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)

Most ocular tumors metastasize from systemic origins in breast carcinoma in females, and bronchial carcinoma in males. Here, we report a case of choroidal carcinoma metastasis from the breast with visual problems being the only initial manifestations. In this case, both eyes were involved at almost the same time, with initial manifestation of blurred vision which progressed to complete visual loss. At first, the patient was diagnosed with malignant melanoma, and enucleation of the right eye was performed in another hospital. However, the tumor had already metastasized rapidly to numerous organs, including the lungs, brain and bone, although it had not affected the liver. Clinical presentations were, therefore, not compatible with those of malignant melanoma, which has usually been reported to metastasize to the liver. Persistent hypercalcemia and raised carcinoembryonic antigen (CEA) concentrations prompted investigations into the possibility of systemic malignancy. A very small breast nodule was finally located by thorough physical examination, and a lumpectomy was performed. A detailed review of the histopathology showed the tumors from the breast and the right eye to have the same origin. Simultaneous bilateral choroidal metastases from other malignancies is not uncommon; however, it is quite rare for breast carcinoma to present with visual problems as a first manifestation. Detailed history taking and physical examination are therefore essential when searching for a primary tumor, so that appropriate therapy can be given earlier.
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PMID:Bilateral choroidal metastases as the initial presentation of a small breast carcinoma: a case report. 953 72

Ameloblastoma is a rare, locally destructive, benign neoplasm of the jawbones, which arises from epithelium derived from the epithelial components of the developing tooth. Ameloblastic carcinoma is the term used to designate any ameloblastoma in which there is histologic evidence of malignancy in the primary tumor, regardless of whether it has metastasized. Most ameloblastic carcinomas are presumed to have arisen de novo, with few cases of malignant transformation of ameloblastoma being apparent. Hypercalcemia is the most common metabolic complication of malignancy. Although malignancy-associated hypercalcemia is often reported in association with other malignancies, it is exceedingly unusual in association with ameloblastoma, malignant ameloblastoma, or ameloblastic carcinoma. We describe a patient with multiple recurrences of ameloblastoma, with subsequent malignant transformation presenting with malignancy-associated hypercalcemia.
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PMID:Ameloblastic carcinoma ex ameloblastoma of the mandible with malignancy-associated hypercalcemia. 1111 17

A transplantable tumor line (IP) was established in syngeneic rats from a spontaneous pulmonary carcinoma found in a male F344 rat aged 25 months. A tissue fragment of IP grew into a nodule, 2-3 cm in diameter, 2-3 weeks after implant, and IP has been serially passed through 26 generations. Lined by cuboidal or columnar epithelial cells, the primary tumor consisted of completely alveolar architecture. However, IP tumors developed various growth patterns such as glandular, acinar, trabecular, cord, and solid, and consisting of epithelial cells showing cellular atypia. Ultrastructurally, neoplastic cells had microvilli, basement membranes, and desmosomes, and occasional cells possessed dense cytoplasmic granules. Interestingly, it was shown by the immunohistochemistry, the RT-PCR method, and immunoradiometric assay that IP tumor cells produce parathyroid hormone-related protein (PTHrP). During a 3-week observation period after implant, IP-bearing rats showed severe emaciation, hypercalcemia, and hypophosphatemia, as well as an increase in osteoclastic areas and a decrease in shaft thickness of the femurs. These were considered to be due to a marked elevation of plasma PTHrP levels. Furthermore, IP-bearing rats developed calcification in various organs including the kidneys, lungs, and heart. These findings in IP-bearing rats were similar to those of humoral hypercalcemia of malignancy (HHM) reported in human cancer patients. PTHrP plays a central role in the development of HHM, but the mechanisms of HHM remain poorly understood. IP may become a useful model for studying the pathogenesis of HHM and the pathophysiological role of PTHrP.
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PMID:Establishment of a transplantable tumor line (IP) derived from rat pulmonary carcinoma, developing humoral hypercalcemia of malignancy in IP-bearing rats. 1196 51

A 73-year-old man was admitted to the hospital complaining of gross hematuria and left flank pain. Abdominal ultrasonography and computed tomography revealed a left renal tumor with extracapsular extension. Laboratory data showed marked leukocytosis of 121,000/mm3 and hypercalcemia of 12.3 mg/dl without any findings of inflammatory disease or bone metastasis. Enzyme immunoassay of the serum demonstrated a high level of granulocyte colony-stimulating factor (250 pg/ml) and parathyroid hormone-related protein (1,069 pmol/l). Pathological diagnosis of needle biopsy specimen of the primary tumor was transitional cell carcinoma which was suspected to have originated from renal pelvis. Immunohistochemical examination with anti-granulocyte colony-stimulating factor monoclonal antibody demonstrated granulocyte colony-stimulating factor production in cancer cells. The patient underwent a course of systemic chemotherapy, but died two months after diagnosis. To our knowledge, this is the first report of renal pelvic cancer representing granulocyte colony-stimulating factor production and hypercalcemia simultaneously.
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PMID:[Renal pelvic cancer representing G-CSF production and hypercalcemia simultaneously: a case report]. 1199 9

Transgenic mouse models of prostate cancer provide unique opportunities to understand the molecular events in prostate carcinogenesis and for the preclinical testing of new therapies. We studied the G gamma T-15 transgenic mouse line, which contains the human fetal globin promoter linked to SV40 T antigen (Tag) and which develops androgen-independent prostate cancer. Using the immunohistochemistry of normal mouse prostates before tumor formation, we showed that the target cells of carcinogenesis in G gamma T-15 mice are located in the basal epithelial layer. We tested the efficacy of the 1,25(OH)(2)D(3) analogue, EB 1089, to chemoprevent prostate cancer in these transgenic mice. Compared with treatment with placebo, treatment with EB 1089 at three different time points before the onset of prostate tumors in mice did not prevent or delay tumor onset. However, EB 1089 significantly inhibited prostate tumor growth. At the highest dose, EB 1089 inhibited prostate tumor growth by 60% (P = 0.0003) and the growth in the number of metastases, although this dose also caused significant hypercalcemia and weight loss. We conducted several in vitro experiments to explore why EB 1089 did not prevent the occurrence of the primary tumors. EB 1089 significantly inhibited the growth of a Tag-expressing human prostate epithelial cell line, BPH-1, and an androgen-insensitive subline of LNCaP cells [which was not inhibited by 1,25(OH)(2)D(3)]. Thus, neither Tag expression nor androgen insensitivity explain the absence of chemopreventive effect. Conversely, neither 1,25(OH)(2)D(3) nor EB 1089 inhibited the growth of the normal rat prostate basal epithelial cell line NRP-152. It is likely that EB 1089 was not effective in delaying the growth of the primary tumor in G gamma T-15 transgenic mice because the target cells of carcinogenesis in these mice are located in the basal epithelial layer. We conclude that G gamma T-15 transgenic mice are a useful model for testing vitamin D-based therapies in androgen-insensitive prostate cancer but are not suitable for studies of vitamin D-based chemoprevention. The superiority of EB 1089 over 1,25(OH)(2)D(3) in the growth suppression of androgen-insensitive prostate cancer cells supports the use of EB 1089 in androgen-insensitive prostate cancer.
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PMID:The G gamma / T-15 transgenic mouse model of androgen-independent prostate cancer: target cells of carcinogenesis and the effect of the vitamin D analogue EB 1089. 1205 97

Prostate cancer is a common malignancy affecting men, which is often associated with skeletal metastases resulting in significant morbidity and mortality. In this hormone-dependent cancer, low levels of a prostate secretory protein of 94 amino acids (PSP-94) are associated with advanced disease stage. In the current study, we have examined the effect of PSP-94 on prostate cancer growth and experimental metastases to the skeleton. For these studies, MatLyLu rat prostate cancer cells were transfected with full-length cDNA encoding parathyroid hormone-related protein [PTHrP (MatLyLu-PTHrP cells)], which is known to be the major pathogenetic factor for malignancy-associated hypercalcemia. MatLyLu-PTHrP cells were inoculated s.c. into the right flank or via intracardiac route into the left ventricle of syngeneic male Copenhagen rats. Intracardiac inoculation of MatLyLu cells routinely results in the development of tumors in the lumbar vertebrae, resulting in hind-limb paralysis. Animals were infused with different doses of PSP-94 (0.1, 1.0, and 10.0 micro g/kg/day) starting on the day of tumor cell inoculation. Time of hind-limb paralysis and tumor volume were determined, and comparison was made between PSP-94-treated animals and control animals receiving vehicle alone. At the end of the study, animals were sacrificed, and plasma calcium, plasma PTHrP, and tumor PTHrP levels were determined. Whereas the highest dose of PSP-94 caused a modest but statistically significant delay in the development of hind-limb paralysis, a marked dose-dependent decrease in primary tumor volume was seen in experimental animals receiving PSP-94 due to its ability to promote tumor cell apoptosis. Furthermore, whereas control animals routinely developed hypercalcemia due to PTHrP production, treatment with PSP-94 led to a near normalization of plasma calcium and a marked reduction in PTHrP production as determined by radioimmunoassay and immunohistochemistry. Collectively, these results demonstrate the ability of PSP-94 to be an effective treatment modality for prostate cancer, where decrease in plasma PTHrP and calcium levels can serve as useful biochemical markers for monitoring the efficacy of this novel antitumor agent.
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PMID:Prostate secretory protein PSP-94 decreases tumor growth and hypercalcemia of malignancy in a syngenic in vivo model of prostate cancer. 1272 22

Many advanced cancers, particularly breast cancer and prostate cancer, metastasize to the bone, resulting in painful lesions and skeletal complications. Intravenous bisphosphonate therapy is an important component of palliative care for patients with bone metastases, and pamidronate has been the standard of care for patients with breast cancer and multiple myeloma since 1996. However, zoledronic acid is the first bisphosphonate shown to significantly reduce skeletal morbidity in patients with a wide range of primary tumor types. Zoledronic acid has demonstrated efficacy in the management of hypercalcemia and metastatic bone disease. In phase III studies involving more than 3000 patients with multiple myeloma, breast cancer, prostate cancer, lung cancer, and other cancers, 4 mg zoledronic acid demonstrated consistent efficacy across a range of clinical end-points, and was safe and well tolerated when infused over 15 min. Based on these studies, zoledronic acid appears to be active in patients with bone metastases irrespective of tumor type, and should be considered as the standard of care for the treatment of bone metastases.
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PMID:Proven efficacy of zoledronic acid in the treatment of bone metastases in patients with breast cancer and other malignancies. 1465 40

Paraneoplastic syndromes are manifestations of malignancies that have produced effects that are distant from the primary tumor or metastases. Paraneoplastic syndromes are not caused by local effects of compression or infiltration into tissues, but are generally due to ectopic hormone production, autoimmune phenomena, or overproduction of cytokines. Paraneoplasia may be the presenting symptom of underlying malignancy and can affect almost any organ system, such as the neurologic syndromes associated with small-cell lung cancer or hypercalcemia associated with squamous cell carcinomas. Lymphoproliferative disorders are also associated with many paraneoplastic disorders; however, to date, most published information has been in the form of case reports and series of small numbers of patients. In this review, the most common paraneoplastic syndromes associated with non-Hodgkin's lymphoma and Hodgkin's disease will be discussed.
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PMID:Paraneoplastic manifestations of lymphoma. 1524 5

Parathyroid carcinoma constitutes less than 1% of primary hyperparathyroidism. The exact etiology is not known. Prior radiation to neck, chronic renal failure and genetic factors are thought to play a role. The male to female ratio is one. Parathyroid carcinomas are slow growing, have a tendency to recur locally and metastasize late. 95% of parathyroid carcinomas are functioning. The major distinguishing features of malignant hyperparathyroidism are presence of a palpable mass in the neck and features of severe hypercalcemia. By far the most important test to diagnose primary hyperparathyroidism is serum level of Immunoreactive PTH. The diagnosis of primary hyperparathyroidism is essentially clinical and biochemical. Biopsy is not necessary before definitive surgery. CT scan appears to be the best investigation for detecting the primary tumor, its local extent and metastases. Most of the symptoms are attributable to hypercalcemia, which needs to be treated aggressively. Early surgery with 'en bloc' resection of the tumor is the only potentially curative treatment. Parathyroid carcinoma is traditionally said to be resistant to radiotherapy. Various chemotherapeutic agents have been used with partial anecdotal responses. The 5-year survival is about 50% and 10-year survival varies from 13-49%.
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PMID:The carcinoma of parathyroid gland. 1531 9

Breast cancer is the malignant neoplasm most commonly associated with hypercalcemia. In breast cancer the majority of the hypercalcemia cases result from osteolytic metastatic bone disease of the primary tumor. In a few patients hypercalcemia results from other conditions like primary hyperparathyroidism. Here, we present two female patients who were treated for breast cancer. Hypercalcemia in these two patients was diagnosed as being due to primary hyperparathyroidism. One of them was submitted to surgery and the calcium level dropped to the normal level thereafter. The other one refused surgery and was treated with biphosphonate and calcitonin. We suggest that when hypercalcemia occurs in breast cancer, primary hyperparathyroidism should be considered as possible cause.
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PMID:Breast cancer and concomitant primary hyperparathyroidism: description of two patients. 1551 83


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