Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report a case of ossified prolactinoma that was identified as a calcified nodule on the roentgenograms. Histologically, the ossified tissues were diffuse, and the osteoid was mineralized in various degrees, subsequently forming bones. Adenoma cells were sparse among the ossified tissues. This is probably the first report of ossified pituitary adenoma associated with osteoid metaplasia. The pathogenesis of osteoid metaplasia in pituitary adenomas is possibly due to proliferative connective tissue resulting from degeneration of the pituitary adenoma; this connective tissue may possess osteogenic potency.
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PMID:Ossified prolactinoma: case report. 310 49

Two monoclonal antibodies with anti-human tumour reactivity were produced by murine hybridomas. One, 791T/36, is an IgG2b which was raised against a cultured human osteogenic sarcoma cell line, 791T. This antibody reacts with a high proportion of osteogenic sarcomas, and also with other tumour types. It has been used successfully as a tumour localising antibody in vivo and a targeting agent in vitro. The other antibody, C14/1/46, was raised against a human colonic adenoma. An IgM antibody, it reacts with most colorectal carcinoma cells but only with a small subpopulation of cells within the normal mucosa. It has been shown to recognise a difucosylated Type-2 blood-group chain, which has raised expression in colorectal carcinoma tissue.
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PMID:Antibodies against osteosarcoma and colon cancer. 659 16

The different subgroups of hypercalciuria cannot be separated clearly by the Pak calcium-load test. To improve the diagnosis and therapy we examined all relevant parameters of calcium metabolism in 32 patients with calcium urolithiasis and hypercalciuria (> 6.25 mmol/day). We also conducted bone mineral density measurements as well as the Pak calcium-load test. In most cases the pathophysiological constellations which Pak takes as the basis for his classification of hypercalciuria could not be shown. To date, diagnostics only insufficiently explains the genesis of hypercalciuria (except pHPT). As a consequence, a therapeutic problem arises: a low-calcium diet should not be generally recommended, since some patients may develop osteopenia. From our investigation the following diagnostic and therapeutic conclusions can be drawn: (1) Hypercalciuria in primary hyperparathyroidism should be treated by surgical removal of the adenoma. (2) The parathormone-independent osteogenic form should be treated with thiazides. (3) Hypercalciuria with increased 1.25-dihydroxyvitamin D should be treated by low-calcium diet.
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PMID:[Studies of calcium metabolism in patients with hypercalciuria]. 899 31

Neurofibromatosis type 1 (NF 1) is a syndrome with a predisposition for benign and malignant tumor development. Of the malignant neoplasms, osteogenic sarcomas are rare but have been described. There are some reports of patients with neurofibromatosis type 1 with a parathyroid adenoma and hyperparathyroidism. Also, there are studies that imply that the parathyroid hormone plays a role in the regulation and modulation of oseogenic sarcomas in vitro. We report about a 50-year-old female suffering from neurofibromatosis type 1, with a 3-year documented history of untreated hyperparathyroidism and a parathyroid adenoma. The patient developed a mandibular osteogenic sarcoma. To our knowledge, this is the first reported case occurring in the mandible. The unusual tumor site for a patient with neurofibromatosis type 1, the conjugation with hyperparathyroidism and the rapid growth of an osteogenic sarcoma are intriguing.
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PMID:Neurofibromatosis type 1, hyperparathyroidism, and osteosarcoma: interplay? 1243 89

Ossifying fibroma is an uncommon benign osteogenic neoplasm arising from cells of the periodontal ligament, typically with a slowly progressive enlargement of the affected bone. The neoplasm sometimes presents with hyperparathyroidism, most of which cases are due to familial parathyroid tumours. We report a rare case of ossifying fibroma of the mandible which showed very rapid growth and presented with primary hyperparathyroidism due to non-familial parathyroid adenoma. Despite improvement of parathyroid dysfunction after removal of the parathyroid adenoma, the tumour continued to grow very aggressively. The case required partial mandibular resection for complete resection of the tumour, and fixation of the remaining mandible with a titanium plate.
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PMID:Ossifying fibroma of the mandible with primary hyperparathyroidism due to non-familial parathyroid adenoma. 1713 36

Discriminant markers are required for accurate cancer screening. We evaluated genes frequently methylated in colorectal neoplasia to identify the most discriminant ones. Four genes specifically methylated in colorectal cancer [bone morphogenetic protein 3 (BMP3), EYA2, aristaless-like homeobox-4 (ALX4), and vimentin] were selected from 41 candidate genes and evaluated on 74 cancers, 62 adenomas, and 70 normal epithelia. Methylation status was analyzed qualitatively and quantitatively and confirmed by bisulfite genomic sequencing. Effect of methylation on gene expression was evaluated in five colon cancer cell lines. K-ras and BRAF mutations were detected by sequencing. Methylation of BMP3, EYA2, ALX4, or vimentin was detected respectively in 66%, 66%, 68%, and 72% of cancers; 74%, 48%, 89%, and 84% of adenomas; and 7%, 5%, 11%, and 11% of normal epithelia (P < 0.01, cancer or adenoma versus normal). Based on area under the curve analyses, discrimination was not significantly improved by combining markers. Comethylation was frequent (two genes or more in 72% of cancers and 84% of adenomas), associated with proximal neoplasm site (P < 0.001), and linked with both BRAF and K-ras mutations (P < 0.01). Cell line experiments supported silencing of expression by methylation in all four study genes. This study shows BMP3, EYA2, ALX4, and vimentin genes are methylated in most colorectal neoplasms but rarely in normal epithelia. Comethylation of these genes is common, and pursuit of complementary markers for methylation-negative neoplasms is a rational strategy to optimize screening sensitivity.
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PMID:Highly methylated genes in colorectal neoplasia: implications for screening. 1808 75