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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To test the hypothesis that interferon-gamma (IFN gamma) and interleukin-1 beta (IL-1 beta) possess antitumor activity on human papillary thyroid carcinoma cells, we studied the in vitro effects of IFN gamma and IL-1 beta on the proliferation and invasiveness of two human PTC cell lines, TPC-1 (TP) and NPA (NP) cells. TP and NP cells were treated with various concentrations of IFN gamma and IL-1 beta alone and in combination. Cell proliferation was assessed by [3H]thymidine incorporation and cell number measurement. Tumor cell invasion was assessed by the ability of cells to penetrate through a Matrigel membrane. Both IFN gamma and IL-1 beta inhibited [3H]thymidine incorporation into TP cells in a dose-dependent manner and decreased TP cell number. In NP cells, treatment with IFN gamma and IL-1 beta also decreased [3H]thymidine incorporation and cell number. The inhibitory effects of IFN gamma and IL-1 beta on tumor cell proliferation were additive in both cell lines. In the invasion experiments, IFN gamma and IL-1 beta reduced the invasiveness of TP and NP cells. Again, the inhibitory effects of IFN gamma and IL-1 beta on tumor cell invasion were additive in both cell lines. In summary, the results showed that both IFN gamma and IL-1 beta are potent inhibitors of the proliferation and invasiveness of TP and NP cells. The additive effects of IFN gamma and IL-1 beta are evidence that they act through different pathways. Our findings suggest that IFN gamma and IL-1 beta are two of the anticancer factors that act to suppress the proliferation and reduce the invasive potential of human papillary thyroid carcinoma cells.
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PMID:Antitumor actions of interferon-gamma and interleukin-1 beta on human papillary thyroid carcinoma cell lines. 774 15

MCF-7 cells, a metastatic human breast carcinoma line, caused dose-dependent platelet aggregation in heparinized human platelet-rich plasma (PRP). MCF-7 tumor cell-induced platelet aggregation (TCIPA) was almost blocked by apyrase (0.5 U/ml) and completely inhibited by hirudin (5 U/ml). This TCIPA was unaffected by cysteine proteinase inhibition with E-64 (10 microM), but was limited by cell pretreatment with phospholipase A2. MCF-7 cell suspension caused marked, dose-dependent decrease in plasma recalcification times using normal, Factor VIII-deficient, and Factor IX-deficient human plasma. This effect was potentiated in cell lysates but was inhibited in intact cells preincubated with sphingosine. MCF-7 cell suspension did not affect the recalcification time of Factor VII-deficient plasma. Taken together, these data suggest that MCF-7 TCIPA arises from MCF-7 tissue factor activity expression. Trigramim and rhodostomin, RGD-containing snake venom peptides which antagonized the binding of fibrinogen to platelet membrane glycoprotein IIb/IIIa, prevented MCF-7 TCIPA. Likewise, synthetic peptide GRGDS as well as monoclonal antibodies against human tissue factor, platelet membrane glycoprotein IIb/IIIa and Ib prevented MCF-7 TCIPA, which was unaffected by control peptide GRGES. On a molar basis, trigramin (IC50, 0.1 microM) and rhodostomin (IC50, 0.03 microM), were about 5,000 and 18,000 times, respectively, more potent than GRGDS (IC50, 0.54 mM).
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PMID:Characterization of platelet aggregation induced by human breast carcinoma and its inhibition by snake venom peptides, trigramin and rhodostomin. 774 50

A 38-year-old male was admitted to our department with jaundice. Imaging studies including ultrasonography, ERCP, PTC and computed tomography (CT) revealed a hilar lesion. Right hepatic lobectomy, caudate lobectomy, excision of CBD and restoration of biloenteric continuity was performed. Pathological examination showed an icteric hepatoma (1.2 x 0.8 x 0.8 cm in size) originating in the caudate lobe. The tumor thrombus occupied the common hepatic duct and the right intrahepatic duct. The postoperative course was fairly unremarkable, and the patient has remained in good health for four years after surgery without any sign of recurrence.
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PMID:Successful resection of a minute icteric hepatocellular carcinoma--case report. 785 62

The purpose of the study was to ascertain whether the prognostic significance of staging in multiple myeloma (MM) is influenced by the aggressiveness of effective induction treatment and/or by continuing or discontinuing maintenance chemotherapy. Patients with untreated stage I MM (defined according to Durie and Salmon) were randomised between being followed without cytostatics until the disease progressed and receiving six courses of melphalan and prednisone (MP-P) just after diagnosis; stage II patients were uniformly treated with MPH-P and stage III patients were randomised between MPH-P and four courses of combination chemotherapy with Peptichemio, vincristine and prednisone (PTC-VCR-P). Within each stage, responsive patients were randomised between receiving additional therapy only until maximal tumour reduction was reached (plateau phase) and continuing induction therapy indefinitely until relapse. With resistant, progressive or relapsing disease, patients originally treated with MPH-P for induction received combination chemotherapy and vice versa. The overall first response rate was 43.8% (42.2% in 206 stage I, II and III patients treated with MPH-P and 48.0% in 75 stage III patients treated with combination chemotherapy, P = NS). Combination chemotherapy was more myelotoxic than MPH-P and, in particular, caused more non-haematological side-effects. Both the less and the more aggressive induction policies gave the same disease control. Progression of disease was statistically similar in stage I patients who were initially left untreated and in t hose who received MPH-P just after diagnosis; median duration of first response was similar in stage III patients receiving MPH-P and in those on combination chemotherapy. In all stages, discontinuing or continuing maintenance did not alter the median duration of first response. The overall second response rate was 28.5% (34.0% to MPH-P and 25.3% to combination chemotherapy, P = NS). Median survival was greater than 78 months in stage I, was 46.3 months in stage II and was 24.3 months in stage III patients, still independent of both induction and post-induction policies. In MM, the significance of staging for survival is independent of both the aggressiveness of induction and of continuing or discontinuing maintenance chemotherapy after the maximal tumor reduction has been achieved. Both MPH-P and and the association of PTC, VCR and P are effective in inducing first response and also second response in patients failing on the alternative regimen, but PTC-VCR-P causes more side effects. Thus, the overwhelming majority of patients with MM can safely be given MPH-P as first therapy, and this treatment may be delayed in early diseases.
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PMID:Treatment of multiple myeloma according to the extension of the disease: a prospective, randomised study comparing a less with a more aggressive cystostatic policy. Cooperative Group of Study and Treatment of Multiple Myeloma. 798 Oct 78

Eighteen patients with main biliary tract cholangiocarcinomas and no spread to the gallbladder and to the papilla of Vater underwent a combined US, ERCP/PTC and CT study. Angiography was performed on a selected group of 12 patients. We divided the infiltrating, polypoid or stenosing lesions in three groups: upper portion tumors, involving the confluence and the common hepatic duct (8 patients); middle portion tumors, originating from the common bile duct between the confluence of the cystic duct and the upper duodenal profile (6 patients); and finally lower third tumors, originating from the common bile duct between the upper rim of the duodenum and the papilla of Vater (4 patients). According to ERCP and/or PTC, US, CT and angiographic findings, only 9 of 18 cholangiocarcinomas were judged as resectable. The authors stress the need to optimize the use of imaging methods: US can locate the biliary obstruction; ERCP and/or PTC can show the tumor and its spread out of the duct, and finally angiography can exclude or confirm the vascular involvement of the hepatic hilum.
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PMID:[Cholangiocarcinoma of the main biliary tract. Judging its resectability by imaging procedures]. 804 36

The prognosis of patients with follicular (FTC) and papillary (PTC) thyroid cancer depends on age and the size and extent of the tumor. Differentiated thyroid cancers bind more epidermal growth factor (EGF) than normal thyroid tissue, but the role of EGF in the proliferation and invasion of thyroid cancer is unknown. We investigated the effects of EGF on growth, migration, and invasion in a follicular thyroid cancer that metastasized to cervical lymph nodes and the lung (FTC 133, primary; FTC 236, lymph node; and FTC 238, lung metastasis) and in a papillary thyroid cancer (PTC-UC3). As measured by the formazan method (dimethylthiazol-diphenyltetrazolium bromide), EGF caused a dose- and time-dependent increase in the growth of FTC 133 and PTC-UC3 by 25%, but its stimulatory effect on growth of the metastatic FTC subclones was smaller (FTC 236, 14%; FTC 238, 8%; P < 0.001). EGF also enhanced the ability of all cell lines to migrate (through 8-microns pore membranes without Matrigel) or invade (membranes with Matrigel). Migration of FTC 133 was enhanced from 86% migrated tumor cells to 95% after 72 h (P < 0.02). Again, stimulation by EGF was lower in FTC 236 and FTC 238. EGF increased migration in PTC-UC3 from 49% to 58%. EGF stimulated invasion of FTC 133 from 17.5% to 24.9%. In the absence of EGF, FTC 238 was the most invasive tumor, but, again, the EGF stimulatory effect was less pronounced than in the primary tumor. EGF stimulated the invasion of PTC-UC3 from 10.9% to 14.3% (P < 0.03). EGF also stimulated the growth of thyroid cancer xenografts in nude mice. Although all FTC cell lines were 100% tumorigenic in nude mice, PTC-UC3 was less tumorigenic. However, after sc inoculation of EGF-pretreated tumor cells, 7 of 10 animals developed tumors (mean size, 2.3 cm3) compared to 2 of 10 animals (mean size, 1.4 cm3) in the control group (P < 0.02). In summary, EGF stimulates the growth and invasion of differentiated thyroid cancer cells in culture and in nude mice. Escape from growth factor control, such as in FTC 236 and FTC 238, may be an important step in the development of metastatic thyroid cancer.
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PMID:Epidermal growth factor enhances proliferation, migration, and invasion of follicular and papillary thyroid cancer in vitro and in vivo. 804 55

This study was aimed at assessing the role of CT in the investigation of extraductal spread of hilar cholangiocarcinoma. October 1990 to November 1993, twenty-one patients with hilar cholangiocarcinoma were examined. The diagnosis was made on the basis of the following CT findings: intrahepatic bile ducts dilatation, nonunion of the right and the left bile ducts, normal size of extrahepatic bile ducts and the tumor depicted "per se". As for extraductal spread, we considered parenchymal invasion, involvement of vascular structures and parenchymal, lymph node and peritoneal metastases. In all cases CT demonstrated intrahepatic bile duct dilatation and nonunion at the confluence. CT demonstrated a hypodense mass in 10/21 cases and an isodense mass in 11/21 cases. Portal vein involvement was detected in 7/10 cases and hepatic artery involvement was correctly suspected in 1/8 cases; CT demonstrated parenchymal and lymph node metastases in 1/6 and 2/7 cases. In conclusion, CT proved to be a valuable technique, like PTC and US, to assess tumor resectability.
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PMID:[Role of computerized tomography in the evaluation of extraductal extension of hilar cholangiocarcinoma]. 806 57

Invasion and metastasis may be caused by the escape of tumor cells from the negative control of growth factors. We analyzed the effects of transforming growth factor-beta 1 (TGF beta 1) on growth, migration, invasion, and adhesion in three follicular thyroid cancer cell lines (FTC133, primary; FTC236, lymph node metastasis; FTC238, lung metastasis) from one patient and in a papillary line (PTC-UC3). Cell growth was measured by dimethylthiazol-diphenyltetrazolium bromide assays, and migration (basal or epidermal growth factor stimulated) was determined by the ability of cells to penetrate 8-microns pore membranes that were covered with Matrigel for invasion assays. Moreover, we studied tumor cell adhesion to collagen type IV, fibronectin, and laminin. TGF beta 1 inhibited growth in FTC (FTC133, by 31%; FTC236, 15%; FTC238, 17%; P < 0.008), but not in PTC. Migration was inhibited in all cell lines. TGF beta 1 inhibited epidermal growth factor-stimulated migration of FTC133 by 43% vs. 29% without epidermal growth factor (P < 0.03). TGF beta 1 also inhibited invasion (FTC133, 32%; FTC236, 18%; FTC238, 16%; PTC-UC3, 32%; P < 0.02). All cell lines adhered preferably to collagen type IV and fibronectin. TGF beta 1 enhanced adhesion. Again, these effects were less pronounced in the FTC metastases. In conclusion, TGF beta 1 inhibits the growth, migration, and invasion of thyroid cancer cells in vitro. It enhances adhesion to components of the extracellular matrix. Metastatic thyroid tumors may be less responsive to the negative regulation of TGF beta 1.
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PMID:Transforming growth factor-beta 1 is a negative regulator for differentiated thyroid cancer: studies of growth, migration, invasion, and adhesion of cultured follicular and papillary thyroid cancer cell lines. 807 65

The RET proto-oncogene encodes a transmembrane receptor of the tyrosine kinase family and has frequently been found activated in human thyroid carcinomas of the papillary subtype. In most cases the activation consisted of the fusion of its tyrosine-kinase domain with the 5'-terminal region of a gene designated H4 or D10S170. We have named the resulting H4/RET chimeric oncogene RET/PTC. Another activated form of the RET oncogene has subsequently been found in a thyroid carcinoma and is now referred to as RET/PTC2. Here we report the identification and cloning of a novel rearranged version of the RET oncogene in a human thyroid papillary carcinoma. In this case the tyrosine-kinase domain of RET was fused to a sequence 790 bp long belonging to a new gene that we have named RFG (RET Fused Gene). This novel chimeric oncogene has been designated RET/PTC3. In order to have more insights into the function of RFG we have completely cloned and sequenced its cDNA. RFG predicted amino-acid sequence does not have any significant homology to any already known genes and is ubiquitously expressed in human and mouse tissues. Finally we provide evidence indicating that the rearrangement leading to the generation of RET/PTC3 occurred in vivo in the original tumor DNA.
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PMID:Molecular characterization of RET/PTC3; a novel rearranged version of the RETproto-oncogene in a human thyroid papillary carcinoma. 829 Feb 61

Follicular thyroid cancer is the second most common thyroid malignancy after PTC. There are marked geographical variations in the relative proportions of FTC and PTC, most likely related to dietary iodine content. In iodine-deficient areas, the relative rate of FTC tends to be increased. Other risk factors for FTC include age over 50 years and female sex. Genetic factors may also have a role in determining disease susceptibility but remain ill-defined. Histologically, FTC is characterized by follicle formation and the absence of any papillary elements in the tumor. Differential diagnosis from a benign adenoma can be difficult. The degree of vascular invasiveness seems to correlate with tumor aggressiveness, and two histologic subtypes, oxyphilic FTC and insular FTC, may be associated with increased morbidity and mortality. Primary treatment for FTC is complete surgical tumor removal. Extensive bilateral surgery beyond this goal may not confer additional benefit but can facilitate adjuvant treatment and follow-up. Postoperative levothyroxine treatment is almost universally used, and patients deemed at high risk of recurrence may benefit from radioiodine remnant ablation. Treatment of metastatic disease involves operation, radioiodine, and, in selected cases, external beam radiation and chemotherapy. Prognosis for patients with metastatic disease is guarded, but most other patients have good outcomes comparable to that in PTC. For nonoxyphilic FTC, high-risk features other than initial metastases include advanced age, locally extensive disease, and the presence of marked angioinvasion. In oxyphilic FTC, DNA aneuploidy is also important. Follow-up should be most intense during the first 5 years after primary treatment and needs to be tailored to the patient's risk of disease progression. For patients at low risk of recurrence (young, small lesions, minimally invasive tumor), serum thyroglobulin measurements may largely suffice, whereas higher risk patients with elevated serum thyroglobulin levels and patients with significant titers of interfering anti-thyroglobulin autoantibodies may also need to undergo periodic diagnostic radioiodine scanning.
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PMID:Follicular thyroid cancer. 860 79


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