line GTn repeat polymorphism (GTn) in the promoter region of the HO-1 gene in PC.

Patients And Methods: We determined the GTn in 100 controls and 150 PC patients.

Heme oxygenase-1 promoter polymorphism is a predictor of disease relapse in pancreatic neuroendocrine tumors.

Background: Current available preoperative diagnostic workup is insufficient to differentiate between benign and malignant pancreatic neuroendocrine tumors (PNET). The aim of the present study was to evaluate the potential prognostic role of the promoter GTn repeat polymorphism (GTn) of the heme oxygenase-1 gene in PNET.

Methods: Tumor, metastasis, corresponding healthy tissue, and peripheral blood leukocyte DNA of 46 patients who underwent surgical resection for PNET were analyzed for GTn by PCR, capillary electrophoresis, and DNA-sequencing.

Extended central pancreatic resection as an alternative for extended left or extended right resection for appropriate pancreatic neoplasms.

Background: Whether patients with focal pancreatic lesions of benign or borderline pathology should be treated by extended central pancreatectomy rather than by extended classic resectional procedures, such as extended right and left resections, is controversial.

Methods: Between 1992 and 2007, 105 patients underwent operation for focal pancreatic lesions of borderline or benign neuroendocrine neoplasms, cystadenoma, intraductal papillary mucinous neoplasia (IPMN), and secondary metastasis. In all, 35 patients were subjected to extended central pancreatectomy, whereas the remaining 70 patients were treated by an extended classic right resection or an extended classic left resection.