Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We found previously that a human renal carcinoma cell line derived from a hypercalcemic patient induces humoral hypercalcemia when grown as allografts in the nude mouse and secretes a protein that activates adenylate cyclase via the PTH receptor. The purpose of this study was to examine the conditioned medium of this cell line for bone-resorbing activity in vitro. Processed conditioned medium produced dose-dependent stimulation of bone resorption in cultured fetal rat limb bone explants. Two PTH antagonists were used to assess the PTH receptor dependence of this bone-resorbing activity. Neither [8Nle,18Nle,34Tyr]bovine (b) PTH-(3-34) amide nor [34Tyr]bPTH-(7-34)amide inhibited bone resorption or limb bone cAMP accumulation induced by either processed conditioned medium or equivalent concentrations of bPTH-(1-34). As an alternate means to assess whether this tumor-derived PTH-like protein had intrinsic bone-resorbing activity, the latter was measured during partial purification of PTH-like adenylate cyclase-stimulating activity (ACSA) from conditioned medium by consecutive gel filtration and reverse phase HPLC. The bone-resorbing activity in conditioned medium could not be resolved from PTH-like ACSA by these two separation techniques, indicating that the activities may be intrinsic to the same protein. These results are consistent with the view that a tumor-derived protein with PTH-like ACSA and bone-resorbing activity may be responsible for hypercalcemia in vivo.
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PMID:Parathyroid hormone-like adenylate cyclase-stimulating activity from a human carcinoma is associated with bone-resorbing activity. 302 77

Fourteen cases of urogenital tumors (9 prostatic carcinomas, 4 renal cell carcinomas and 1 bladder carcinoma) which had bone metastases were treated with eel-calcitonin, Elcitonin injections for relief of bony pain. Forty mgs. of Elcitonin was injected intramuscularly, 2 to 3 times a week, to out-patients. Forty to 80 mgs. of Elcitonin was injected intramuscularly, daily to hospitalized patients. Relief of the pain was obtained in 71.4% of all patients (71.4% of out-patients and 71.4% of hospitalized patients) and especially in 88.9% of prostatic carcinoma patients. Hypercalcemia was seen in only one patient of renal cell carcinoma. It is considered that Elcitonin treatment is useful for relief of bony pain in the patients with bone metastases, with or without hypercalcemia.
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PMID:[Experience of Elcitonin treatment in metastatic bony pain of urological tumors]. 317 47

It is noted that while a wide variety of syndromes have been associated with hypernephroma in the clinical literature, there is clear understanding of the pathophysiology of these effects only in the cases of the endocrine disorders where direct tumor production of hormone can be demonstrated in vitro. Furthermore, this knowledge has done little to alter the care of patients with the disease, except for indications that indomethacin might be of benefit in some patients with hypercalcemia and that one might consider the use of converting enzyme inhibitors in patients with hypernephroma and hypertension. The overall approach to the disease is still surgical. Resection of the tumor also removes the paraneoplastic syndrome. Persistence or recurrence of a syndrome suggests the continued presence of the neoplasm, with the considerations for prognosis which that fact entails. To that degree, at least, these conditions are useful as tumor markers, but such use is limited because they are inconsistent. Further studies of pathophysiology of paraneoplastic syndromes will lead to better understanding of processes of cell differentiation and regulation, and possibly better ways to manage the patients in which they occur.
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PMID:Paraneoplastic syndromes in hypernephroma. 330 61

The success of cancer therapy depends on the destruction of all viable cancer cells in the primary site, as well as in metastatic areas. Surgery alone can do little for the patient whose tumor has produced distant involvement except in those situations where surgical excision, radiotherapy, chemotherapy, or immunotherapy can be relied on to eradicate metastatic disease. Because of the paucity of systemic therapy for renal cell carcinoma, an aggressive surgical approach to the primary tumor is justifiable when all metastatic lesions can be excised or otherwise definitively treated and in experimental protocols in which adjuvant therapy of possible benefit can be combined with palliative nephrectomy. There is no evidence, however, in reported studies to suggest that routine palliative nephrectomy in patients who will not be offered adjuvant systemic therapy or radiation is beneficial. Such practice is also associated with a higher incidence of complications and mortality than is expected for resection of localized renal cell carcinoma. For these reasons, it is reasonable to recommend adjunctive nephrectomy only in certain selected instances, which include (1) the control of a patient's current symptoms related to the primary disease, for example, flank pain, hematuria, fever and toxicity, anemia, erythrocytosis, and hypercalcemia; (2) nephrectomy with the excision of a solitary metastasis; and (3) the patient who is willing to undergo experimental therapy, part of which involves removal of the primary tumor.
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PMID:The failure of infarction and/or nephrectomy in stage IV renal cell cancer to influence survival or metastatic regression. 331 66

A variety of solid tumors secrete proteins that are immunochemically distinct from parathyroid hormone (PTH) but activate PTH-responsive adenylate cyclase. Such PTH-like proteins have been proposed as mediators of the hypercalcemia and hypophosphatemia frequently associated with malignancies. We purified to apparent homogeneity a PTH-like protein with a molecular weight of 6,000, that is produced by human renal carcinoma cells. The amino-terminal sequence of the PTH-like protein and that of human PTH were found to display at least five identities in the first 13 positions. The purified protein bound to PTH receptors, activated adenylate cyclase in renal plasma membranes, and stimulated cAMP formation in rat osteosarcoma cells. The PTH-like protein reproduced two additional effects of PTH, stimulation of bone resorption in fetal rat limb bone cultures and inhibition of phosphate uptake in cultured opossum kidney cells. These properties are consistent with a role for PTH-like proteins as mediators of the syndrome of malignancy-associated hypercalcemia.
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PMID:Parathyroid hormonelike protein from human renal carcinoma cells. Structural and functional homology with parathyroid hormone. 368 May 30

Serum concentrations of immunoreactive parathyroid hormone (iPTH) measured with a mid-region specific radioimmunoassay and total calcium were correlated in 300 healthy subjects and 158 patients with surgically verified primary hyperparathyroidism (HPT). All the healthy individuals could be separated from the patients by a monoexponential declining curve in which iPTH at concentrations of 0.60 micrograms/l and 0.33 micrograms/l corresponded to calcium concentrations of 2.20 mmol/l and 2.60 mmol/l, respectively. In 22 patients more than one sample was analysed and serum iPTH and calcium were inversely correlated. In contrast, three patients with parathyroid carcinoma showed no reciprocal fluctuations between serum iPTH and calcium. Of 75 patients with hypercalcaemia due to malignant diseases (metastatic mammary carcinoma, bronchial carcinoma, renal carcinoma, myelomatosis), 62 had a normal iPTH/calcium relationship. Two patients with myelomatosis had a temporary elevation of serum iPTH and calcium due to renal impairment. One patient with bronchial carcinoma probably had ectopic production of iPTH. The remaining 10 patients (six mammary carcinomas and four bronchial carcinomas) were found in the pathological iPTH/calcium range. In conclusion, we have demonstrated that an inverse relationship exists between serum iPTH and calcium in patients with non-malignant, primary HPT. Evaluation of iPTH and calcium in the same serum sample gave a correct diagnosis in more than 90% of patients with primary HPT.
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PMID:Improved diagnosis of primary hyperparathyroidism by defining the inverse relationship between serum immunoreactive parathyroid hormone and calcium. 374 90

We measured serum 1,25-dihydroxyvitamin D concentrations in 18 patients with renal cell carcinoma-associated hypercalcemia. Only 2 patients (11%) had low serum 1,25-dihydroxyvitamin D (less than 15 pg/ml) levels, and the mean 1,25-dihydroxyvitamin D level in the 18 patients was 44 +/- 30 (+/- SD) pg/ml, not different from the value of 42 +/- 22 pg/ml in 75 age-matched normocalcemic patients with various malignancies. Eighty-seven percent (26 of 30) of the hypercalcemic patients with extensive skeletal metastases due to other malignancies or with hematological malignancies had suppressed serum 1,25-dihydroxyvitamin D levels (less than 15 pg/ml). In hypercalcemic patients with other malignancies and no skeletal metastases, only 54% (21 of 39) had low serum 1,25-dihydroxyvitamin D levels. The mean serum 1,25-dihydroxyvitamin D level in the latter group was 21 +/- 26 pg/ml, significantly lower than that in normocalcemic patients. In renal cell carcinoma-associated hypercalcemia, suppression of circulating 1,25-dihydroxyvitamin D concentrations is uncommon.
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PMID:Circulating 1,25-dihydroxyvitamin D concentrations in patients with renal cell carcinoma-associated hypercalcemia are rarely suppressed. 378 32

A hypercalcemia frequency of 1.5% was found in patients with malignant disease attending a large oncological center. Eighty per cent of hypercalcemias were of obvious malignant etiology. Hypercalcemia was most frequent in multiple myeloma, renal carcinoma, squamocellular carcinomas of different sites and breast cancer. Most patients had advanced metastasized disease. In 80% of those with solid tumors malignant hypercalcemia was associated with bone metastases. Serum calcium could almost invariably be reduced by treatment, and active treatment was associated with a more favorable prognosis. One year actuarial survival of patients with malignant hypercalcemia was 31%.
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PMID:Malignant hypercalcemia--a hospital survey. 381 29

A very rare case of renal cell carcinoma of the horseshoe kidney that produced AFP and caused hypercalcemia is reported. The relationship between this renal cell carcinoma and hypercalcemia was obvious, but the mechanism of hypercalcemia was not revealed. The presence of AFP in cancer cells was demonstrated using the "ABC" method.
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PMID:[A case of renal cell carcinoma of horseshoe kidney that produced AFP and caused hypercalcemia]. 608 18

Today the indication for palliative embolization of inoperable renal carcinoma is more restricted than several years ago. Reviewing 31 own palliative occlusions of the renal artery in 29 patients over a period of 5 1/2 years two main reasons for this attitude are presented: 1. Because of collateral or parasitic vascular supply of kidney tumors the occlusion of the renal arteries only results in a retarded tumor growth rate and does not seem to prolong patient survival. 2. the "postembolization syndrome" after tumor occlusion has a relatively high complication rate and lethality (20% serious side effects, 3% deaths directly related to embolization). Therefore embolization of inoperable renal carcinomas is justified only in patients whose remaining lifetime can be alleviated by this measure. Certain indications are: massive hematuria, severe local pain due to the tumor and life endangering endocrine tumor activity, e.g. hypercalcemia. Uncertain indications such as recurring but not perilous hematuria causing progressive anemia and refusal of tumor surgery should be carefully balanced against the hazards of embolization.
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PMID:[Limitations and hazards of palliative renal tumor embolization]. 618 73


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