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)

14 patients with osteolytic bone disease due to breast cancer or myeloma, 7 of whom had hypercalcaemia, received oral treatment with (3-amino-1-hydroxypropylidene)-1, 1-bisphosphonate (A.P.D.). Serum-calcium dropped to low normal values in all 14 patients, accompanied by a decrease in urine calcium and hydroxyproline excretion-rate. The results show that A.P.D. may inhibit tumour-induced osteolysis.
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PMID:Inhibition of osteolytic bone lesions by (3-amino-1-hydroxypropylidene)-1, 1-bisphosphonate (A.P.D.). 8 43

A specific receptor for 1,25-dihydroxyvitamin D has been demonstrated in a cultured human breast cancer cell line. This is the first such demonstration in any cancer cell. It may explain the high incidence of metastatic bone destruction and hypercalcaemia in this common malignancy, and the limited success of other steroid-receptor assays in predicting the response of breast cancer to therapy.
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PMID:1,25-dihydroxyvitamin-D-receptor in breast cancer cells. 9 76

Urinary adenosine -3' ,5' - cyclic monophosphate was measured in 14 patients with hypercalcaemia not caused by primary hyperparathyroidism. Increased levels were found in patients with malignant disease without bone metastases and believed to be examples of paraendocrine syndrome. Decreased levels were found in patients with metastatic carcinoma involving bone, and in patients with multiple myeloma, lymphoma and immobilisation after fracture. Results obtained during treatment for hypercalaemia are described in three patients. In two hypercalcaemic patients (one with hyperthyroidism and one with breast cancer with bone metastases) normal levels were found. This measurement is a useful substitute for assay of serum parathyroid hormone and is of value in the diagnosis of hypercalcaemia, in monitoring effects of treatment and in revealing underlying mechanisms.
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PMID:Urinary cyclic AMP in diagnosis and management of hypercalcaemia: studies of patients without primary hyperparathyroidism. 16 77

A woman with metastatic carcinoma of the breast developed hypercalcemia 39 months after mastectomy. The hypercalcemia remitted after treatment but recurred 12 months later, accompanied by elevated levels of serum immunoreactive parathyroid hormone (PTH). A urea/HC1 extract of hepatic metastases contained immunoreactive PTH, material which stimulated the resorption of fetal rat bone in tissue culture, and material which stimulated chick renal adenylate cyclase activity. These findings strongly suggest that this breast cancer produced a PTH-like substance.
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PMID:Carcinoma of the breast associated with hypercalcemia and the presence of parathyroid hormone-like substances in the tumor. 42 76

Four antisera raised in the goat have very different properties: all recognized the immunoreactive calcitonin (iCT) of medullary carcinoma of the thyroid (MCT), one the response of normal subjects to induced or endogenous hypercalcemia and 2 others a different molecular species which occurs in half the patients with cancer of breast and 3/4 of patients with cancer of the lung. The latter two antisera are most sensitive to the 22-32 sequence of human calcitonin. Depending on the antiserum used, 4 or 7 peaks of immunoreactivity are found in eluates by column chromatography or stimulated serum from MCT. Not all elevated levels of iCT in serum are diagnostic of MCT and ectopic production by lung and breast cancer must be considered. Presence of higher levels of iCT with greater amounts of cancer tissue and undetectable levels after surgery or radiotherapy when using antisera which require intact molecule of calcitonin for recognition suggest the possibility that sequential calcitonin levels with differentiating antisera may be helpful in assessing the extent of disease and response to therapy.
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PMID:Immuno-heterogeneity of the calcitonins of hypercalcemia, breast and lung cancers and medullary carcinoma of thyroid. 47 68

Seventy-eight advanced breast cancer patients, most of whom had had prior treatment, were treated with the synthetic antiestogen tamoxifen. The overall objective response rate was 27% (21/78). An additional 19% (15/78) showed disease stabilization. Sixty-seven percent (14/21) of the responses were in soft tissue sites, 24% (5/21) on bony sites and one each occurred in liver and nodular lung disease. Forty percent of patients with soft-tissue disease alone responded, while less than 10% of patients with visceral disease showed responses in visceral sites. The response rate was 28% among patients with a known positive estrogen receptor (ER) assay. It was 21% among patients who had previously received cytotoxic drugs. Toxicity was mild and was seen in nausea and vomiting, hot flushes and vaginal bleeding, and occasional myelosuppression. One patient was withdrawn from the study because of a rash. In two patients the disease flared, once with concomitant hypercalcemia. Tamoxifen is a useful agent for advanced breast cancer even in some patients with visceral disease.
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PMID:Phase-II trial of tamoxifen in advanced breat cancer. 53 27

Various hormones have been implicated in the genesis of hypercalcemia in patients with malignancy. Ectopic secretion of PTH by tumor has been documented in only a few patients; rather, elevated levels of circulating iPTH have been presumed to reflect tumor production of hormone in most patients. Small fragments of PTH, as well as polypeptides larger than native PTH, have been described; their biological roles are unclear. The pattern of immunoreactivity, however, has been used to differentiate patients with ectopic hyperparathyroidism from patients with concomitant primary hyperparathyroidism. Vitamin D-like sterols produced by breast cancer seldom reach plasma levels necessary for physiological effects. Members of the prostaglandin family have been proposed to induce hypercalcemia through osteoclast activation or alteration of the immune system and also to affect the frequency of bone metastases. At present, no direct evidence is available to prove a direct role for these effects and prostaglandins are most useful as possible indicators of disease activity.
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PMID:Mechanisms of hypercalcemia in malignancy. 65 92

Patients with breast cancer and bone destruction were found to have a pattern of calcium metabolism which was broadly similar to that found in other malignancies, but different from that in primary hyperparathyroidism. Thus, they tended to have reduced absorption of calcium from the intestine, elevated endogenous faecal calcium and normal or reduced urinary cyclic AMP excretion. Since prostaglandin synthetase inhibitors have been shown to inhibit breast cancer-induced osteolysis in vitro we have attempted to reduce bone destruction and serum calcium in patients with hypercalcaemia complicating breast cancer using these agents. High doses failed to reduce the serum calcium or the urinary hydroxyproline: creatinine ratio in ten patients with skeletal metastases, four of whom had hypercalcaemia.
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PMID:Calcium metabolism in breast cancer. 87 Sep 1

The pathogenesis of hypercalcemia in cancer continues to challenge the clinical investigator. Some aspects of this subject have been reviewed, notably with respect to the possible roles of prostaglandins and osteoclast activating factor, with particular reference to breast cancer. There is considerable evidence that the former humoral factor is operative and beginning evidence that the latter may be also. The hope in this continued work is that with better understanding of the mechanisms of hypercalcemia and bone loclization of tumors we will be in a far better position to control and interdict this localization.
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PMID:Studies on the pathogenesis of cancer hypercalcemia. 89 35

Prostaglandin synthetase inhibitors have, in the past, been shown to inhibit osteolysis caused by breast carcinoma tissue in vitro. We therefore assessed the effect of Indomethacin and aspirin on some parameters of calcium metabolism in patients with breast cancer. Neither drug reduced the serum calcium in pateints with hypercalcemia, nor reduced skeletal destruction as measured by the urinary hydroxy proline: creatinine ratio and urinary calcium in normocalcemic or hypercalcemic patients with osteolytic metastases. A possible reason for the discrepancy between results obtained in vitro and in vivo is that there are two phases of bone destruction in breast cancer; the early phase dependent and the late phase independent of prostaglandin synthesis.
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PMID:Failure of indomethacin to reduce hypercalcemia in patients with breast cancer. 100 35


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