Neuroendocrine tumors: A European view

Oncogene expression in gastroenteropancreatic neuroendocrine tumors

“…This tumor register was established in 1978 by the Department of Medicine, the Queen's University understanding of the molecular genetics of cancer, and many of these advances have stemmed from studof Belfast. 1 Detailed clinicopathologic data on patients (including age, gender, symptoms, tumor location, tuies of cellular oncogenes and tumor-suppressor genes. Several oncogenes have been well studied over the mor size, and occurrence of metastases) were available, and each patient's clinical progress had been years and characterized with regard to their roles in the development of specific human tumors.…”

“…About one-third of PNTs fail to produce study, we have analyzed, by immunohistochemistry using monoclonal antibodies, the expression of five any hormone-related syndrome and are therefore described as nonfunctioning. 1 Carcinoid tumors are the dominant oncogenes-c-myc, bcl-2, c-erb B-2, c-erb B-3, and c-jun-in a retrospective series of 116 primost common of the gastrointestinal tract (GI) neuroendocrine neoplasms and account for 55-86% of all mary human GPNTs, including islet cell tumors of the pancreas and carcinoids of foregut, midgut, and hindsuch tumors. 3,4 According to the site of origin, carcinoid tumors have been classified as tumors of the foregut origin, and we have attempted to correlate this expression with the clinicopathologic outcome of the gut (bronchus, pancreas, stomach, and proximal duodenum), midgut (distal duodenum, jejunum, ileum, disease.…”

Hypomethylation of LINE-1 and Alu in well-differentiated neuroendocrine tumors (pancreatic endocrine tumors and carcinoid tumors)

“…1,2 The molecular mechanisms of neuroendocrine tumors are poorly understood but have been the focus of many recent reports. [3][4][5][6][7][8][9][10] The methylation of cytosine in CpG dinucleotides is an important epigenetic modification of DNA in the vertebrate genome.…”

Chemo-hormone therapy of non-well-differentiated endocrine tumours from different anatomic sites with cisplatinum, etoposide and slow release lanreotide formulation

“…In this case, the derivative cells may dynamically undergo a caricatural differentiation that may resemble epithelial, glandular, or neuroendocrine cells. On the basis of different kinds and levels of molecular and genetic alterations, these cells may follow distinct differentiation pathways and may stop their distinct differentiation programmes at different stages of maturation (Buchanan et al, 1986;Hansson and Abrahamsson, 2003;Wright et al, 2003;Bishop, 2005;Long et al, 2005). Respiratory, gastroenteric, and urinary tracts, as well as the prostate, are physiologically under strict neurovegetative control, and so it is not surprising that the majority of neuroendocrine tumours arise in these anatomic sites.…”

“…In some cases, they may be very difficult to recognise because there is no single marker to identify an undifferentiated neuroendocrine tumour; so, diagnosis must rely on the correct interpretation of pathological data (histology, immunohistochemistry, and sometimes electronic microscopy), biohumoral studies, blood/urinary tests, biological behaviour of the neoplasia, the natural history and the progression of the disease, and patients' symptoms (Wiedenmann and Huttner, 1989;Polak, 1993;Nicholson and Ryan, 2000;De Lellis, 2001;Bishop, 2005). Neuroendocrine tumours may arise with clinically different modalities and signs (paraneoplastic syndromes), which are often related to the different degrees of biological aggressiveness and to the different levels of production of specific hormones and peptides (Buchanan et al, 1986;Moertel, 1987). When well differentiated, they retain a low level of local and metastatic aggressiveness.…”