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)

Humoral hypercalcemia secondary to the production of parathyroid hormone-related peptide has been reported to occur in up to 17% of patients with renal cell carcinoma but has been reported only rarely in patients with other genitourinary cancers and never in patients with testicular or extragonadal nonseminomatous cancers. A 54-year-old man is reported who had an extragonadal nonseminomatous germ cell tumour with hypercalcemia that masqueraded as a renal cell carcinoma with metastases. The hypercalcemia was suspected to be humorally mediated.
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PMID:Extragonadal nonseminomatous germ cell tumour with hypercalcemia, masquerading as renal cell carcinoma: a case report. 788 17

Parathyroid gland carcinoma is a rare cause of primary hyperparathyroidism. The authors discuss the case of a 56-year-old man who presented with hypercalcemia and multiple bone lesions suggestive of tumor metastases. Laboratory and radiological investigations revealed primary hyperparathyroidism in a patient with evidence of osteitis fibrosa cystica, sustained by carcinoma of a mediastinal parathyroid gland. Early titration of parathyroid hormone (PTH) levels in all patients with hypercalcemia of unclear cause is important for early diagnosis of cases that are tumor-sustained and prevention of the most severe complications. The role of immunostaining with anti-PTH antibodies in demonstrating parathyroid gland tissue in ectopic and/or non-functioning primary tumors, as well as metastases, is also discussed.
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PMID:[Hyperparathyroidism due to parathyroid carcinoma located in the mediastinum]. 800 90

A two-site immunoradiometric assay (IRMA) of parathyroid hormone-related protein (PTHrP) was employed to react with circulating concentrations of PTHrP in 14 patients with hepatocellular carcinoma (HCC) and hypercalcemia (> 10.6 mg/dl). Eleven of them had unresectable lesions and three received transcatheter arterial chemo-embolization (TACE) treatment. Patients had no evidence of bony metastases and only one had evidence of a parathyroid lesion (by bone scan and serum parathyroid hormone level, respectively). The urinary cAMP level was increased in all patients, but the serum 1,25-dihydroxyvitamin D and plasma cAMP levels varied. Twelve patients had elevated alpha-fetoprotein (AFP) (> 400 ng/ml) and two of them had mildly elevated AFP levels (11 and 147 ng/ml). Their PTHrP concentrations were elevated (7.1 to 33.2 pmol/l), compared with normal levels obtained in our laboratory (< 3.5 pmol/l). A significant decrease in plasma PTHrP (from 27.4 to 5.2 pmol/l), serum calcium concentrations (from 16.3 to 9.4 mg/dl) and AFP levels (from 64,787 to 3129 ng/ml) was observed on the day following TACE treatment. These results, by using an improved technique, extend the findings that hypercalcemia in patients with HCC is associated with increased renal reabsorption of calcium and increased bone resorption of PTHrP generated by HCC.
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PMID:Hypercalcemia and parathyroid hormone-related protein in hepatocellular carcinoma. 829 94

We present herein the case of a 60-year-old man found to have a rare type of cloacogenic anal carcinoma. The disease was advanced and aggressive with local invasion to the prostate as well as distant lymph node metastases to the neck and paraaortic region on presentation. Therefore, a palliative abdominoperineal resection was performed, 10 weeks following which the patient developed humoral hypercalcemia. Despite treatment with hydration, furosemide, steroids, and calcitonin, serum calcium continued to rise and the patient died on the 95th postoperative day. Laboratory findings revealed a decreased parathyroid hormone (PTH) level and marked elevation of parathyroid hormone-related protein (PTHRP). The detection of the PTHRP in the tumor extract and the positive immunohistochemical staining for this in the tumor cells suggested that the humoral hypercalcemia was definitely caused by its associated tumor production. Although hypercalcemia is not an uncommon complication of solid cancers in their late stage, only three other cases of rectal cancer with hypercalcemia have ever been reported. To our knowledge, this is the first documentation of cloacogenic anal carcinoma accompanied by PTHRP-induced severe humoral hypercalcemia.
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PMID:Cloacogenic anal carcinoma presenting with humoral hypercalcemia: report of a case. 864 24

Serum bone alkaline phosphatase (BALP), serum carboxy-terminal propeptide of type I procollagen (PICP) and serum bone gla protein (BGP) as markers of bone formation, serum carboxy-terminal telopeptide of type I collagen (ICTP) as a marker of collagen resorption and fasting molar ratio of urinary calcium to creatinine (CaCr) and serum parathyroid hormone (PTH) were determined in two groups of cancer patients: 48 with advanced or metastatic disease with negative bone scan and 174 with bone metastases categorised as having lytic, mixed or blastic lesions and with more or fewer than or equal to three sites involved. In patients without apparent bone involvement, bone formation markers were rarely elevated. Conversely, serum ICTP was frequently found to be supranormal, showing it to be a non-specific marker for early detection of bone metastases. As expected, values of bone formation markers progressively increased in patients with lytic, mixed and blastic lesions, but ICTP levels did not show any differences according to the types of bone appearances, confirming previous reports of elevated osteoclast activity also in patients with apparent blastic lesions. Serum PTH increased significantly in patients with lytic compared with patients with mixed and blastic appearances, paralleling the bone formation markers, but CaCr showed the opposite pattern. These data are compatible with calcium entrapment in the bone in patients with increased osteoblast activity. This so called 'bone hunger syndrome' is further confirmed by the finding that in the subgroup of blastic appearances CaCr diminished whereas both ICTP and PTH increased according to the extent of tumour load in the bone.
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PMID:Biochemical evaluation of bone turnover in cancer patients with bone metastases: relationship with radiograph appearances and disease extension. 866 34

The pancreatic somatostatinoma belongs to the type of rare endocrine tumors of the pancreas. We report the observation of a 54 year old woman. Previously she was suffering from diabetes mellitus. An abdominal ultrasonography revealed an endocrine tumor of the pancreatic tail. There was no specific symptomatology, with the exception for the hyperglycaemia. The diagnosis of somatostatinoma was certified post operatively by the immunocytochemistry of the tumor. Then, the patient developed a hypercalcaemia associated with an increase of parathyroid hormone. The surgery of the neck revealed three hyperplastic parathyroids, inducing this association as a multiple endocrine neoplasia type 1 (MEN 1). The patient did not develop pituitary tumor. Afterwards, scintigraphy with 111 Indium- octreotide showed a residual tumor at the head of pancreas. Basal levels of somatostatine and calcium, pentagastrine test, computed tomography scan, arteriography were negative. The presence of a second somatostatinoma was confirmed by surgery and immunohistology. One year after the surgery, the patient remains clinically well. The pancreatic localization of the somatostatinoma in a MEN 1 is poorly documented. Its malignant nature can only be assured by the presence of metastases. The genetic detection of the MEN 1 becomes possible. Above all, the treatment is based on surgery and/or chemotherapy (Fluoro-Uracile; Streptozotocine). In our case, 111 In-octreotide scintigraphy was the only method demonstrating a residual focus, suggesting it could be an element of reference for the diagnosis and survey of somatostatinoma the watch of patients having a treatment for somatostatinoma.
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PMID:[Pancreatic somatostatinoma and MEN 1. Apropos of a case. Review of the literature]. 873 92

Remodeling the cyclical replacement of old bone by new, serves to maintain its mechanical and metabolic functions. In each cycle a circumscribed volume of bone is removed by osteoclastic resorption and subsequently replaced by osteoblastic formation at the same location. Remodeling is carried out by elongated structures known as basic multicellular units (BMU) that travel through or across the surface of bone. Each BMU lasts about six months, with continued sequential recruitment of new osteoclasts and osteoblasts. Abnormal bone remodeling involves some combination of loss of directional control, increase in number of remodeling cycles and incomplete replacement. In metastatic bone disease, tumor cells find the hematopoietic bone marrow conducive to their survival and growth, because they can manipulate the local cytokine network to increase recruitment of osteoclasts from local precursors and so increase bone resorption. The effect on bone formation is biphasic; an initial increase is due partly to the normal evolution of the BMU, and partly to the induction of reparative woven bone formation. Later, normal BMU-based bone formation may fall to subnormal levels. In some tumors, a generalized increase in osteoclast recruitment and decline in bone formation are the systemic responses to one or more agents released by tumor cells into the circulation, of which the most frequent is parathyroid hormone-related peptide, but in both metastatic and non-metastatic disease, the cellular events in bone are essentially the same. Cancer-related bone disease is amenable to treatment with drugs that inhibit osteoclast recruitment, of which the bisphosphonates are the most effective. Treatment should be started before there has been irreparable damage to bone structure and before the onset of hypercalcemia. Although bisphosphonates remain in bone for a long time, adverse effects are very unlikely within the patient's lifetime.
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PMID:Bone remodeling, normal and abnormal: a biological basis for the understanding of cancer-related bone disease and its treatment. 885 18

Cancers from patients with tumor-induced hypercalcemia usually produce a circulating factor that mimics the parathyroid hormone activity, termed parathyroid hormone-related protein. Incidence of tumor-induced hypercalcemia appears to be high in patients with squamous cell carcinoma of the esophagus, and the presence of parathyroid hormone-related protein have been shown in some primary esophageal cancers. In the present study, we have investigated the presence of parathyroid hormone-related protein in a patient with metastasized squamous cell carcinoma of the esophagus complicated with tumor-induced hypercalcemia. Protein was searched by immunohistochemistry, and messenger RNA was investigated by reverse transcriptase-polymerase chain reaction and S1 nuclease assay. Both messenger RNA and protein were detected in hepatic metastases, whereas normal esophageal mucosa and primary cancer did not express detectable protein or messenger RNA using the S1 nuclease assay. Reverse transcriptase-polymerase chain reaction was positive in all these tissues, including normal esophageal mucosa. In conclusion, the present case suggests that tumor-induced hypercalcemia due to esophageal squamous cell carcinoma may be caused by parathyroid hormone-related protein mostly released by liver metastases.
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PMID:Parathyroid hormone-related protein in an esophageal squamous cell carcinoma with tumor-induced hypercalcemia. 904 Feb 21

The pathogenesis of tumor-induced osteolysis (TIO) following breast cancer metastases in bone remains unclear. We postulated that osteoblasts could be target cells for the secretory products of breast cancer cells. We previously showed that serum-free conditioned medium (CM) of the breast cancer cell line MCF-7 inhibits DNA synthesis by 75% of control values in osteoblast-like cells SaOS-2 and that this effect is only in a minor part due to transforming growth factor beta secretion. To establish the specificity of our observations and to look for other biologically active factors, we have tested the effects of medium conditioned by several cancer and noncancer cell lines (breast, colon, placenta, or fibrosarcoma) on the proliferation of osteoblast-like cells (SaOS-2, MG-63), normal human osteoblasts, human fibrosarcoma cells, and normal human fibroblasts. Culture medium (1:2) of the breast cancer cell lines MCF-7, T-47D, MDA-MB-231, and SK-BR-3 inhibited by 25-50% the proliferation of osteoblast-like cells SaOS-2, MG-63, and normal osteoblasts as evaluated by the MTT survival test or [3H]thymidine incorporation. MCF-7 cells completely inhibited the proliferation of normal human osteoblasts in coculture. This inhibitory effect was reversible and not due to cytotoxicity. Moreover, the cyclic adenosine monophosphate (cAMP) response to parathyroid hormone (PTH) of osteoblast-like cells SaOS-2 was also increased by 100-240% by the same CM. Such activities were, however, not detected in medium from the breast noncancer cell line HBL-100 or in the medium conditioned by non-breast cancer cell lines (COLO 320DM, HT-29, JAR, or HT-1080). Medium from the breast cancer cells had no effect on normal human fibroblasts or fibrosarcoma cells (HT-1080), suggesting the specificity of their action on human osteoblasts. After partial purification by ultrafiltration and size-exclusion chromatography, we found that medium of T-47D cells contained at least three nonprostanoid factors of low molecular weights (apparent MW of 700, 1500, and 4000 D) which affected human osteoblast-like cells. These factors were heat stable and could be peptides without disulfide bonds. In summary, our data show that human breast cancer cells release soluble factors that inhibit osteoblast proliferation and increase their cAMP response to PTH, indicating that osteoblasts could be important target cells for breast cancer cells and could be involved in the process of TIO.
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PMID:Secretory products of breast cancer cells specifically affect human osteoblastic cells: partial characterization of active factors. 910 66

Hypercalcaemia, a common complication of malignancy, may result from either the lytic effect of multiple osseous metastases or the effect of tumour-derived humoral factors. Excessive secretion of parathyroid hormone-related peptide (PTHrP), a major cause of humoral hypercalcaemia of malignancy, has been incriminated as the cause of hypercalcaemia in patients with lung, breast, renal, head and neck and, occasionally, haematological malignancies. Carcinoid tumours, while frequently the source of ectopic hormone secretion, are infrequently associated with hypercalcaemia. We report the case of a 59-year-old woman with fulminant hypercalcaemia due to excessive PTHrP secretion from a hepatic carcinoid and we present the change in her serum PTHrP concentrations during infusion of a somatostatin analogue.
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PMID:Intractable hypercalcaemia due to parathyroid hormone-related peptide secretion by a carcinoid tumour. 915 50


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