Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the thyroid cell adhesion receptors and gap junctions establish a complex modular network defining the structural properties of cells, their interactions with neighboring cells and the extracellular matrix. Neoplastic alterations of this network can lead to an imbalance of cell to cell communication and allows transformed cells to escape from the tissue to generate metastases. The present manuscript summarizes general and thyroid-specific aspects of the molecular basis of cell-cell contacts, an expanding field of tumor biology.
Exp Clin Endocrinol Diabetes 1996
PMID:Cell adhesion receptors and gap junctions in normal and neoplastic transformed thyrocytes. 898 Sep 95

Invasion and metastasis are the primary cause of death in patients with follicular thyroid cancer (FTC). The thyroid is a micro-economic system in which proliferation and differentiation was supposed to be under the major control of only a single hormone (thyroid stimulating hormone-TSH). It has shown, however, that a complex network of various growth factors regulates growth and invasion of thyroid cancer cells. A growing literature has established the close association between malignant tumor progression and growth regulatory aberrations in cancer cells. Most of these studies have focused on the phenomenon, that advanced and more aggressive tumors or metastases lost the sensitivity to growth inhibitors, such as transforming growth factor beta. These findings highlight two aberrations of growth regulation which may favour progression of malignant disease and acquisition of metastatic competence: (1) Resistance to growth factor inhibitors and (2) growth autonomy of metastatic follicular thyroid cancer cells.
Exp Clin Endocrinol Diabetes 1996
PMID:The regulation of proliferation and invasion in differentiated thyroid cancer by growth factors. 898 Sep 96

Oncogene amplification is frequent in many epithelial tumors and often associated with advanced tumor progression. In different epithelial neoplasias it helps to provide prognostic information on individual patients. The present study was performed to evaluate the hitherto unknown prevalence of INT-2 gene amplification and its potential usefulness as prognostic marker in patients with human thyroid cancer. We used differential quantitative polymerase chain reaction and fluorescent DNA technique as a reliable method to detect low copy-number amplification of oncogenes from archival carcinoma specimens. Sequences from the int-2 gene and the single copy gamma-interferon gene were amplified simultaneously by PCR and quantified on a fluorescence activated sequencer. Native tumor tissue from 63 patients with differentiated thyroid cancer (43 papillary, 3 oncocytary, and 17 follicular) and from 12 goiters was analyzed by differential quantitative polymerase chain reaction. The study group contained many far advanced tumors. 40% of tumors were recurrent, 35% were staged T4 tumors and 70% presented with lymph node metastases. The prevalence of INT-2 amplification was 12% for follicular and 7% for papillary carcinomas. In goiter tissue no amplification was found. Amplification was only 2-4fold in positive cases. Low grade amplification is of no apparent importance in differentiated thyroid cancer.
Exp Clin Endocrinol Diabetes 1996
PMID:INT-2 gene amplification in differentiated human thyroid cancer. 898 Oct 13

In spite of efforts to reduce complications associated with inguinal-femoral lymphadenectomy (IFL), morbidity continues to be substantial. We sought to assess the efficacy of sartorius transposition (ST) in reducing groin wound complications following IFL, in patients with vulvar malignancy. The records of 101 patients with vulvar cancer undergoing IFL through separate incisions between March 1975 and December 1994 were examined. Sixty-two patients undergoing ST (group 1) were compared to 38 who did not (group 2). The groups were similar with respect to age, weight, tobacco/alcohol use, prior abdominal/vulvar surgery, prevalence of diabetes, hypertension, or peripheral vascular disease, and previous exposure to irradiation or chemotherapy. Additionally, there was no significant difference with respect to extent of disease, incidence of macro-/microscopic groin metastases, use of groin drains, and use of perioperative antibiotics or deep venous thrombosis prophylaxis. Groin wound complications were less frequent in patients undergoing ST (group 1). The incidence of groin cellulitis was 30% in group 1 compared with an incidence of 58% in group 2 (P = 0.011). Significant groin wound morbidity, defined as either wound breakdown or cellulitis, was seen less frequently in group 1 (41% vs 66%; P = 0.029). Employing a multivariate analysis, only patient weight < 150 lbs and performance of ST were established as independently associated with a reduction in groin morbidity following IFL (P = 0.0281 and P = 0.0075, respectively). In conclusion, despite waning enthusiasm for its performance, ST appeared to significantly reduce the incidence of wound morbidity after IFL. Our data confirmed that separate incisions, and improved perioperative antibiotics, have not eliminated the value inherent in this surgical modification. We suggest a prospective trial to further establish the benefit of sartorius transposition during IFL.
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PMID:The effect of sartorius transposition on wound morbidity following inguinal-femoral lymphadenectomy. 903 69

A 52-year-old-woman with non-insulin-dependent diabetes mellitus developed carcinoma of the pancreas and had a Whipple's resection performed. She required pancreatic exocrine supplements and insulin post-operatively. Five years later metastatic disease became apparent, and was accompanied by episodic spontaneous hypoglycaemia necessitating the cessation of insulin therapy. Hormonal analysis was performed, off insulin, at a time of hypoglycaemia (glucose 0.9 mmol l-1) and showed negligible insulin concentrations (< 2 mU l-1) but raised IGF-II together with low IGF-I concentrations (1.85 and 0.1 U ml-1, respectively). The association between diabetes and pancreatic carcinoma, and the pathogenesis of non-islet cell tumour induced hypoglycaemia (NICTH) are discussed.
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PMID:Spontaneous hypoglycaemia in a noninsulin-dependent diabetes mellitus patient with disseminated pancreatic carcinoma. 911 88

A 50-year-old male presented with diabetes mellitus and Cushing's syndrome associated with a large mediastinal mass. The levels of serum cortisol were high (1500-1800 nmol/l) without diurnal variation. Plasma ACTH levels (200-250 ng/l) and urinary excretion of cortisol were also increased. The levels of these hormones did not change in response to stimulation with corticotrophin releasing hormone (CRH) or suppression with high doses of dexamethasone. The patient had an elevated baseline GH level (7.3 mU/l), and the levels of immunoreactive GH-releasing hormone (GHRH) in eight plasma samples were markedly increased (600-1500 ng/l). Circulating levels of IGF-1, chromogranin A and neuropeptide Y (NPY) were also increased. Computer-assisted tomography and octreotide scintigraphy revealed a large mediastinal tumour and metastases in the left supraclavicular fossa. During treatment with octreotide, the baseline GH level was decreased (to 4.4 mU/l), while the GH pulse height was unchanged. Surgical removal of most of the tumour tissue resulted in a further decrease in the baseline serum GH level to a value (1.6 mU/l) about 20% of that before treatment, while the pulse height and mean GH were affected to a lesser extent. Postoperatively, circulating levels of cortisol and IGF-1 decreased, and the patient exhibited clinical improvement. Histological examination showed a neuroendocrine tumour with characteristics consistent with a foregut carcinoid of thymic origin. Immunoreactive GHRH, ACTH and NPY, but not immunoreactive GH, were detected in 80-90% of the tumour cells and the three peptides appeared to be co-localized. In primary culture, cells from this tumour displayed calcium influx in response to GHRH or GH releasing peptide-6 (GHRP-6), while there were not such responses by cells from another carcinoid not producing GHRH, ACTH or NPY. These results demonstrate a rare case of ectopic production of GHRH, ACTH and NPY, and indicate that the tumour cells were responsive to GHRH and GHRP-6 as well as octreotide.
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PMID:Acromegaly and Cushing's syndrome due to ectopic production of GHRH and ACTH by a thymic carcinoid tumour: in vitro responses to GHRH and GHRP-6. 957 39

Hepatocellular carcinoma with chondrosarcomatous variation is very rare. We report a case with the results of pathology examination, and review the literature. The patient, a 72-year-old may had a very large tumor in the liver revealed during follow-up for diabetes mellitus. The liver mass, which was 14 cm in diameter, was diagnosed as hepatocellular carcinoma by abdominal ultrasonography. Anterior segmentectomy and partial liver resection were performed. Histopathology examination revealed that the tumor consisted of two different components: the major one was hepatocellular carcinoma (HCC), which occupied most of the tumor; and a sarcomatous component, which occupied a smaller area, and included spindle-shaped cells with chondroscarcomatous variation. Intrahepatic metastases and tumor thrombi of HCC were also found in portal and hepatic veins. Investigations of the immunohistochemical localization of keratin (KRT), vimentin (VMT), and S-100 protein (S 100) were performed by the avidin-biotin complex method. Some of the spindle cells were immunohistochemically positive for both KRT and VMT, and the chondrosarcomatous cells were positive for S 100. These results strongly suggested that the sarcomatous lesion resulted from a sarcomatous change of HCC.
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PMID:Hepatocellular carcinoma with chondrosarcomatous variation: case report with immunohistochemical findings, and review of the literature. 974 92

In adults, marked angiogenesis takes place only during the female reproductive cycles, during wound healing, and accompanying some disease processes, such as tumor development. Vascular endothelial growth factor (VEGF) is a secreted, endothelial cell-specific growth factor, which is induced by tissue hypoxia and is angiogenic in vivo. We measured serum VEGF (S-VEGF) concentrations by ELISA in patients with a variety of types of cancer, as well as in healthy volunteers, and in patients with diabetes or rheumatoid arthritis. Elevated S-VEGF concentrations were found in patients with locoregional (n = 39; median, 158 pg/ml; range, 8-664 pg/ml) or disseminated (n = 58; median, 214 pg/ml; range, 17-1711 pg/ml) cancer in comparison to individuals without cancer (n = 113; median, 17 pg/ml; range, 1-177 pg/ml; P < 0.0001 for both comparisons). Values higher than 200 pg/ml were observed in 74% of patients with untreated metastatic cancer, and high serum levels were measured regardless of the histological type of cancer. S-VEGF levels were found to be higher in untreated patients with disseminated cancer than in those with local cancer (P = 0.006), and patients undergoing cancer therapy had lower values than those without cancer therapy (P = 0.03). The results indicate that both patients with locoregional cancer and patients with disseminated cancer may have elevated S-VEGF levels, regardless of the histological type of cancer, and that S-VEGF is often elevated in cancer with distant metastases.
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PMID:Serum vascular endothelial growth factor is often elevated in disseminated cancer. 981 32

Of the rare pancreatic endocrinomas, glu-cagonomas, either with or without diabetico-dermatogenic syndrome (DDS), are probably third in frequency after insulinomas and gastrinomas. This study was carried out to evaluate the present status of glucagonoma/DDS in a statistically reliable number of cases and to provide precise information to investigators actively working in this particular field of research. A total of 407 cases of glucagonoma were collected from the international literature and evaluated according to characteristic clinicopathologic features. Findings were: (1) The incidence of DDS was 57.2% (233/407). (2) The tail of the pancreas was predominantly involved, in 53.7% (213/397). (3) One-third of the tumors (80 of 276 for whom size was recorded; 29.0%) measured 20 mm or less. (4) Metastases occurred in 51.4% (209/407) and malignant tumors in 60.7% (247/407). (5) Multiplicity occurred in 11.8% (48/407), and associated multiple endocrine neoplasia type 1 in 13. 0% (53/407). (6) In the patients with DDS, the rates of hyperglucagonemia, necrolytic migratory erythema, diabetes mellitus, loss of weight, hypo-aminoacidemia, or anemia, as representative constituents of DDS, were all higher than rates in the overall series (P < 0.01). (7) The 10-year survival rate in the 233 patients with DDS was 51.6% in those with metastases and 64.3% in those without metastases (P < 0.001).
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PMID:Glucagonomas/diabetico-dermatogenic syndrome (DDS): a statistical evaluation of 407 reported cases. 988 Jul 81

The diagnosis of pancreatic cancer usually depends upon symptoms; consequently it is late when there is no chance for cure. At this point, pain, anorexia, early satiety, sleep problems and weight loss are present. Back pain also may be prominent, which predicts unresectability and shortened survival after resection. However, earlier recognition of symptoms of pancreatic cancer might improve early detection of the cancer. For example, 25% of patients have symptoms compatible with upper abdominal disease up to 6 months prior to diagnosis and 15% of patients may seek medical attention more than 6 months prior to diagnosis. These symptoms erroneously may be attributed to problems such as irritable syndrome. Symptoms, however, may be less common. For example a quarter of patients with pancreatic cancer may have no pain at diagnosis, and half, particularly those with pancreatic head tumors, may have little pain compared with patients with body-tail tumors. However, if the tumor is suspected because of predisposing conditions, earlier diagnosis may be possible. These conditions include diseases such as chronic pancreatitis, intraductal papillary mucinous tumor (IPMT), and recent onset of diabetes mellitus, particularly if the diabetes occurs during or beyond the sixth decade. In addition inherited syndromes also are associated with an increased risk of pancreatic cancer including familial pancreatic cancer, hereditary pancreatitis, familial adenomatous polyposis syndrome (FAP) and familial atypical multiple mole melanoma (FAMMM) syndrome (hereditary dysplastic nevus syndrome). Of these conditions, recent onset of diabetes may be the best clue and should be included in a clinical profile of patients prior to the onset of symptoms to identify a high-risk group to apply screening strategies for detection of early disease. Contrary to a clinical aphorism that pancreatic cancer patients are elderly, lean and recently may have developed diabetes, we found that patients who develop pancreatic cancer are overweight prior to onset of symptoms compared to controls (body mass index, 28 vs 25). Forty percent had the diagnosis of diabetes made at the time of diagnosis of pancreatic cancer and more patients with a resectable tumor had diabetes (58%) compared to patients with locally unresectable or metastatic disease (37%). Perhaps, screening overweight persons who have new-onset diabetes may lead to a diagnosis of asymptomatic, early, resectable pancreatic cancer.
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PMID:Pancreatic cancer: clinical presentation, pitfalls and early clues. 1043 7


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