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)

We reported earlier that oncolysate retained in the excision wound of a local tumor inhibits growth of remote tumor in the rat. We further studied this effect on pulmonary metastasis. C57BL/6 mice were given B16 melanoma F10 cells subcutaneously into the gluteal area (Day 0) and then intravenously on Day 10. On Day 14, mice were divided into four groups. Group 1 received a sham operation and no further treatment. Tumors were excised in the remaining mice. Group 2 received tumor excision alone. Groups 3 and 4 received injections of freeze-lysed tumor cells (TC) and lysate modified (PTC) with a hapten, L-phenylalanine mustard (PhM), respectively, into excision wounds. On Day 24, metastases were assessed by determining metastatic burden. Average diameters of excised tumors in repeated experiments ranged from 8.7 to 10.9 mm. In repeat experiments, pulmonary metastatic burden increased by as much as 52 to 181% in the tumor excised group (Group 2) in comparison with those receiving sham surgery (Group 1). However, metastatic burden was always reduced in Group 3. An even greater reduction was seen in Group 4. To study the possible involvement of macrophages, the production of prostaglandin-E2 (PGE2) and cytotoxicity of macrophages in these animals were examined. It was found that tumor excision enhanced PGE2 production by macrophages and suppressed their cytotoxicity, while TC inoculation prevented both of these changes. An even greater prevention was observed with PTC inoculation. These results indicate an association among macrophage cytotoxicity, PGE2 production of macrophages, and metastasis. In order to clarify the mechanism for these reactions, we did experiments using adherent splenic macrophages from the four groups of animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of local tumor removal and retained oncolysate on lung metastasis. 140 87

Thyroid carcinoma may invade the mediastinum by direct extension of the primary tumor or metastases to the paratracheal or retroclavicular-parajugular lymph nodes. From 1975 to 1991 in 47 out of 622 thyroid cancer patients (7.6%) [14 papillary (PTC), 5 follicular (FTC), 16 medullary (MTC) and 12 undifferentiated carcinoma (UTC)] transsternal tumor resection has been performed. Four patients (UTC three, MTC one) deceased 7, 8, 35, and 41 days after resection of the primary tumor due to cardiac or tumor disease, and in one patient because of acute arteriotracheal haemorrhage after external irradiation; no patient deceased after transsternal resection as a result of cervicomediastinal lymphadenectomy. At the time of primary operation 80% of patients showed an advanced tumor stage (greater than pT3). In 34% of patients (PTC 64%, FTC 40%, MTC 13%, UTC 25%) no tumor recurrence was observed neither by imaging nor by biochemical methods. In 18 patients a transsternal microdissection of all four cervicomediastinal lymph node compartments has been performed. Histological analyses of excised and tumor involved lymph nodes revealed in 9 patients unilateral cervical and mediastinal and in 9 patients bilateral cervical and mediastinal lymph node metastases. In the case of unilateral cervicomediastinal lymph node metastases 2 out of 2 patients with papillary and 2 out of 6 patients with medullary thyroid carcinoma could be cured surgically. In the case of bilateral cervicomediastinal lymph node metastases 3 out of 4 patients with papillary thyroid carcinoma, but no other thyroid cancer patient were free of disease. In conclusion, main indications for transsternal cervicomediastinal resection in thyroid carcinoma are (1) primary tumors extending to the upper mediastinum, but without lymph node metastases, and (2) thyroid carcinomas with unilateral cervicomediastinal lymph node metastases. In the case of bilateral cervicomediastinal lymph node metastases probable only papillary thyroid carcinomas are supposed to be curable by transsternal multicompartmentectomy.
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PMID:[Trans-sternal cervico-mediastinal primary tumor resection and lymphadenectomy in thyroid gland cancer]. 156 3

We have investigated the PTC/retTPC oncogene, an activated form of ret proto-oncogene with a specific rearrangement, in thyroid malignancies. Southern analysis was used to screen 36 thyroid papillary carcinomas (PC), 22 normal thyroid tissues from glands with PC elsewhere, three follicular carcinomas, eight follicular adenomas and 30 other non-malignant thyroids. Rearrangements were detected in four PCs (11%) using probes derived from the ret proto-oncogene. Genomic breakpoints from a PC and a PC cell line (TPC-1) were cloned and sequenced. The rearrangement points of ret proto-oncogene were found in the intron between the exon for the transmembrane domain and the first exon for the tyrosine kinase domain. Furthermore, the PTC/retTPC chimeric transcripts were detected in two PCs with the rearrangement by reverse transcription polymerase chain reaction. Distant metastases were present in 50% (2/4) of PCs with the rearrangement, but in only two out of 32 PCs without a detectable rearrangement (P = 0.05, Fisher exact test). Our study suggests that the rearrangement of the ret proto-oncogene may be involved in the development of distant metastases in patients with papillary thyroid carcinomas. However, a larger clinical study will be required to verify this observation.
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PMID:Detection of the PTC/retTPC oncogene in human thyroid cancers. 162 May 47

We recently detected a novel activated oncogene by transfection analysis on NIH 3T3 cells in five out of 20 primary human thyroid papillary carcinomas and in the available lymph node metastases. We designated this transforming gene PTC (for papillary thyroid carcinoma). Here we describe the molecular cloning and sequencing of the gene. The new oncogene resulted from the rearrangement of an unknown amino-terminal sequence to the tyrosine kinase domain of the ret proto-oncogene. This gene rearrangement was detected in all of the transfectants and in all of the original tumor DNAs, but not in normal DNA of the same patients, thus indicating that this genetic lesion occurred in vivo and is specific to somatic tumors. Moreover, the transcript coded for by the fused gene was detected in an additional PTC-positive human papillary carcinoma for which mRNA was available.
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PMID:PTC is a novel rearranged form of the ret proto-oncogene and is frequently detected in vivo in human thyroid papillary carcinomas. 240 25

The records of 121 patients who presented for PTC and biliary drainage within a five-year period were reviewed. Fifty-eight bile samples had been obtained from 38 of these patients for cytologic analysis. Malignancy was detected in 14 of 32 patients with carcinoma (sensitivity 44%). Repeat sampling was positive in four of nine patients whose initial specimen contained no tumor cells. Bile duct carcinoma, pancreatic carcinoma, and metastatic disease were all detected. An approach to biliary cytodiagnosis is offered that, it is hoped, will further minimize future false negative results.
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PMID:Biliary cytodiagnosis. Bile sampling for cytology. 398 69

Metastatic obstructive jaundice usually results from an occlusion of the common hepatic or bile duct. More rarely, the underlying cause is a disseminated intrahepatic infiltration that has led to the occlusion of the bile canaliculi. The endoscopic-radiological examination techniques usually permit a reliable differentiation between neoplasms originating primarily in the biliary tract, and ductal occlusions caused by metastatic disease. In addition to this, both ERC and PTC permit the placement of an internal or external biliary drain during one and the same procedure. ERC represents a highly suitable method for the follow-up monitoring or documentation of the therapeutic effect of biliary drainage, radiotherapy and/or polychemotherapy. With the aid of regular follow-up examinations, recurrent disease can be detected early on, and appropriately treated.
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PMID:Endoscopic-radiological findings in metastatic obstructive jaundice. 682 22

Mutational changes in the p53 tumor suppressor gene are the most frequent genetic alterations in human malignant tumors. Studies have shown a correlation of p53 expression in breast cancer with tumor prognosis. In contrast to mutational activation of ras and GSP in thyroid tumors, little is known about the role of p53 in thyroid tumor development. Therefore thyroid tumors and thyroid tumor cell lines were studied for the presence of p53 mutations. Snap-frozen tissues from 57 differentiated thyroid carcinomas (DTCs) and 5 goiters were studied by immunohistochemical methods. A panel of six antibodies (pAb 240, 421, 1620, 1801, DO7, and CM1) was employed by using the ABC technique. Five cell lines from DTCs (FTC133, 236, 238, PTC337, MTC164) were examined by the same technique. Additionally, genomic DNA from the cells was amplified by the polymerase chain reaction (PCR) and the PCR product studied for p53 mutations (R273H) by mutation-specific oligonucleotide hybridization (MOH) and temperature gradient gel electrophoresis (TGGE) for the p53 exon 8. None of the benign thyroid tumors and 7 of 57 (12%) DTCs strongly express p53 with a heterogeneous distribution in the tumor tissue. All seven patients have metastatic disease or dedifferentiated tumors G3 (three of seven). CM1 was positive in two cell lines (FTC-133, PTC-337), questionable in FTC-238, and negative in FTC-236 and MTC-164. All three follicular cell lines, however, and the original tumor tissue showed the same p53 mutation (R273H) in MOH analysis and TGGE. P53 mutations are rare in thyroid tumors, but the presence of p53 mutations indicates a poor prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Significance of P53 in human thyroid tumors. 772 41

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

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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