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)

Receptors for 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] have been described in several human breast cancer cell lines and more recently in human melanoma. The presence of 1,25-(OH)2D3 receptor (1,25-DR) in two cultured breast cancer cell lines was associated with receptors for calcitonin, another hormone thought to have effects on calcium handling. Therefore, it seemed important to examine a range of established human cancer cell lines for the presence of receptors for 1,25-(OH)2D3 and calcitonin. Thirty-three cancer cell lines were examined. 1,25-DR was found to be present in 23 lines, while calcitonin receptors were not detected in any of them. The 1,25-DR from several cell lines sedimented at about 3.5S in sucrose density gradients, had the appropriate specificity for vitamin D metabolites, had Kds of 0.8 to 2.2 x 10(-11) M, and had receptor concentrations of 12 to 99 fmol/mg protein. Ten malignant melanoma and nine colonic carcinoma lines constituted the largest groups of carcinoma cell lines, and seven and eight, respectively, of these were 1,25-DR positive. The high frequency of 1,25-DR positivity in the cultured colonic carcinoma cells is quite different from the low frequency of 1,25-DR in primary colonic carcinomas. It was also interesting that both of two cell lines derived from patients who had had both bone metastases and malignant hypercalcemia were 1,25-DR positive. These various cell lines may provide useful models for the examination of 1,25-(OH)2D3 action in vitro.
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PMID:Presence of 1,25-dihydroxyvitamin D3 receptors in established human cancer cell lines in culture. 627 75

A case of humoral non-parathyroid hypercalcemia in a breast cancer patient is discussed. Bone metastases developed 23 months after the first clinical evidence of increased serum calcium levels and did not appear to be etiologically involved in this case of hypercalcemia. Serum levels of I-PTH and PGE2 were normal, as were urinary c-AMP levels. Furthermore, no significant response to corticosteroid therapy was observed. However, the correlation between the activity of metastatic disease and calcemia suggests that this cancer produced humoral factor(s) with calcium-mobilizing activity.
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PMID:Humoral nonparathyroid hypercalcemia without evidence of bone involvement. 630 87

In a total of 277 patients with advanced breast cancer treated between July 1977 and November 1983 at Cancer Institute Hospital, there were 26 cases (9.4%) showing hypercalcemia (Ca greater than or equal to 11.0 mg/dl). All these patients had bone metastasis examined by either X-ray films or bone scintigram during clinical course of the disease and confirmed at the time of autopsy, thus an overall incidence of hypercalcemia in 149 patients with bone metastasis was 17.4%. Major clinical signs due to hypercalcemia were gastrointestinal symptoms such as anorexia, nausea and vomiting, renal dysfunction and neurological symptoms but there was no definitive correlation in between clinical signs and values of serum calcium. Among various treatments performed, a combination of hydration, steroids and calcitonin was the most effective. Mean survival time from the diagnosis of hypercalcemia was 288 + days for responders, and 28.8 days for non-responders (p less than 0.001). Seven patients expired due to hypercalcemia and were died suddenly, while others died of renal failures.
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PMID:[Hypercalcemia in breast cancer]. 674 68

In 51 women with metastatic breast cancer calcium excretion per litre of glomerular filtrate (CaE) values were persistently higher in those with bone secondaries than in those with only soft tissue involvement despite a normal range of serum calcium in both groups. Measurement of CaE in 8 further patients who were severely hypercalcaemic as a result of their advanced breast cancer revealed the degree to which calcium resorption from bone secondaries and renal dysfunction contributed to the hypercalcaemia. Thus, in patients with breast cancer, CaE provides a reliable indicator of early changes of calcium homeostasis. It may provide an objective indication of progression of bone secondaries and also has important therapeutic implications in established hypercalcaemia.
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PMID:Calcium excretion (CaE) in metastatic breast cancer. 683 Nov 70

We used a sensitive and specific hybridization assay that detects evidence of parathyroid hormone synthesis in tumors to investigate whether this hormone mediates the hypercalcemia of malignant disease. The assay uses radiolabeled, cloned parathyroid hormone DNA to hybridize selectively with parathyroid hormone messenger RNA. We assayed 13 human and 3 animal tumors of diverse cell origins that are frequently associated with the hypercalcemia of cancer. Five of the human tumors were obtained from patients known to be hypercalcemic at the time of tumor excision, two were from normocalcemic patients, and six were from patients with breast cancer whose serum calcium levels were unknown. Messenger RNA was prepared from cultured cell lines or tumors; active RNA fractions were hybridized with either human or bovine cloned parathyroid hormone DNA that had been labeled to a high specific activity with [32P]nucleotide. We were unable to detect parathyroid hormone RNA transcripts in any of the tumors. Our results indicate that parathyroid hormone rarely, if ever, causes hypercalcemia in malignant disease.
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PMID:Absence of parathyroid hormone messenger RNA in nonparathyroid tumors associated with hypercalcemia. 686 67

Although hypercalcemia is a well-known complication of malignant diseases, hypocalcemia seems to be a rather rare one. A 34-yr-old woman with advanced breast cancer who presented hypocalcemia is described. She had generalized multiple osteolytic bone metastases which were progressive in spite of chemo-endocrine and radiation therapy. She was admitted because of severe bone pain and dyspnea caused by bilateral pleural effusion. Laboratory examination on admission showed that the serum calcium was 9.6 mg/dl, serum total protein 5.9 g/dl, serum inorganic phosphorus 4.6 mg/dl, and serum alkaline phosphatase 29.6 King-Armstrong units. The serum calcium gradually fell to 7.0 mg/dl on the 45th hospital day when the serum total protein was 6.8 g/dl and she complained of paresthesia in the extremities. On the 58th day, severe tachycardia and hypotension developed and she died of congestive heart failure on the 67th hospital day. At that time the serum calcium was 5.4 mg/dl. During her hospital course, the plasma parathyroid hormone levels were examined repeatedly and were 0.4, 0.6, 0.6 and 0.7 ng/ml (normal; less than 0.5 ng/ml). Autopsy revealed that cancer invaded the space between the thyroid and the trachea and no parathyroid glands could be found even in the mediastinum. Microscopically the parathyroid glands were replaced completely by the cancer cells. These observations indicate that metastasis of breast cancer to the parathyroid glands caused relative hypoparathyroidism, resulting in hypocalcemia. In addition, congestive heart failure which was refractory to digitalis and diuretics might have been caused by impaired contractility of the myocardium associated with hypocalcemia.
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PMID:A case of advanced breast cancer associated with hypocalcemia. 688 61

Hypercalcemia is a life threatening complication of generalized breast cancer. It developed in 28 out of 205 patients (13.5%) treated in the Department of Medicine of the Cancer Institute of Piraeus during the years 1974-1978. 32 hypercalcemic episodes appeared in these 28 patients and of these episodes, 15 were hormone induced and 16 spontaneous. The interval between hormone institution and appearance of hypercalcemia never exceeded one month. Hypercalcemia was moderate to severe in 81% of the spontaneous hypercalcemic episodes and only in 40% of those hormone induced. The clinical manifestations varied from no symptoms to a severe clinical picture. The most frequent biochemical abnormality was hyperuricemia; azotemia and hypokalemia were also frequent. Administration of phosphates is the most effective therapeutic agent in this complication. When the diagnosis was made promptly and correct treatment initiated without delay, no patient in our material died of hypercalcemia.
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PMID:Hypercalcemia in breast cancer. 694 66

Studies have suggested that both natural and synthetic retinoids have extensive chemopreventive activity against a variety of carcinogens in vivo and in vitro. We have previously shown that growth of human breast cancer cells can be inhibited by retinoids, and retinoic acid-binding proteins have been demonstrated in these cell lines and tumor biopsies. We studied the activity of 13-cis-retinoic acid in the treatment of 18 patients with advanced breast cancer refractory to standard cytotoxic and/or endocrine therapy. Patients began on 0.5 mg/kg and escalated to 8 mg/kg over a one-month period unless toxicity (dry skin, dry mucosa, cheilitis, conjunctivitis) forced dose reduction. All these toxicities responded promptly to dose reduction. Four patients exhibited drug related hypercalcemia, 2 complained of severe earache and several had nausea, vomiting and abdominal cramping. There were no objective responses as defined by standard criteria. One patient with thrombocytopenia secondary to documented marrow involvement demonstrated a recovery of platelet count from 9000 to 110,000. 13-cis-Retinoic acid is not of apparent value in women with heavily pretreated breast cancer.
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PMID:Phase II trial of 13-cis-retinoic acid in metastatic breast cancer. 696 67

Breast cancer is the malignant neoplasm most commonly associated with hypercalcemia. At the University of Texas M. D. Anderson Hospital, Houston, during the fiscal year 1977 to 1978, of 16,887 patients having calcium determinations, 7.8% had hypercalcemia. From 1969 to 1979, 13 patients had proved and three had presumed primary hyperparathyroidism associated with breast cancer. Two other patients had pseudohyperparathyroidism. Selective neck vein catheterization was used in 17 of the 18 patients and helped localize and confirm the diagnosis of primary hyperparathyroidism. Chloride-phosphate ratios were elevated in 13 of the 14 patients with proved or presumed primary hyperparathyroidism. This condition may mimic osseous metastases by producing brown tumors or compression fractures. In patients with breast cancer and hypercalcemia, particularly without osseous metastases, a careful diagnostic evaluation is warranted to rule out primary hyperparathyroidism.
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PMID:Hypercalcemia in patients with breast cancer. Osseous metastases, hyperplastic parathyroid tissue, or pseudohyperparathyroidism? 723 46

In a randomized study, 63 postmenopausal patients with advanced breast cancer were treated with ethinyl estradiol (EE2) or the antiestrogen tamoxifen to compare the efficacy and side effects of both drugs. EE2 was always given in combination with chlorothiazide to prevent fluid retention. Pretreatment characteristics of the patients of both groups did not differ significantly. Objective remissions were achieved in 31% of the EE2-treated patients and in 33% of the tamoxifen-treated patients. The median duration of remission was 12 months (range, 5-32) for the EE2 group and 11 months (range, 5-26) for the tamoxifen group (P greater than 0.1), and the estimated median survival times from the start of treatment were 31 and 25 months, respectively (P greater than 0.1). The best treatment results in both groups were obtained in patients with estradiol receptor-positive tumors and less advanced disease. After therapy was stopped, objective withdrawal responses were observed in EE2- but not in tamoxifen-treated patients. Two patients receiving EE2 had to discontinue treatment because of drug-related liver function impairment. Both patients had cholelithiasis. Two patients in the tamoxifen-treated group discontinued therapy because of nausea. Deep venous thrombosis occurred in one patient receiving EE2, whereas two patients receiving tamoxifen developed superficial thrombophlebitis. Other side effects in both groups of patients, including initial hypercalcemia, were mild. It is concluded that both treatment regimens, EE2 or tamoxifen, are equally effective with respect to induction and duration of remission in postmenopausal patients with advanced breast cancer. Side effects of EE2 therapy appeared to be more serious than those of tamoxifen treatment.
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PMID:Tamoxifen versus ethinyl estradiol in the treatment of postmenopausal women with advanced breast cancer. 723 48


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