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National Cancer Institute®
Ultima Vez Modificado: 1 de mayo del 2002
UI - 11929809
AU - Lott ST; Chandler DS; Curley SA; Foster CJ; El-Naggar A; Frazier M;
TI - Strong LC; Lovell M; Killary AM High frequency loss of heterozygosity in von Hippel-Lindau (VHL)-associated and sporadic pancreatic islet cell tumors: evidence for a stepwise mechanism for malignant conversion in VHL tumorigenesis.
SO - Cancer Res 2002 Apr 1;62(7):1952-5
AD - Department of Molecular Genetics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030-4009, USA.
Germ-line mutation of the von Hippel-Lindau (VHL) gene predisposes to the development of multifocal, benign lesions, including retinal and central nervous system hemangioblastomas, pheochromocytomas, and renal and pancreatic cysts. Progression to malignancy in VHL disease is associated primarily with the development of renal cell carcinoma (RCC) and pancreatic islet cell tumors (PICT). Although many reports have documented the multiple functions of the VHL protein, few have investigated the intriguing question related to the tissue-specificity of malignant conversion in VHL disease, a problem not easily explained by strict genotype-phenotype correlations. We investigated a novel VHL kindred with a preponderance of PICTs to determine whether loss of additional genetic loci associated with the sporadic forms of RCC and PICTs might play a role in malignant conversion in this disease. We report the high frequency loss of heterozygosity (LOH) of genetic loci distinct from and mapping proximal to VHL within human chromosome 3p in the VHL kindred under study. Furthermore, chromosome 3p LOH occurs subsequent to VHL mutation and cyst formation, and correlates with malignant progression in VHL-associated PICTs. High frequency LOH was also observed in sporadic PICTs in regions of 3p associated with LOH in sporadic clear cell RCC as well as homozygous deletion in lung cancer. A stepwise model for malignant conversion in VHL disease is herein proposed.
UI - 11965607
AU - Anthony LB; Woltering EA; Espenan GD; Cronin MD; Maloney TJ; McCarthy KE
TI - Indium-111-pentetreotide prolongs survival in gastroenteropancreatic malignancies.
SO - Semin Nucl Med 2002 Apr;32(2):123-32
AD - Louisiana State University Medical Center, Department of Medicine, the Louisiana State University Health Sciences Center (LSUHSC), Stanley S. Scott Cancer Center, New Orleans, LA 70112, USA.
Somatostatin and its analogues bind to somatostatin receptors (sst) 1 through 5 that are overexpressed in neuroendocrine neoplasms such as gastroenteropancreatic (GEP) malignancies. After ligand-receptor binding, a fraction of the ligand-receptor complexes internalize. This internalization process is an effective means of delivering cytotoxic radiolabeled somatostatin analogues, especially those emitting short-range decay particles such as Auger electrons, to the neoplastic cell nucleus. Indium-111-pentetreotide, an sst 2 preferring somatostatin analogue with gamma and Auger electron decay characteristics, is commonly used for the scintigraphic evaluation and management of neuroendocrine cancer patients. This clinical trial was performed to determine the effectiveness and tolerability of therapeutic doses of (111)In-pentetreotide in patients with GEP tumors. GEP tumor patients who had failed all forms of conventional therapy, with worsening of tumor-related signs and symptoms and/or radiographically documented progressive disease, an expected survival less than 6 months, and sst positivity as determined by the uptake on a 6.0 mCi (111)In-pentetreotide scan (OctreoScan; Mallinckrodt Medical, Inc, St. Louis, MO), were treated with at least 2 monthly 180-mCi intravenous injections of (111)In-pentetreotide. Baseline clinical assessments, serum chemistries, and plasma pancreastatin levels were measured and and 3 pancreatic islet cells) patients were accrued, with 26 patients evaluable for clinical and radiographic responses, 21 patients evaluable for biochemical assessments, and 27 patients evaluable for survival analysis and safety. Toxicity was evaluated by using standard National Cancer Institute (NCI) Common Toxicity Criteria guidelines. Clinical benefit occurred in 16 (62%) patients. Pancreastatin levels decreased by 50% or more in 81% of the patients. Objective partial radiographic responses occurred in 2 (8%) patients, and significant tumor necrosis (defined by 20 Hounsfield units or greater decrease from baseline) developed in 7 (27%) patients. The following transient Grades 3/4 NCI Common Toxicity Criteria side effects were observed, respectively: leukocyte: 1/1; platelets: 0/2; hemoglobin: 3/0; bilirubin: 1/3; creatinine: 1/0; neurologic: 1/0. Myeloproliferative disease and/or myelodysplastic syndrome have not been observed in the 6 patients followed-up for 48+ months. The median survival was 18 months (range, 3-54+ mo). Two doses (180 mCi) of (111)In-pentetreotide are safe, well-tolerated, and improve symptoms in 62% of patients, decrease hormonal markers in 81% of patients, decrease Hounsfield units on computed tomography (CT) scans in 27% of patients, with 8% partial radiographic responses and increased expected survival in GEP cancer patients with somatostatin receptor-expressing tumors. The maximal tolerated dose of (111)In-pentetreotide and the optimal dosing schedules remain under investigation. Copyright 2002, Elsevier Science.
UI - 10707036
AU - Frittitta L; Sbraccia P; Costanzo BV; Tassi V; D'Adamo M; Spampinato D;
TI - Ercolino T; Purrello F; Tamburrano G; Vigneri R; Trischitta V High insulin levels do not influence PC-1 gene expression and protein content in human muscle tissue and hepatoma cells.
SO - Diabetes Metab Res Rev 2000 Jan-Feb;16(1):26-32
AD - Institute of Internal Medicine, Endocrine and Metabolic Diseases, University of Catania, Garibaldi Hospital, Catania, Italy. firstname.lastname@example.org
BACKGROUND: To verify whether insulin levels influence PC-1 tissue content, we studied PC-1 gene expression and protein content in skeletal muscle of patients with insulinoma, a model of primary hyperinsulinemia. Data were compared with those obtained in matched insulin sensitive or resistant healthy subjects. In addition, the effect of high insulin concentration on PC-1 protein content was studied in HepG2 cells. METHODS: The following measurements were performed: insulin sensitivity by euglycemic clamp; PC-1 protein content and insulin receptor autophosphorylation by specific ELISAs; PC-1 gene expression by competitive polymerase chain reaction (PCR); phosphatidyl-inositol-3 kinase by immunoprecipitation and thin layer chromatography; glycogen synthesis by (14)C-glucose incorporation. RESULTS: Muscle PC-1 content was similar in the insulinoma patients and in insulin sensitive controls but higher (p<0.01) in insulin resistant controls (21.9+/-4.6 ng/mg protein, 23.8+/-3.9, 48.0+/-8.7, respectively). PC-1 protein content was inversely correlated with insulin sensitivity (r=-0.5, p<0.015) but with neither plasma insulin nor glucose levels. PC-1 protein content was correlated with PC-1 gene expression (r=0.53, p<0.05, n=14). Exposure to high insulin (100 nmol/l for 16 h) caused a significant (p<0.05-0.01) impairment of insulin receptor autophosphorylation, phosphatidyl-inositol-3 kinase activity and glycogen synthesis, but not of PC-1 protein content (114+/-3 vs 102+/-14 ng/mg protein) in HepG2 cells. CONCLUSION: These findings suggest that chronic high insulin levels do not influence PC-1 expression. Copyright 2000 John Wiley & Sons, Ltd.
UI - 11961649
AU - Takamatsu S; Teramoto K; Inoue H; Goseki N; Takahashi S; Baba H; Iwai T;
TI - Arii S Laparoscopic enucleation of an insulinoma of the pancreas tail.
SO - Surg Endosc 2002 Jan;16(1):217
AD - Department of Surgery, Tokyo Medical and Dental University, School of Medicine, 1-5-45 Yushima, Bunkyo-ku, Tokyo, Japan.
A 29 year-old woman with a tumor of the pancreatic tail was referred to our institute. The tumor was confirmed to be a solitary benign insulinoma that protruded from the pancreas and was distant from the main pancreatic duct. A laparoscopic enucleation was performed with Laparoscopic Coagulating Shears (LCS). The postoperative course was uneventful. The laparoscopic enucleation for benign pancreatic tumor was thought to be a feasible procedure when the appropriate instruments were used.
UI - 11961650
AU - Tagaya N; Ishikawa K; Kubota K
TI - Spleen-preserving laparoscopic distal pancreatectomy with conservation of the splenic artery and vein for a large insulinoma.
SO - Surg Endosc 2002 Jan;16(1):217-8
AD - Second Department of Surgery, Dokkyo University School of Medicine, 880 Kitakobayashi, Mibu, Tochigi 321-0293, Japan.
We report a successful spleen-preserving laparoscopic distal pancreatectomy for a large insulinoma with conservation of the splenic artery and vein. The patient was a 48-year-old man with syncope due to hypoglycemia. Abdominal computed tomography (CT) and ultrasonography revealed a large 6-cm mass located in the tail of the pancreas. We adopted the laparoscopic approach to remove the tumor. After careful dissection and an accurate hemostasis between the pancreas and splenic vessels, laparoscopic distal pancreatectomy was carried out using a linear stapler. There were no perioperative complications. The patient was discharged uneventfully. He had no hypoglycemic episodes or abdominal symptoms during 8 months of follow-up. When performed by experienced laparoscopic surgeons in conjunction with intraoperative ultrasonography, spleen-preserving laparoscopic distal pancreatectomy with conservation of the splenic artery and vein is a technically feasible procedure for the treatment of benign lesions of the tail or body of the pancreas.
UI - 11964041
AU - Barth PJ; Ebrahimsade S; Hellinger A; Moll R; Ramaswamy A
TI - CD34+ fibrocytes in neoplastic and inflammatory pancreatic lesions.
SO - Virchows Arch 2002 Feb;440(2):128-33
AD - Institute of Pathology, Philipps University Marburg, Germany. email@example.com
Besides its function as a matrix-producing cell, the CD34+ fibrocyte has been reported to be an antigen-presenting cell capable of priming naive T cells in situ. Therefore, it has been claimed that the CD34+ fibrocyte may play an important role in host response to tissue damage. The objective of the present study was to analyze the presence and distribution of CD34+ fibrocytes and smooth muscle actin (SMA) reactive myofibroblasts in relation to the underlying pancreatic disease. We investigated a total of 12 pancreatic adenocarcinomas, 7 endocrine tumors of the pancreas, and 8 cases of chronic pancreatitis; in 11 cases, normal pancreatic tissue was available. The stroma of normal pancreatic tissue harbored diffusely scattered CD34+ fibrocytes. Chronic pancreatitis was characterized by an increased number of stromal CD34+ fibrocytes paralleled by a gain of SMA reactive myofibroblasts which were not observed in the normal pancreatic stroma. The stroma of pancreatic ductal adenocarcinomas and endocrine tumors was devoid of CD34+ fibrocytes or showed at least a focal loss of this cell type, whereas SMA reactive myofibroblasts were detected in both endocrine tumors and adenocarcinomas. We conclude that detection of CD34+ fibrocytes may constitute an adjunctive tool in distinguishing chronic pancreatitis from ductal adenocarcinoma since the absence of this cell population strongly favors a neoplastic process. Moreover, CD34+ fibrocytes and myofibroblasts appear to be involved in stromal remodeling associated with chronic pancreatitis and ductal adenocarcinoma.
UI - 11964045
AU - Scarpa A; Orlandini S; Moore PS; Lemoine NR; Beghelli S; Baron A;
TI - Falconi M; Zamboni G Dpc4 is expressed in virtually all primary and metastatic pancreatic endocrine carcinomas.
SO - Virchows Arch 2002 Feb;440(2):155-9
AD - Dipartimento di Patologia, Universita di Verona, Italy. firstname.lastname@example.org
DPC4/Smad4 is inactivated in about 50% of pancreatic ductal cancers. It has been recently reported that this gene is also inactivated in neoplasms arising from pancreatic islet cells, a phenomenon suggested to be related to similar progressions of malignancy found in common ductal cancers. To evaluate this possibility, we analysed 20 metastases of pancreatic endocrine carcinomas and their corresponding primary lesion for inactivation of DPC4 using immunohistochemical staining. In fact, immunohistochemical labelling has been shown to correlate with DPC4 gene status with high sensitivity and specificity. The cancers included 18 nonfunctioning tumours, one gastrinoma and one ViPoma all with liver, nodal and/or adrenal metastases. Seventeen were well-differentiated and three poorly differentiated endocrine carcinomas. Dpc4 expression was absent in only one primary well-differentiated endocrine cancer and its liver metastasis, while all the remaining 19 primary tumours and their metastases stained positive for the protein. All positively staining cases showed diffuse cytoplasmic and nuclear staining in virtually all neoplastic cells. Our data suggest that DPC4 is only rarely involved in pancreatic endocrine tumourigenesis and give further weight to the hypothesis that tumours arising from pancreatic exocrine and endocrine epithelia are genetically distinct.
UI - 11959716
AU - Oshikawa O; Tanaka S; Ioka T; Nakaizumi A; Hamada Y; Mitani T
TI - Dynamic sonography of pancreatic tumors: comparison with dynamic CT.
SO - AJR Am J Roentgenol 2002 May;178(5):1133-7
AD - Division of Digestive Organs, Department of Cancer Survey, Osaka Medical Center for Cancer and Cardiovascular Diseases, 1-3-3, Nakamichi, Higashinari, Osaka, 537-8511, Japan.
OBJECTIVE: The aim of this study was to examine the usefulness of dynamic sonography in the characterization of pancreatic tumors. MATERIALS AND METHODS: IV contrast-enhanced pancreatic sonography (dynamic sonography) with Levovist was performed in 43 patients with pancreatic mass lesions (32 with pancreatic adenocarcinomas, four with inflammatory pancreatic masses, three with islet cell tumors, two with serous cystadenomas, one with a solid and cystic tumor, and one with metastatic pancreatic cancer). We calculated a contrast index using a time-intensity curve: contrast index equals elevation of intensity in the tumor divided by elevation of intensity in the pancreatic parenchyma. We classified the tumors into three groups according to the contrast index: a slightly enhanced group (contrast index < 0.5), a moderately enhanced group (contrast index = 0.5-1.5), and a well-enhanced group (contrast index > 1.5), and we compared these results with those from dynamic CT. RESULTS: The contrast indexes of 32 adenocarcinomas, four inflammatory pancreatic masses, three islet cell tumors, two serous cystadenomas, one solid and cystic tumor, and one metastatic tumor were, respectively, 0.12 +/- 0.095 (mean +/- SD), 0.54 +/- 0.420, 1.74 +/- 0.555, 1.09 +/- 1.380, 1.67, and 2.07. Thirty-five tumors, including all 32 adenocarcinomas, were classified in the slightly enhanced group, three were classified in the moderately enhanced group, and five were classified in the well-enhanced group. In 93% (40/43) of tumors, the grade of enhancement on dynamic sonography was closely correlated with the grade of enhancement on dynamic CT. CONCLUSION: Dynamic sonography can assist in the characterization of pancreatic tumors.
UI - 11753234
AU - Camera L; Bresciani M; Soscia E; Percopo V; Mainenti PP; Salvatore M
TI - [Morphological imaging of gastroenteropancreatic neuroendocrine tumours]
SO - Minerva Endocrinol 2001 Sep;26(3):123-8
AD - Consiglio Nazionale delle Ricerche, Dipartimento di Scienze Bio-morfologiche, Universita degli Studi Federico II, Naples, Italy.
Biologically active neuroendocrine tumours produce early symptoms and are often difficult to diagnose owing to their small dimensions (<1 cm), whereas biologically inactive forms are often coarse and sometimes found by chance. As well as identifying the lesion, locoregional staging is also particularly important for therapeutic planning. Morphological imaging plays an important role in the identification of gastroenteropancreatic neuroendocrine tumours, providing an anatomic substrate for receptorial imaging which usually precede it in the diagnostic work-up, whereas it plays a primary role in the locoregional staging of these neoplasms for which surgery is the first and essential therapeutic approach. In the case of endocrine tumours of the pancreas alone, the most accurate method of diagnosis is currently echo-endoscopy using high-frequency probes. Two-phase spiral CT and dynamic MR have proved equally effective means of identifying endocrine tumours of the pancreas with slightly higher sensitivity for MR, both playing a role in the locoregional staging of biologically active and inactive tumours. Traditional radiology also plays a role in the identification of intestinal carcinoids.
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