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)

A series of rasH oncogene-transformed cell lines were established from NIH-3T3 cells using the calcium phosphate precipitation method of transfection. The transfectant lines formed highly-invasive tumors when injected into athymic mice while the parent cells did not. When examined for motility in the micropore filter assay, all of the transfectant lines were motile in response to either laminin or fibronectin while the parent cells were not stimulated by either factor. These studies, therefore, indicate that transformation of NIH-3T3 cells with the rasH oncogene results in the generation of cells with increased capacity for motility relative to the parent cells.
Invasion Metastasis 1986
PMID:Motility of rasH oncogene transformed NIH-3T3 cells. 380 40

The author writes about some facts related to the use of 99m-Tc-phosphate in skeletal scanning, specially to recognize cancer metastases, and vascular and inflammatory osseous diseases, and indicates some conditions to carry out the study.
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PMID:[Nuclear medicine in osteoarticular pathology]. 391 1

A 47-year-old man was admitted because of a left axillary tumor. A biopsy of the tumor disclosed adenocarcinoma. The bone survey showed multiple sclerotic metastases. Thirteen months after his first admission, a left breast tumor developed and a simple mastectomy revealed a papillotubular carcinoma. Skin metastases appeared postoperatively and were exacerbated with accumulation of pericardial effusion and a high CEA level (401.7 ng/ml) despite radiation and chemotherapy. Estrogen therapy with diethylstilbestrol sodium phosphate was started, resulting in the disappearance of pericardial effusion and skin metastases. The patient remains well 10 months after starting estrogen therapy with a normal CEA level.
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PMID:[A case of advanced male breast cancer treated effectively with estrogen]. 392 44

To investigate the mechanisms of hypercalcaemia in carcinoma of the breast, 22 patients with hypercalcaemia due to metastatic carcinoma were studied and the findings compared with those obtained in normal subjects and patients with benign and malignant breast disease without hypercalcaemia. As expected, patients with metastases of bone showed biochemical evidence of increased bone resorption. Whereas all patients with hypercalcaemia had skeletal metastases, not all patients with skeletal metastases had hypercalcaemia despite considerable degrees of bone resorption. The presence of hypercalcaemia was associated with a significant increase in renal tubular reabsorption of calcium (p less than 0.001) and decreased reabsorption of phosphate (p less than 0.001) despite adequate rehydration of patients. These studies suggest that increased renal tubular reabsorption of calcium, possibly mediated by a humoral factor with activity similar to that of parathyroid hormone, contributes appreciably to the hypercalcaemia of malignant breast disease.
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PMID:Mechanism of malignant hypercalcaemia in carcinoma of the breast. 392 36

Natural stable isotope fractionation is a potential tool in investigation of metabolic process, since rigid mass balance considerations rule the changes in the isotopic ratio. As the natural changes in 13C/12C ratio of total CO2 between blood and urine served for studying renal bicarbonate reabsorption, studying changes in 18O/16O ratio of phosphate are suggested to investigate deranged phosphate metabolism. The 18O/16O ratio in serum phosphate is constant, determined by the ratio in the environmental drinking water. Therefore, measurements of this ratio in normal individuals, after modifications in phosphate metabolism and in diseases with high alkaline phosphatase activity are proposed. The main purpose of the proposed study is to assess whether measurements of 18O/16O ratio can detect malignant metastases in bones due to deranged phosphate metabolism. An assumption that these determinations might precede other tests for detecting bone metastases and can serve as an oncogenic marker is made.
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PMID:Determination of 18O/16O ratio in inorganic phosphate as an oncogenic marker and indicator for disturbances in phosphate metabolism. 406 37

We looked systematically for the presence of receptor like binding sites for 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) in the cytosol from 22 breast cancers. Cytosols were centrifuged on 5-20% sucrose gradients after labeling with tritiated 1,25 (OH)2D3 (3H-1,25(OH)2D3 or 25-hydroxyvitamin D3 (25(OH)D3 alone or in the presence of a large excess of these unlabeled sterols. Binding sites for 1,25 (OH)2D3 migrating in the 3.5-3.7 S region were found in 7 out of 22 cancers, while 5.5-6.5 binding sites for 25 (OH)D3 were found in all cytosols. In a patient in whom cytosol containing a 3.5-3.7 S binding site was in sufficient amount, quantification of 1,25 (OH)2D3 binding indicated a KD of 0.28 nM and a maximal binding capacity of 0.15 pmol/mg prot. No relation was found between the presence or the absence of 1,25 (OH)2D3 binding sites and the histological type, the extension of the cancer, the presence of radiological or histological calcifications, the amount of estrogen or progesterone receptors, the plasma calcium or phosphate concentration and the emergence of metastases after 1 year. The significance of the presence of receptor-like binding sites for 1,25-(OH)2D3 in one third of breast cancers remains therefore unknown at the present time.
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PMID:Systematic search for 1 alpha,25-dihydroxy-vitamin D3 receptors in human breast carcinomas. 609 7

The relative importance of different causes of hypercalcaemia was studied, and diagnostic tests were evaluated as predictors of the cause of hypercalcaemia. In one year, hypercalcaemia was identified in 166 hospital inpatients. Serum-calcium was below 3.00 mmol/l in 63%. Among 153 patients investigated the commonest cause of hypercalcaemia was malignancy (89 cases), especially breast and bronchial tumours. 75% of the 89 patients had obvious metastases at presentation. 51 patients had primary hyperparathyroidism: their symptoms were non-specific and only 20% had renal stones. Other causes of hypercalcaemia were rare (9% of patients seen). Of patients with no diagnosis initially, 64% had hyperparathyroidism and 32% malignancy, but this was demonstrated early in the illness. Serum phosphate and chloride and acid/base status were unsatisfactory as diagnostic tests; multivariate analysis was more discriminating overall, but incorrect classification was still a significant problem.
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PMID:Hypercalcaemia in hospital patients. Clinical and diagnostic aspects. 610 66

Bone imaging with Tc-99m labelled phosphate compounds is a very sensitive but less specific method for detection of bone metastases, the lack of false-negative findings in prostatic cancer is of additional value. Preoperative bone scans should be obtained from all patients with prostatic cancer, the frequency of controls depends on the tumor stage and on the individual course of the illness. Serial bone scintigraphy is able to assess the effectiveness of treatment. Normalisation of the bone scan is synonymous with good response, the occurrence of new bone metastases indicates failure of treatment. Relief of pain is obtained in some patients after application of P-32 or Sr-89, intense uptake in the metastases is necessary but does not guarantee successful treatment.
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PMID:[Radionuclide diagnosis and therapy of skeletal metastases of prostatic cancer]. 620 Aug 97

The low incidence of measurable or evaluable metastases in patients with prostatic cancer makes evaluation of response difficult. This is particularly true in patients with bone metastases only. With a digital model it is possible to measure quantitatively from the radioisotope bone scan the total area of skeletal involvement by metastatic tumor. Definitions of response in bone have been derived from this model. These response criteria have been compared to response in acid phosphatase determinations and clinical status in a study of 44 patients with advanced prostatic cancer treated with estramustine phosphate. Based on serial quantitative bone scans, serial measurements of acid phosphatase levels and repeat clinical evaluations a system is proposed for defining response to systemic therapy that is applicable to the majority of patients with metastatic prostatic cancer.
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PMID:Systemic treatment of advanced prostatic cancer: development of a new system for defining response. 625 76

Some relations between metastatic bone disease and calcium homoeostasis were determined in a consecutive series of 81 patients with solid malignant tumours attending for radionuclide bone scans. Biochemical evaluation showed that bone resorption from metastatic disease was generally not enough to account for hypercalcaemia. While skeletal metastases were present in about half of the patients who developed hypercalcaemia, biochemical indices of bone resorption in these subjects were greatly increased and disproportionate to the extent of metastatic disease detected by the bone scans. Furthermore, a reduced renal phosphate threshold and increased tubular calcium reabsorption were generally observed in hypercalcaemic patients when compared with their normocalcaemic counterparts. These findings suggest that in most cases malignancy associated hypercalcaemia may be caused by the release of a humoral factor by tumour tissue which exhibits "parathyroid-hormone-like" activity with regard to bone resorption, renal phosphate threshold, and renal calcium handling. It may be postulated that this putative humoral mediator predisposes to hypercalcaemia both by stimulating generalised osteolysis and in most cases also by impairing the renal excretion of the resultant increase in filtered calcium load. While hypercalcaemia may arise as a result of metastatic bone disease alone, these data indicate that this may be the exception rather than the rule. Hence the term "metastatic hypercalcaemia" should probably be reserved for patients with extensive skeletal tumour disease in whom biochemical evaluation fails to yield evidence of an underlying humorally mediated cause.
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PMID:Relative contribution of humoral and metastatic factors to the pathogenesis of hypercalcaemia in malignancy. 642 77


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