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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Childhood hypophosphatemic rickets (HR) is most often caused by a defect in renal tubular resorption of filtered phosphorus. However, HR can also be caused by secretion of a phosphaturetic factor from a tumor. The presentation of patients with the different HR syndromes may be identical. Distinguishing between the HR syndromes is essential, however, because HR caused by renal defect requires life-long therapy with Vitamin D and phosphate replacement, but tumor-associated HR is cured by removal of the tumor. A case of hemangiopericytoma occurring in bone and causing HR is reported. Children with HR typically have normal levels of serum calcium and parathyroid hormone but very low levels of serum phosphorus. In a child with HR, the following features should prompt a thorough evaluation for a causative tumor: lack of other family members who have hypophosphatemia; presence of aminoaciduria, particularly glycinuria. Causative lesions are most commonly found in the bone or skin.
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PMID:Surgically curable hypophosphatemic rickets. Diagnosis and management. 273 55

A case of oncogenous osteomalacia due to a fibrosarcoma of the maxilla is reported, with a 19 year course before treatment. Metabolic studies of calcium and phosphorus were performed 3 and 19 years after the first symptomology. There was a negative balance for both phosphorus and calcium with low serum levels of 1,25-dihydroxyvitamin D which were corrected by resection of the tumor. Portions of the tumor were cultured and the supernatant did not affect phosphorus transport by a proximal tubule kidney cell line. Other portions were injected into athymic nude mice where they resulted in hypophosphatemia and phosphaturia, thus confirming the endocrine nature of the oncogenous osteomalacia factor.
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PMID:Oncogenous osteomalacia: a case study. 276 8

Magnetic resonance (MR) imaging was performed on 14 patients with histologically proved osteosarcoma (mean age, 14.4 years). There was excellent correlation of intramedullary tumor extent as determined with MR imaging and pathologic examination (r = 99%). This was facilitated by the presence of a chemical shift artifact at the tumor-marrow interface on the T1-weighted images. The correlation between CT and pathologic findings was not as good (r = 84%). In a single patient, however, a 10-cm length of sclerotic bone was incorrectly interpreted as being tumor. If this case is excluded, the correlation between CT and pathologic findings improves significantly (r = 96%). T2-weighted images were optimal in demonstrating soft-tissue bulk and breach of the epiphysis or cortex. Vascular involvement was also readily defined. The T2 value of the tumor soft-tissue component decreased in patients who were deemed to have responded well to therapy. Two patients with very high T2 values after chemotherapy developed wide-spread metastatic disease and died. Phosphorus-31 MR spectroscopy of five patients with osteosarcoma showed elevated levels of phosphomonoesters (PMEs), inorganic phosphate (Pi), and phosphodiesters (PDEs). PME and PDE peak areas decreased in three patients after chemotherapy, while Pi peak areas increased.
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PMID:Osteosarcoma: use of MR imaging and MR spectroscopy in clinical decision making. 277 93

The authors report a case of primary urethral carcinoma which seems to be linked to human papillomavirus (HPV) infection. Southern blot hybridization of phosphorus 32 (32P)-labeled DNA extracted from the cancer tissue gave a positive reaction with HPV-6. Specimens of the tumor material subjected to in situ hybridization with 3H-labeled HPV-6 DNA showed numerous tumor cell clusters with clearly labeled nuclei. Using immunoperoxidase staining the authors found papillomavirus structural antigen within cell nuclei of the tumor tissue.
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PMID:Detection of human papillomavirus-6 in primary carcinoma of the urethra in men. 282 May 63

Studies on the pathogenesis of hypercalcemia in canine lymphosarcoma have led to conflicting results. The biochemical and bone histomorphometric findings in canine lymphosarcoma were examined in 19 hypercalcemic and 17 nonhypercalcemic dogs with lymphosarcoma. Compared to the nonhypercalcemic group, the hypercalcemic dogs demonstrated an increase in fasting and 24-h calcium excretion, an increase in fractional phosphorus excretion, and a significant increase in nephrogenous AMP excretion. Plasma 1,25-dihydroxyvitamin D and immunoreactive PTH levels were equivalent in the two groups. Quantitative bone histomorphometry performed on iliac crest biopsies revealed increased parameters of bone resorption in those hypercalcemic dogs with no evidence of tumor at the biopsy site, without a compensatory increase in bone formation. Acid-urea tumor tissue extracts from eight hypercalcemic and six nonhypercalcemic dogs were examined for adenylate cyclase-stimulating activity (ACSA). All tumors from hypercalcemic dogs contained ACSA, whereas none of the tumors from nonhypercalcemic dogs had ACSA. Further purification of one tumor extract yielded an adenylate cyclase-stimulating protein which appeared to interact specifically with the PTH receptor. We conclude that in some cases, hypercalcemia in canine lymphosarcoma is mediated by a tumor-derived circulating bone-resorbing factor which is distinct from PTH. ACSA detected in tumor tissue appears to be a reliable marker for the syndrome in vivo. The role of this activity in the pathogenesis of the syndrome remains to be determined.
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PMID:Humoral hypercalcemia of malignancy in canine lymphosarcoma. 282 6

Although more than 50 patients with the tumor-induced osteomalacia syndrome, characterized by remission of unexplained osteomalacia after resection of a coexisting tumor, have been reported, the pathogenesis of this syndrome is still not clear. We investigated the cause of biopsy-confirmed osteomalacia which was resistant to treatment with 1 alpha-hydroxyvitamin D3 in a 54-yr-old man. He had severe hypophosphatemia, a high serum alkaline phosphatase level, a low plasma 1,25-dihydroxyvitamin D level, and remarkably increased urinary phosphorus excretion. A tumor, with histological characteristics of a hemangiopericytoma, was found on his left thigh. After surgical removal of this tumor, his plasma 1,25-dihydroxyvitamin D and serum phosphorus levels increased to normal levels, and his bone pain subsided. The tumor was transplanted to athymic nude mice. A nodule formed in each mouse, with histological features identical to those of the original tumor, and the tumor-bearing mice had hypophosphatemia, high serum alkaline phosphatase levels, and increased urinary phosphorus excretion. When extracts of the original tumor were added to primary cultures of renal tubular cells, renal cAMP levels did not change, but 25-hydroxyvitamin D-1 alpha-hydroxylase activity was significantly inhibited. These data indicate tumoral production of some humoral factor(s) inhibiting 25-hydroxyvitamin D-1 alpha-hydroxylase activity and phosphorus reabsorption unrelated to adenylate cyclase-cAMP production in proximal renal tubules.
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PMID:Hemangiopericytoma-induced osteomalacia: tumor transplantation in nude mice causes hypophosphatemia and tumor extracts inhibit renal 25-hydroxyvitamin D 1-hydroxylase activity. 283

To assess the potential of in vivo magnetic resonance (MR) spectroscopy for breast cancer, hydrogen-1 and phosphorus-31 MR spectra of five malignant human breast tumors were compared with those of unaffected breast tissue. The water-to-fat ratio was high in the tumors (average, 2.2) but low in the unaffected tissue (average, 0.3). The P-31 spectrum of normal breast tissue showed low levels of phosphomonoesters (PMEs), inorganic phosphate, phosphodiesters (PDEs), and ATP. In addition, an intense phosphocreatine (PCr) signal was observed in breast tissue of young women: The relative intensities of the PCr and ATP signals had a mean value of 1.9. The tumor spectrum showed elevated levels of PMEs, Pi, and PDEs, while no PCr was seen (PCr/ATP less than 0.2). In two breast cancers treated with radiation therapy, resulting in a decrease of tumor volume of more than 50%, a similar change in the tumor P-31 spectrum was observed: An intense PCr signal developed (PCr/ATP = 1.1). Control experiments indicated that the appearance of PCr after radiation therapy was the result of a radiation-induced metabolic change in the tumor itself.
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PMID:Human breast cancer in vivo: H-1 and P-31 MR spectroscopy at 1.5 T. 284 30

Medullary carcinoma of the thyroid (MCT) develops from the thyroid C-cells. Thyroid C-cells and MCTs secrete calcitonin (CT), a 32 amino acid polypeptide hormone. The author has described a sensitive direct sequential radioimmunoassay of CT in human serum. The vast majority of healthy subjects had detectable values of serum immunoreactive calcitonin (iCT) and elevated levels were found in patients with MCT. Besides CT, several higher molecular weight substances contribute to CT-immunoreactivity. These substances may represent metabolic products in the processing of a glycosylated procalcitonin to CT. Calcium, several gastrointestinal hormones and ethanol increases CT secretion from normal and neoplastic C-cells, but the physiological regulation of CT secretion has not been firmly established. The author has shown that the levels of serum iCT vary little during day and nighttime. CT acutely reduces bone resorption and, in pharmacological doses, increases urinary electrolyte excretions. A lowering in serum calcium, magnesium and phosphorus levels result but the effect is pronounced only in disease states with a high bone turnover. The physiological role for CT may be preservation of the skeleton at times of increased need for calcium. A causal relationship between postmenopausal osteoporosis and CT deficiency has been proposed. The author has described increased serum 1,25-dihydroxyvitamin D levels and increased trabecular bone remodeling in patients with MCT and normalization of these parameters following surgical cure for MCT. These results were interpreted to indicate that chronic endogenous CT excess directly enhances the renal production of 1,25-dihydroxyvitamin D which, acting synergistically with parathyroid hormone, increases trabecular bone remodeling. Elevated serum iCT is almost invariably found in patients with clinically manifest MCT as well as in several patients with clinically occult MCT. An exaggerated increase in serum iCT levels after provocative testing with pentagastrin and/or calcium can disclose early C-cell neoplasia. Elevated serum iCT may be encountered in non-C-cell neoplasias and in renal insufficiency. Compared to MCT, circulating iCT may show a different immunochemical profile and the response to provocative testing is blunted in these conditions. MCT occurs in a sporadic variety, and in a familial variety as part of two related multiple endocrine neoplasia (MEN) syndromes. MEN IIa consists of MCT and often phaeochromocytomas and/or hyperparathyroidism and invariably exhibits an autosomal dominant mode of inheritance but a variable age of expression.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Medullary thyroid carcinoma and calcitonin. 285 45

Phosphorus-31 magnetic resonance spectra were obtained from the RIF-1 tumor in C3H mice before and up to 2 days after various doses of X rays. Parallel studies were performed to measure relative changes in tumor blood perfusion using [14C]iodo-antipyrine and changes in % tumor necrosis using Chalkley's method. Tumor ratios of phosphocreatine to inorganic phosphate (PCr/Pi) and nucleotide triphosphates to inorganic phosphate (NTP/Pi) as well as pH as measured by 31P-MRS increased significantly at most time points after irradiation with doses of 5, 10, and 20 Gy. Tumor blood perfusion was found to significantly improve after a dose of 20 Gy but not after a dose of 2 Gy. Percent tumor necrosis increased to about 3 times its control level at 1 day after a dose of 20 Gy and then declined to about twice its control value at 2 days. The magnitude of the changes in the 31P-MRS parameters makes it unlikely that any of them are entirely due to radiation-induced changes in the radiobiologically hypoxic fraction of these tumors. Changes in the necrotic fraction did not appear to influence the tumor spectra. However, the observed improvement in tumor blood perfusion may have resulted in an increase in oxidative phosphorylation of the whole tumor population as well as a clearance of inorganic phosphate and acid metabolites, so that 31P-MRS changes may indirectly reflect changes in tumor blood perfusion.
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PMID:Phosphorus-31 magnetic resonance spectroscopy and blood perfusion of the RIF-1 tumor following X-irradiation. 291 37

Thirty-five human neoplasms from various sites and of various histologic types and stages were examined with phosphorus-31 magnetic resonance spectroscopy in situ. The tumors included 13 squamous cell carcinomas of the head and neck (lymph nodes), eight Hodgkin lymphomas, six non-Hodgkin lymphomas, four carcinomas of the breast, one melanoma, one sarcoma, one neuroblastoma, and one mucoepidermoid sarcoma of the salivary glands. Thirty-four of the neoplasms had normal to slightly alkaline pH before irradiation. During fractionated radiation therapy, the pH stayed in a range of from near neutral to alkaline and rose to 7.6-8.0 at several time points of radiation therapy for some tumors. These results suggest that most tumor cells in human neoplasms are well oxygenated and that only a negligible fraction are chronic hypoxic cells. The fluctuating alkaline pH during radiation therapy occurred regardless of the responsiveness of the treated tumors.
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PMID:Human neoplasm pH and response to radiation therapy: P-31 MR spectroscopy studies in situ. 261 Jul 57


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