Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metastases were detected in 120 out of 598 cancer patients (20.2%). 96 patients underwent a close clinical examination. Symptoms produced by mediastinal and lung metastases were the first clinical manifestations of the disease in 23% of cases, whereas in 38.5%, both metastases and primary tumor were detected simultaneously. Metastatic cancer of lung and mediastinum was mostly symptom-free. Metastases most frequently occurred in lungs, less frequently in mediastinal lymph nodes and rarely in the pleura. Lung metastases usually disseminated in foci. Spherical metastases and foci of shadowed lung tissue were less frequent. In cases of thyroid cancer disseminated into mediastinum, all groups of lymph nodes were involved. If slightly enlarged, regional lymph nodes located behind manubrium sterni were most difficult to detect.
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PMID:[Clinical characteristics of metastases of thyroid cancer to the lungs]. 686 76

Genetic factors in the etiology of carotid body tumors (CBT) were sought in a medical record review of 222 histologically diagnosed cases at 12 U.S. medical centers. Patients in the series, which had a marked female predominance (146 females:76 males), usually developed tumors between the fourth and seventh decades of life (mean, 44.7 yr). In 16 patients who also had other extra-adrenal paragangliomas, suggesting a multiple primary tumor syndrome, CBT were diagnosed significantly earlier (mean, 35.4 yr; P less than 0.01). The occurrence of thyroid cancer in 5 other patients appeared to be excessive. Familial CBT was recognized in 16 patients from 13 affected families, including 9 newly ascertained kindreds. Compared with non-familial lesions, familial CBT tended to develop bilaterally (38% vs. 8% unilaterally) and at slightly earlier ages (41.6 vs. 44.9 yr). CBT was reported to occur in an autosomal dominant pattern in some families and within sibships in others; relatives were not examined for confirmation. The familial findings are generally consistent with a two-step mutation model of the development of hereditary and nonhereditary CBT; apparent deviations from the model might be clarified with additional data on this rare neoplasm.
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PMID:Carotid body tumors in humans: genetics and epidemiology. 695 Oct 72

The approach to management of an isolated thyroid nodule requires some understanding of the natural history of thyroid cancer and other forms of nodular thyroid disease. The histologic classification of thyroid cancer is an important determinant of survival, as are the size of the primary tumor, presence of thyroid capsule invasion, and presence of distant metastases. Therapeutic radiation and radioactive fallout increase the risk that a thyroid nodule is malignant. Autonomously functioning thyroid nodules are usually benign follicular adenomas and may cause thyrotoxicosis.
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PMID:Solitary thyroid nodule. 1. Clinical characteristics. 724 4

Differentiated thyroid carcinoma is a relatively indolent disease. Despite the usually favorable prognosis, differentiated thyroid cancer is fatal in some patients. In the past, treatment strategies were often based upon incomplete knowledge or inaccurate assumptions regarding the significance of the presenting characteristics of the tumor and patient. More recently, several large retrospective reviews have analyzed various presenting factors and have identified those that have prognostic significance and those that do not. Significant prognostic factors are age, primary tumor size, histology, grade, local tumor extension, and M stage. N stage appears to be a significant factor in older patients but not in younger patients. Gender, focality, and a history of prior irradiation are not significant prognostic factors. Using this knowledge, patients can be grouped into low, intermediate, and high risk groups. Prognostic factor and risk group analysis has facilitated the development of more rational treatment algorithms. Low risk patients can usually be treated with lobectomy and suppression therapy. For high risk patients, total thyroidectomy and adjuvant radioiodine is advocated. Treatment for patients in the intermediate risk group should be individualized. Prognostic factor and risk group analysis makes a selective approach to differentiated thyroid cancer possible. Such an approach can spare many patients the morbidity and expense of unnecessarily aggressive treatment without compromising outcome.
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PMID:Therapeutic implications of prognostic factors in differentiated carcinoma of the thyroid gland. 763 12

The rationale for TSH suppression in the treatment of follicular thyroid cancer (FTC) and papillary thyroid cancer (PTC) is to inhibit tumor growth, prevent recurrent disease, and eventually prolong survival. We analyzed the effects of TSH on invasion and growth of 3 FTC cell lines from 1 patient (FTC133, primary; FTC236, lymph node; FTC238, lung metastasis) and 2 PTC cell lines (PTC-UC1, PTC-UC3). Cell growth and invasion through an 8-micron pore polycarbonate membrane coated with Matrigel were measured using the MTT assay. The dose-response to TSH was biphasic, stimulating invasion and growth of FTC and PTC at low concentrations (0.1-10 mU/mL), and inhibiting them at high concentrations (100 mU/mL). Interestingly, the metastatic FTC cell lines had higher basal invasion, but were less responsive to TSH than the primary tumor. TSH (1 mU/mL) stimulated invasion of FTC133 by 21%, FTC236 by 8%, and FTC238 by 8% (p < 0.01). At 100 mU/mL, TSH inhibited invasion of FTC133 by 21%, compared to 11% in FTC236 and 12% in FTC238. Also, TSH dose-dependently influenced proliferation of follicular thyroid cancer cells. At low concentrations it stimulated growth of FTC133 (20%) and inhibited it at high concentrations (23%; p < 0.01). Again, the amplitude of TSH effects was significantly smaller in the cell lines from metastatic tumors. TSH affected invasion and growth of PTC-UC1 and PTC-UC3 also biphasically. These results show that TSH may act as a mitogenic and antimitogenic growth factor for invasion and proliferation of well-differentiated thyroid cancer cells in vitro.
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PMID:Biphasic effects of thyrotropin on invasion and growth of papillary and follicular thyroid cancer in vitro. 778 31

This study is a retrospective analysis of 248 thyroid cancer patients who received their primary treatment in the Chang Gung Memorial Hospital during the period January 1979 to December 1992. Among these cases, there were 173 papillary thyroid cancers (69.8%), 52 cases of follicular thyroid cancer (21%), 7 cases of medullary thyroid cancer (2.8%), and 16 cases of anaplastic thyroid cancer (6.5%). The subjects included 184 female patients with a mean age of 40.7 +/- 14.3 years and 64 males patients with a mean age of 49.2 +/- 14.3 years. Most of the cases had a nearly total thyroidectomy after the diagnosis was confirmed by frozen section during the operation. During the follow-up period, 19 (8.2%) patients diagnosed with well-differentiated thyroid cancer died of thyroid cancer in contrast to 12 patients (75%) with anaplastic thyroid cancer. The 1-year Greenwood survival probabilities after the disease is diagnosed in papillary, follicular, and anaplastic thyroid cancer are 0.98, 0.86, and 0.25, respectively. For the analysis of prognostic variables in well-differentiated thyroid cancer patients, 16 factors were entered for univariate and multivariate analysis. Using a log-rank univariate analysis, survival was significantly associated with the cell type of the primary tumor, age, clinical staging, postoperative 131I pattern, tumor size, postoperative thyroglobulin (Tg) level and postoperative x-ray results. In the Cox multivariate regression analysis the combination factors that gave the best prognostic value were the association of x-ray finding (P = .004), age (P = .017), and Tg level (P = 0.19). In conclusion, thyroid cancer is not an unusual disease in Taiwan. As previously reported anaplastic thyroid cancer has a poor prognosis. In this limited period of follow-up study, the patients' age with postoperative first positive x-ray finding and Tg level may provide the prognostic factors for patients with well-differentiated thyroid cancer.
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PMID:Thyroid cancer treated in Chang Gung Memorial Hospital (northern Taiwan) during the period 1979-1992: clinical presentation, pathological finding, analysis of prognostic variables, and results of treatment. 799 Apr 81

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

Among the patients who were examined with bone scintigraphy between April 1985 and March 1991, there were 27 patients whose initial clinical manifestation was bone metastasis and who were surveyed for the primary tumor site. The primary tumor site could be identified in 20 patients (74%), consisting of 9 patients with lung cancer, 3 with prostate cancer, 3 with hepatoma, 2 with renal cancer, and one each with thyroid cancer, adrenal cancer, and pleural malignant mesothelioma. In 17 of the 20 patients, the primary site had been detected within two months after presentation. Examinations which were helpful in identifying the primary site included chest radiography, sputum cytology, abdominal sonography, serum prostatic acid phosphatase level and pathologic examination of biopsy specimens. 99mTc-PMT scintigraphy was useful in the diagnosis of the hepatoma when accumulation was observed at the metastatic sites. In 2 patients, lung cancer had been recognized using follow-up chest radiography 3 and 6 months after presentation, respectively. One patient was diagnosed at autopsy as having adrenal cancer. In 7 patients the primary site remains unknown. Histology examination of the biopsy specimen performed in 6 of these patients revealed 4 to be adenocarcinoma and 2 undifferentiated carcinoma. The average survival period of the 17 patients who died was 9.5 months. Four patients are alive, and the outcome in the remaining 6 could not be determined.
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PMID:[Survey for primary tumor site in patients with initial clinical presentation of bone metastasis]. 823 Aug 25

When solitary pulmonary tumors are observed in patients with a history of cancer, differentiation between metastasis and primary lung cancer is crucial for appropriate therapy. Assuming that p53 mutations are conserved in metastases, mutation analysis of the p53 gene would be a valuable tool in differentiating metastases from primary carcinomas of the lung. In nine of 267 resected lung tumors, the origin of the lung tumor could not be defined histologically. Five patients had a history of colorectal carcinoma, one had a history of breast carcinoma, one had a history of soft-tissue carcinoma, and one had a history of head and neck carcinoma. One patient with a clear cell carcinoma of the lung had been surgically treated for both renal and thyroid cancer. Material from one patient with adenocarcinoma of the lung, histologically defined regional lymph nodes, and distant brain metastasis served as a control. We extracted deoxyribonucleic acid from the snap-frozen tissue of the unclassified lung tumors, from paraffin-embedded tissue of the previously removed primary cancers, and also from peripheral blood of the patients. Exons 2 to 11 of the p53 gene were amplified in separated polymerase chain reactions and directly sequenced. In all cases, the presence of germline mutations was excluded by analysis of peripheral blood deoxyribonucleic acid. The p53 mutation detected in the deoxyribonucleic acid of the lung tumor of the control patient proved to be conserved in the lymph nodes as well as in the brain metastasis. In two cases, the lung tumors exhibited a p53 mutation not present in the previously removed primary tumor and were therefore classified as new primary lung cancers. In five cases, the lung tumors proved to be metastases of the first tumor, exhibiting the identical p53 mutation. One of these lung tumor samples could be identified as a metastasis from the renal cancer, but the corresponding thyroid cancer material was different. For two cases, molecular analysis remained inconclusive. In one case, no p53 mutation could be found in the compared samples; in the other, no deoxyribonucleic acid could be extracted. Analysis of p53 mutations allowed exact classification in tumors for which standard methods failed to distinguish between metastasis or primary tumor. More than two thirds of lung tumors in patients with previous gastrointestinal carcinoma were revealed to be metastases, but second primary lung cancer could also be diagnosed. This diagnosis allowed correct surgical and adjuvant treatment of these patients.
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PMID:Molecular genetic differentiation between primary lung cancers and lung metastases of other tumors. 861 43

Metastases from differentiated thyroid cancer are usually seen in the cervical or mediastinal lymph nodes, lung or bone. We report a case of papillary thyroid cancer metastasizing to lymph nodes in the porta hepatis. No other site of metastasis was apparent on neck or abdominal exploration or on iodine whole-body scans. The primary tumor was a multifocal papillary thyroid cancer arising on a background of multinodular goiter. The metastasis was observed on a diagnostic radioiodine scan after surgical resection of the primary tumor despite significant (11%) radioiodine uptake by residual thyroid tissue in the neck and was proven by histologic examination and thyroglobulin immunohistochemistry. Although rare, metastasis to porta hepatis lymph nodes should be considered in the differential diagnosis of abdominal radioiodine uptake in patients with differentiated thyroid cancer.
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PMID:Isolated porta hepatis metastasis of papillary thyroid cancer. 868 30


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